Spider venom molecule meets benchmarks to treat heart attack and stroke

 There is a venom library. What the fuck are our stroke researchers doing with this to help with stroke recovery? There is already this out there:

Snake Venom Helps Hydrogels Stop the Bleeding

Intravenous Ancrod for Treatment of Acute Ischemic Stroke

Biting back - snake venom contains toxic clotting factors

 

Snake Venom Could Hold Key To Alzheimer’s Breakthrough

Metrion taps Venomtech’s venom library for ion channel modulator discovery

The latest here:

Spider venom molecule meets benchmarks to treat heart attack and stroke

A spider venom molecule being investigated by a University of Queensland team has met critical benchmarks towards becoming a treatment for heart attack and stroke.

Associate Professor Nathan Palpant and Professor Glenn King from UQ's Institute for Molecular Bioscience have previously shown that the drug candidate Hi1a protects cells from the damage caused by heart attack and stroke.

Dr Palpant said a subsequent study has put the drug through a series of preclinical tests designed to mimic real-life treatment scenarios.

These tests are a major step towards helping us understand how Hi1a would work as a therapeutic – at what stage of a heart attack it could be used and what the doses should be.

We established that Hi1a is as effective at protecting the heart as the only cardioprotective drug to reach Phase 3 clinical trials, a drug that was ultimately shelved due to side effects.

Importantly, we found that Hi1a only interacts with cells in the injured zone of the heart during an attack and doesn't bind to healthy regions of the heart – reducing the chance of side effects."

Dr. Nathan Palpant, Associate Professor, UQ's Institute for Molecular Bioscience

Professor King, who recently won the Prime Minister's Prize for Innovation for developing the world's first insecticides from spider venom, discovered Hi1a in the venom of the K'gari funnel web spider.

"Hi1a could reduce damage to the heart and brain during heart attacks and strokes by preventing cell death caused by lack of oxygen," Professor King said.

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"Our testing and safety studies from independent contract research organisations has provided evidence that Hi1a could be an effective and safe therapeutic."

Infensa Bioscience, a company co-founded by the researchers, raised $23 million in 2022 to develop Hi1a for commercial purposes.

Infensa CEO and UQ researcher, Associate Professor Mark Smythe, said cardiovascular disease is the leading cause of death globally.

"Most deaths from cardiovascular disease are caused by heart attacks and strokes, yet there are no drugs on the market that prevent the damage they cause," Dr Smythe said.

"An effective drug to treat heart attacks would have worldwide impact, providing a breakthrough to improve the lives of millions of individuals living with heart disease."

The research team included Dr Meredith Redd from IMB as well as Dr Melissa Reichelt and Dr Yusuke Yoshikawa from UQ's School of Biomedical Sciences.

The study was published in the world's leading cardiac journal The European Heart Journal.

Source:

University of Queensland

Journal reference:

Redd, M. A., et al. (2023). Acid-sensing ion channel 1a blockade reduces myocardial injury in rodent models of myocardial infarction. European Heart Journal. doi.org/10.1093/eurheartj/ehad793.

Exploring How Low Oxygen Post Conditioning Improves Stroke-Induced Cognitive Impairment: A Consideration of Amyloid-Beta Loading and Other Mechanisms

 This is interesting because almost all other research works on delivering more oxygen to the brain. Ask your doctor to reconcile. Can both be done at different times?

• supersaturated oxygen therapy (1)

• cortical oxygenation (1)

• Extracorporeal membrane oxygenation (2)

• Normobaric oxygen (12)

• oxygen (17)

• oxygen delivery (11)

• oxygen saturation (1)

• oxygen therapy (2)

• oxygen uptake (5)

Exploring How Low Oxygen Post Conditioning Improves Stroke-Induced Cognitive Impairment: A Consideration of Amyloid-Beta Loading and Other Mechanisms

Zidan Zhao^1,2,3, Rebecca J. Hood^1,2,3, Lin Kooi Ong^1,2,3,4,5, Giovanni Pietrogrande^1,2,3, Sonia Sanchez Bezanilla^1,2,3, Kirby E. Warren^1,2,3, Marina Ilicic^1,2,3, Murielle G. Kluge^1,2,3, Clifford TeBay^1,2,3, Ole P. Ottersen^6,7, Sarah J. Johnson^8,9, Michael Nilsson^2,3,4,9† and Frederick R. Walker^{1,2,3,4,9*†}

• ¹School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, NSW, Australia
• ²Priority Research Centre for Stroke and Brain Injury, University of Newcastle, Newcastle, NSW, Australia
• ³Hunter Medical Research Institute, Newcastle, NSW, Australia
• ⁴National Health and Medical Research Council Centre of Research Excellence in Stroke Rehabilitation and Brain Recovery, Heidelberg, VIC, Australia
• ⁵School of Pharmacy, Monash University Malaysia, Bandar Sunway, Malaysia
• ⁶Division of Anatomy, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway
• ⁷Office of the President, Karolinska Institutet, Stockholm, Sweden
• ⁸School of Electrical Engineering and Computing, University of Newcastle, Newcastle, NSW, Australia
• ⁹Centre for Rehab Innovations, University of Newcastle, Newcastle, NSW, Australia

Cognitive impairment is a common and disruptive outcome for stroke survivors, which is recognized to be notoriously difficult to treat. Previously, we have shown that low oxygen post-conditioning (LOPC) improves motor function and limits secondary neuronal loss in the thalamus after experimental stroke. There is also emerging evidence that LOPC may improve cognitive function post-stroke. In the current study we aimed to explore how exposure to LOPC may improve cognition post-stroke. Experimental stroke was induced using photothrombotic occlusion in adult, male C57BL/6 mice. At 72 h post-stroke animals were randomly assigned to either normal atmospheric air or to one of two low oxygen (11% O₂) exposure groups (either 8 or 24 h/day for 14 days). Cognition was assessed during the treatment phase using a touchscreen based paired-associate learning assessment. At the end of treatment (17 days post-stroke) mice were euthanized and tissue was collected for subsequent histology and biochemical analysis. LOPC (both 8 and 24 h) enhanced learning and memory in the 2nd week post-stroke when compared with stroke animals exposed to atmospheric air. Additionally we observed LOPC was associated with lower levels of neuronal loss, the restoration of several vascular deficits, as well as a reduction in the severity of the amyloid-beta (Aβ) burden. These findings provide further insight into the pro-cognitive benefits of LOPC.

Introduction

Cognitive impairment has been reported as one of the most debilitating side-effects of stroke, impacting up to 80% of survivors (1, 2). Problems with memory, learning, and attention can significantly impact a survivor's functional independence and several studies have reported that increased levels of cognitive impairment are associated with lower levels of self-reported quality of life (3). This situation has triggered a substantial effort both clinically and pre-clinically to develop effective strategies to improve cognitive function post-stroke (4, 5).

Currently, there are no approved therapeutic interventions for post-stroke cognitive impairment. Although promising, the use of individual pharmacological strategies e.g., donepezil and memantine, have a patchy record of success (2). Recent evidence has shown pro-cognitive effects of exogenously delivered growth hormone post-stroke (6–9). Another equally promising pro-cognitive therapy has been the use of intermittent exposure to a reduced oxygen environment (10, 11). This non-pharmacological approach has numerous advantages over current strategies including its well-characterized and acceptable safety-profile, relatively low cost, ease of delivery and scalability.

In the context of stroke, exposure to a low oxygen environment prior to induction of an ischemic event (up to and including 4 weeks prior) has been shown to produce robust neuroprotection (10). Whilst the exposure to low oxygen prior to an ischemic event is of interest, exposure post ischemic event is arguably a more translationally relevant time to evaluate. In this context, low oxygen post-conditioning (LOPC) has been demonstrated to exhibit significant therapeutic properties in the context of heart attack (12) and spinal cord injury (13) and there is a growing body of evidence to support its application post-stroke (14–19). Preclinical studies have shown LOPC to be neuroprotective (15), enhance neurogenesis (18, 19), and reduce the severity of secondary neuronal loss and atrophy in the thalamus (14, 17). LOPC has also been shown to improve motor function (15) and cognition (18, 19).

Despite evidence indicating the potential utility of LOPC as a therapy, the underlying mechanisms involved in driving the positive post-stroke exposure outcomes are relatively unknown. We have recently identified a number of mechanisms that correlate with post-stroke cognitive impairment including loss of neural tissue and vasculature, the accumulation of neurotoxic proteins including amyloid-beta (Aβ) (20), vascular leakage and aquaporin four (AQP4) depolarization (associated with effective clearance of neurotoxic proteins) (20). It is clear that post-stroke exposure to LOPC promotes neuronal survival and vascular growth (14, 15, 17), yet what remains unclear is whether LOPC improves other aspects of vascular function (i.e., AQP4 polarization), or whether these improvements can modulate the Aβ burden. Therefore, in this study we sought to consider whether LOPC influenced these mechanisms. We have also considered the impact of LOPC on several genes involved in regulating the expression of Aβ including production of Aβ [amyloid precursor protein (APP) (21); beta secretase enzyme−1 (BACE) (22); tumor necrosis factor α (TNFα) converting enzyme (TACE) (23)], transport of Aβ across the blood-brain barrier into the parenchyma [receptor for advanced glycation end products (RAGE) (24)], Aβ degrading enzymes [neprilysin (NEP) (25), endothelin-converting enzyme (ECE) (26) and insulin-degrading enzyme (IDE) (25)] and clearance of Aβ [low-density lipoprotein receptor-related protein 1 (LRP1) (27–29)].

 

Oxygen Cost During Walking in Individuals With Stroke: Hemiparesis Versus Cerebellar Ataxia

Useless. You describe a problem, give NO SOLUTION.  Not even any mention of normobaric oxygen. Does anybody in stroke have any clue at all in what they are doing?

• Normobaric oxygen (9)

Possible solutions: Obviously not vetted coming from me. Don't do them.

How to Improve Your Brain Function with An Oxygen Concentrator April 2018 

Or is it more important to increase the loading ability of red blood cells to carry more oxygen? 

Like this?

University of Glasgow Study Demonstrates the Ability of Oxycyte® to Supply Oxygen to Critical Penumbral Tissue in Acute Ischemic Stroke  August 2012

Or like this?

chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers. August 2017

 

The latest here:

Oxygen Cost During Walking in Individuals With Stroke: Hemiparesis Versus Cerebellar Ataxia

Show all authors

Maxence Compagnat, Jean-Christophe Daviet, Charles Batcho, ...

First Published February 24, 2020 Research Article Find in PubMed

https://doi.org/10.1177/1545968320907076

Article information

Abstract

Background.
Understanding the factors that limit mobility in stroke patients is fundamental for proposing appropriate rehabilitation strategies. A high oxygen cost during walking (Cw) has a strong impact on the community ambulation of hemiparetic patients. The Cw in poststroke cerebellar ataxia is poorly evaluated, unlike hemiparetic gait.  
Objective.
To compare the oxygen cost/self-selected walking speed (S) relationship in stroke individuals with cerebellar ataxia or hemiparetic gait.  
Methods. Thirty-three subjects were included (14 cerebellar stroke, 19 hemispheric stroke), with stroke confirmed by brain imaging and able to walk without human assistance. We measured Cw using the Metamax3B. The relationship between Cw and self-selected walking speed was modelled by logistic regression and then compared between the cerebellar and hemispheric groups.  
Results.
No significant difference was found between the 2 groups for all characteristics of the population, except motor impairments, spasticity, and ataxia (P < .01). We identified 2 separate Cw/S relationships with different logistic regression equations for the 2 groups. Faster than 0.4 m s⁻¹, Cw was 30.6% to 39.9% higher in patients with cerebellar stroke in comparison with hemispheric stroke individuals. The Cw was correlated with ataxia (r = 0.88; P < .001) in the cerebellar group, whereas there was a correlation with motor impairments (r = −0.61; P < .01), spasticity (r = 0.59; P < .01), and ataxia (r = 0.81; P < .01) in hemispheric stroke individuals.  
Conclusion.
The Cw in poststroke cerebellar ataxia is significantly higher compared with hemiparetic patients at an equivalent walking speed. The impact on community walking needs to be explored in stroke survivors with cerebellar stroke.

Keywords oxygen cost, walking, cerebellar stroke, hemispheric stroke, energy expenditure

Introduction

Walking is a meaningful activity in view of social participation and quality of life in individuals with poststroke sequelae.¹ Unfortunately, at 6 months after stroke, less than 30% of patients have regained the ability to walk independently, and almost 50% believe they have restricted mobility in the community.² The limitation of walking activity may be due to metabolic factors, because individuals with stroke suffer from significant cardiorespiratory deconditioning. The VO₂ peak in these patients was found to be 26% to 87% lower than that of age- and sex-matched healthy control subjects.³ In addition, secondary to their neurological impairments, stroke individuals consume between 1.5 and 2 times more oxygen when walking than healthy subjects, which causes intense metabolic strain, leading to an increase in fatigability and consequently to limitation of activity.⁴ The walking efficiency of an individual can be quantified by measuring the oxygen cost of walking (Cw), which is the consumption of oxygen per meter expressed in mL kg⁻¹ m⁻¹.⁵ The Cw is of crucial importance in stroke individuals, because this parameter is associated with walking ability⁴ and social participation.⁶ Franceschini et al reported that stroke individuals with a Cw greater than 0.55 mL kg⁻¹ m⁻¹ have walking restrictions for community activities.⁶
Neurological impairments following stroke depend on the damaged neurological structure. Thus, after a hemispheric stroke, damage to the pyramidal pathway is classically responsible for spastic hemiparesis, associated or not with cognitive, sensory, and neuro-vegetative impairments, depending on the extent of the injury. These impairments lead to a stiff knee gait and circumduction of the impaired lower limb.⁷ After a cerebellar stroke, individuals typically have coordination and balance disorders, resulting in characteristic ataxic walking.⁸
Among these 2 types of clinical conditions, several deficiencies may induce an increase in Cw. The presence of co-contractions related to spasticity are associated with an increase in Cw.^9,10 The increase in the variability of the trajectories of the limb segments due to the loss of selectivity of the central control¹¹ is also associated with the increase in Cw.^9,12
The gait patterns of cerebellar stroke and hemispheric stroke patients are very different. Cerebellar ataxic gait is typically characterized by an increased step width, variable foot placement, irregular foot trajectories, and a resulting unstable, stumbling walking path with very high movement variability and a high risk of falling. This type of gait is clinically recognizable and is easily differentiated from the gait pattern of hemiparetic individuals, who have a loss of symmetry, with a tendency for increased stance time on the unaffected limb. The affected lower limb appears stiff-legged, demonstrating a synergy pattern with extension, adduction, internal rotation of the hip, extension of the knee, and plantarflexion/inversion of the foot/ankle. This extended limb posture leads to an impairment of limb clearance during the swing phase, and compensatory maneuvers include hip hiking, lateral trunk sway, circumduction, and, less commonly, contralateral vaulting (Olney and Richards, 1996)¹³. In a previous study, we showed that the relationship between the Cw and self-selected walking speed (S) was strong in individuals with poststroke hemispheric sequelae (r = −0.94; R² = 0.97, P < .001).¹⁴ We assumed from this work and our clinical experience that this strong relationship is explained by the fact that the walking pattern was similar from one hemiparetic individual to another. In addition, Zamparo et al, in a similar study, compared the Cw of 20 hemiparesis patients and 17 healthy subjects. The authors found different Cw/S relationships between the groups of subjects (P < .001 in the covariance analysis).¹⁵
The Cw/S relationship seems to be a characteristic of the walking efficiency of individuals that would be specific to the individual’s walking pattern. To support this hypothesis, it must be compared with a very different gait pattern, that of ataxic individuals with post–cerebellar stroke. To our knowledge, no studies have explored the Cw of cerebellar stroke individuals or the Cw/S relationship.
The objective of this study was to compare the relationship between Cw and S in individuals with cerebellar and hemispheric stroke. Our hypothesis is that individuals with cerebellar stroke sequelae do not have the same Cw/S relationship as hemiparetic stroke individuals, due to the differences in impairments and gait patterns between these 2 stroke types. If this hypothesis is confirmed, this would imply that a specific Cw/S relationship could be identified for patients, depending on the stroke location.

More at link. 

Mortality and morbidity in acutely ill adults treated with liberal vs conservative oxygen therapy (IOTA): A systematic review and meta-analysis

Useless since they excluded HBOT from the research.
https://www.mdlinx.com/internal-medicine/medical-news-article/2018/05/01/oxygen-therapy-acutely-ill-adults-systematic/7512097/?

The Lancet — | May 01, 2018

Chu DK, et al. - The efficacy and safety of liberal vs conservative oxygen therapy were systematically reviewed in acutely ill adults. Researchers gained high-quality evidence indicating that liberal oxygen therapy increases mortality without improving other patient-important outcomes. Above saturation of peripheral oxygen range of 94–96%, supplemental oxygen might become unfavourable. The conservative administration of oxygen therapy was thus supported.

sponsor

Methods

• Researchers searched for randomised controlled trials comparing liberal and conservative oxygen therapy in acutely ill adults (aged ≥18 years) via inquiring the Cochrane Central Register of Controlled Trials, MEDLINE, Embase, HealthSTAR, LILACS, PapersFirst, and the WHO International Clinical Trials Registry from inception to Oct 25, 2017, in the Improving Oxygen Therapy in Acute-illness (IOTA) systematic review and meta-analysis.
• They limited the studies to patients with chronic respiratory diseases or psychiatric disease; patients on extracorporeal life support, or patients treated with hyperbaric oxygen therapy or elective surgery were excluded.
• Studies were screened and summary estimates were extracted independently and in duplicate.
• Individual patient-level data from survival curves was also extracted.
• Mortality (in-hospital, at 30 days, and at longest follow-up) and morbidity (disability at longest follow-up, risk of hospital-acquired pneumonia, any hospital-acquired infection, and length of hospital stay) assessed by random-effects meta-analyses were the main outcomes.
• Quality of evidence was assessed using the grading of recommendations assessment, development, and evaluation approach. 

Results

• Researchers identified 25 randomised controlled trials enrolling 16,037 patients with sepsis, critical illness, stroke, trauma, myocardial infarction, or cardiac arrest, and patients who had emergency surgery.
• They noted that in comparison to a conservative oxygen strategy, a liberal oxygen strategy (median baseline saturation of peripheral oxygen [SpO₂] across trials, 96% [range 94–99%, IQR 96–98]) increased mortality in-hospital (relative risk [RR] 1·21, 95% CI 1·03–1·43, I²=0%, high quality), at 30 days (RR 1·14, 95% CI 1·01–1·29, I²=0%, high quality), and at longest follow-up (RR 1·10, 95% CI 1·00–1·20, I²=0%, high quality).
• The groups were similar in terms of morbidity outcomes.
• Findings were noted to be robust to trial sequential, subgroup, and sensitivity analyses.

Read the full article on The Lancet

Too Liberal Use of Oxygen Increases Risk of Death in Acutely Ill Adult Patients

How is your hospital addressing the pros and cons of oxygen therapy?

How to Improve Your Brain Function with An Oxygen Concentrator April 2018 

Then there are the 30 posts on HBOT.

Too Liberal Use of Oxygen Increases Risk of Death in Acutely Ill Adult Patients

Tags:

• Angina Pectoris/MI
• Intensive Care
• Sepsis
• Stroke

Read/Add Comments | Email This | Print This

HAMILTON, Ontario -- April 27, 2018 -- Researchers have found there is such a thing as too much oxygen for acutely ill adults.

Extensive data analyses in a study published in The Lancet showed that supplemental oxygen, when given liberally to these patients, increases the risk of death without improving other health outcomes.

“Supplemental oxygen is administered to millions of acutely unwell patients around the world every day,” said senior author Waleed Alhazzani, MD, St. Joseph’s Healthcare Hamilton, and McMaster University, Hamilton, Ontario. “Despite this, there is a striking lack of definitive, high-quality evidence related to this common intervention.”

The researchers searched electronic academic databases from their inception through to October 2017 for randomised controlled trials done worldwide which compared liberal versus conservative oxygen therapy and death rates, as well as impacts on such aspects as disability, infections, and hospital length of stay.

The 25 randomised controlled trials comprised more than 16,000 adult patients with sepsis, stoke, trauma, emergency surgery, myocardial infarction or cardiac arrest.

Data analysis demonstrated that, compared with the conservative strategy, liberal administration of oxygen resulted in increased in-hospital death by 21%. Additional analyses suggested that the more supplemental oxygen patients were given, the higher their risk was for death.

The incidence of other conditions, such as infections or length of hospital stay, were similar between the 2 groups.

The researchers estimated 1 additional death for every 71 patients treated with a liberal oxygen strategy.

“Our findings are distinct from the pervasive view that liberal oxygen therapy for acute illnesses is at worst, harmless,” said Dr. Alhazzani.

“Prior practice guidelines and medical directives on oxygen therapy for acute illnesses have been inconsistent,” said first author Derek Chu, MD, McMaster University. “Our results provide much-needed clarification by showing, with high-quality evidence, that administering too much supplemental oxygen increases mortality among a broad range of acute illnesses. Currently, patients are frequently given supplemental oxygen and at excessive levels. A simple change to current practice -- being more moderate and cautious with how much oxygen is administered to acutely unwell patients -- could save lives.”

Reference: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)30479-3/fulltext

SOURCE: McMaster University

Effect of Routine Low-Dose Oxygen Supplementation on Death and Disability in Adults With Acute Stroke

Well, well you fucking idiots you used the Rankin scale which has no objectivity and discriminatory power at all. If you truly wanted to know if it helped you would do PET scans to see if the extent of penumbra damage was less. It really chaps my ass on reading bad research trials that stroke leadership doesn't prevent.
I bet they had no clue how much extra oxygen got to the brain because they didn't do this:

Brain Tissue Oxygen Monitoring and the Intersection of Brain and Lung: A Comprehensive Review

Hopefully this latest result doesn't stop further research since this 2005 pilot study showed promise:

 

A Pilot Study of Normobaric Oxygen Therapy in Acute Ischemic Stroke 2005

 

Or is it more important to increase the loading ability of red blood cells to carry more oxygen? 

Like this?

University of Glasgow Study Demonstrates the Ability of Oxycyte® to Supply Oxygen to Critical Penumbral Tissue in Acute Ischemic Stroke  August 2012

 

Or like this?

chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers.

 

Or maybe you want to starve your brain of oxygen, tested in mice;

This is a fascinating idea, treat your recently oxygen starved brain with more reduced oxygen supply.

 

 

The failed and bad research trial here.

Effect of Routine Low-Dose Oxygen Supplementation on Death and Disability in Adults With Acute Stroke 

Christine Roffe, MD^1,2; Tracy Nevatte, PhD^2,3; Julius Sim, PhD²; et al Jon Bishop, PhD⁴; Natalie Ives, MSc⁴; Phillip Ferdinand, MRCP¹; Richard Gray, MSc^4,5; for the Stroke Oxygen Study Investigators and the Stroke OxygenStudy Collaborative Group

Author Affiliations

JAMA. 2017;318(12):1125-1135. doi:10.1001/jama.2017.11463

Key Points

Question  Does routine prophylactic low-dose oxygen supplementation after acute stroke improve functional outcome?
Findings  In this randomized clinical trial, 8003 patients with acute stroke were randomized within 24 hours of admission to 3 days of continuous oxygen, nocturnal oxygen, or control. After 3 months, there was no significant difference in death and disability for the combined oxygen groups compared with control (odds ratio, 0.97) or for the continuous oxygen group compared with the nocturnal oxygen group (odds ratio, 1.03).
Meaning  Routine low-dose oxygen did not improve outcomes in nonhypoxic patients after acute stroke.

Abstract

Importance  Hypoxia is common in the first few days after acute stroke, is frequently intermittent, and is often undetected. Oxygen supplementation could prevent hypoxia and secondary neurological deterioration and thus has the potential to improve recovery.
Objective  To assess whether routine prophylactic low-dose oxygen therapy was more effective than control oxygen administration in reducing death and disability at 90 days, and if so, whether oxygen given at night only, when hypoxia is most frequent, and oxygen administration is least likely to interfere with rehabilitation, was more effective than continuous supplementation.
Design, Setting, and Participants  In this single-blind randomized clinical trial, 8003 adults with acute stroke were enrolled from 136 participating centers in the United Kingdom within 24 hours of hospital admission if they had no clear indications for or contraindications to oxygen treatment (first patient enrolled April 24, 2008; last follow-up January 27, 2015).
Interventions  Participants were randomized 1:1:1 to continuous oxygen for 72 hours (n = 2668), nocturnal oxygen (21:00 to 07:00 hours) for 3 nights (n = 2667), or control (oxygen only if clinically indicated; n = 2668). Oxygen was given via nasal tubes at 3 L/min if baseline oxygen saturation was 93% or less and at 2 L/min if oxygen saturation was greater than 93%.
Main Outcomes and Measures  The primary outcome was reported using the modified Rankin Scale score (disability range, 0 [no symptoms] to 6 [death]; minimum clinically important difference, 1 point), assessed at 90 days by postal questionnaire (participant aware, assessor blinded). The modified Rankin Scale score was analyzed by ordinal logistic regression, which yields a common odds ratio (OR) for a change from one disability level to the next better (lower) level; OR greater than 1.00 indicates improvement.
Results  A total of 8003 patients (4398 (55%) men; mean [SD] age, 72 [13] years; median National Institutes of Health Stroke Scale score, 5; mean baseline oxygen saturation, 96.6%) were enrolled. The primary outcome was available for 7677 (96%) participants. The unadjusted OR for a better outcome (calculated via ordinal logistic regression) was 0.97 (95% CI, 0.89 to 1.05; P = .47) for oxygen vs control, and the OR was 1.03 (95% CI, 0.93 to 1.13; P = .61) for continuous vs nocturnal oxygen. No subgroup could be identified that benefited from oxygen. At least 1 serious adverse event occurred in 348 (13.0%) participants in the continuous oxygen group, 294 (11.0%) in the nocturnal group, and 322 (12.1%) in the control group. No significant harms were identified.
Conclusions and Relevance  Among nonhypoxic patients with acute stroke, the prophylactic use of low-dose oxygen supplementation did not reduce death or disability at 3 months. These findings do not support low-dose oxygen in this setting.(That is an incorrect statement you blithering idiots)
Trial Registration  ISRCTN Identifier: ISRCTN52416964

 

Study: Giving Oxygen No Help After Stroke

Well, well you fucking idiots you used the Rankin scale which has no objectivity and discriminatory power at all. If you truly wanted to know if it helped you would do PET scans to see if the extent of penumbra damage was less.
I bet they had no clue how much extra oxygen got to the brain because they didn't do this:

Brain Tissue Oxygen Monitoring and the Intersection of Brain and Lung: A Comprehensive Review

Hopefully this latest result doesn't stop further research since this 2005 pilot study showed promise:

 

A Pilot Study of Normobaric Oxygen Therapy in Acute Ischemic Stroke 2005

 

Or is it more important to increase the loading ability of red blood cells to carry more oxygen? 

Like this?

University of Glasgow Study Demonstrates the Ability of Oxycyte® to Supply Oxygen to Critical Penumbral Tissue in Acute Ischemic Stroke  August 2012

 

Or like this?

chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers.

 

Or maybe you want to starve your brain of oxygen, tested in mice;

This is a fascinating idea, treat your recently oxygen starved brain with more reduced oxygen supply.

 

 

The failed and bad research trial here.

Study: Giving Oxygen No Help After Stroke

Trial showed no effect on death, disability in non-hypoxic acute stroke

• by Crystal Phend, Senior Associate Editor, MedPage Today September 26, 2017
• This article is a collaboration between MedPage Today® and:
  

Acute stroke patients with sufficient oxygenation levels didn't benefit from provision of low-dose supplemental oxygen, whether continuous or at night only, the SO₂S trial showed.
Three days of oxygen therapy -- given at 3 L/min for a baseline oxygen saturation of 93% or less and at 2 L/min over that -- had no impact on death and disability at 3 months as measured by modified Rankin Scale score with ordinal logistic regression (common OR 0.97 for a one level improvement, 95% CI 0.89-1.05) compared with oxygen given only when clinically indicated.
Those pooled results held also for the two oxygen arms individually, with no significant difference between continuous administration and nighttime use only (OR 1.03, 95%CI 0.93-1.13), reported Christine Roffe, MD, of Keele University in Stoke-on-Trent, England, and colleagues in the Journal of the American Medical Association.
"No subgroup could be identified that benefited from oxygen," they wrote, concluding that "These findings do not support low-dose oxygen in this setting."
The findings from the pragmatic clinical trial of 8,003 patients with acute stroke randomized to the three treatment groups within 24 hours of admission came on the heels of another large trial negative for supplemental oxygen in a different setting -- acute MI.
DETO2X-AMI, reported at the European Society of Cardiology (ESC) meeting and online in the New England Journal of Medicine in August 2017, showed no impact on 1-year all-cause mortality, rehospitalization for MI, extent of myocardial injury, or other outcomes from routine use of 6 L/min oxygen supplementation versus room air for 6 to 12 hours.
While supplemental oxygen has been routine in the U.S. in acute MI, cardiologists at ESC agreed with an editorialist regarding patients without hypoxemia: "It is clearly time for clinical practice to change to reflect this definitive evidence."
In stroke, though, Roffe's group suggested their results might still leave a chance at benefit for one group.
Whether very early administration of high-dose oxygen might help at-risk brain tissue or broaden the the time window for neuroprotection or thrombolysis remains to be seen definitively in the PROOF trial. An underpowered subgroup analysis in SO₂S showed no difference in the 101 participants enrolled within 3 hours of symptom onset as in those enrolled later.
For other subgroups though, the researchers wrote: "Because of the large overall size of this trial, these patient subgroups were each sufficiently large for the lack of observed benefit to be likely real and not a false negative."
They noted that low-dose oxygen supplementation as used in their trial probably wasn't enough to prevent severe desaturation, which occurred similarly with oxygen and without. But randomized trials of high-flow oxygen treatment in acute stroke haven't suggested higher doses are any better for outcomes.
The low-dose oxygen tested in SO₂S wasn't associated with more treatment-related adverse events or a difference in serious adverse events overall.

The project was funded by the NIHR Health Technology Assessment Programme and the Research for Patient Benefit Programme.
Roffe disclosed support from the Research for Patient Benefit Programme and the Health Technology Assessment Programme of the National Institute for Health Research and relevant relationships with Air Liqude and the PROOF trial.

• Primary Source

  Journal of the American Medical Association

  Source Reference: Roffe C, et al "Effect of routine low-dose oxygen supplementation on death and disability in adults with acute stroke, The Stroke Oxygen Study Randomized Clinical Trial" JAMA 2017;318:1125-1135; DOI:10.1001/jama.2017.11463.

You could stay forever young (or young for a long time) with this diabetes drug

This highlighted possibility seems like a great idea for hyperacute use for extra oxygen, much easier than HBOT. All we need to do is to run some research trials on this which won't occur because we have NO strategy to solve any of the problems in stroke and NO one who is actively engaged in solutioning stroke problems. Our stroke associations are sitting on their asses just putting out press releases. They are not for survivors so don't expect anything from them. You're screwed unless you are wealthy enough to hire your own researchers to solve these problems. Do not ask for this drug from your doctor, that would be prescribing your own medicine which is illegal.
http://finance.yahoo.com/news/could-stay-forever-young-young-205518256.html

We can’t live forever yet, but we may be getting closer to living a bit longer. Thanks to a new anti-aging drug, scientists believe they may have found a way to stop the body from falling victim to the perils of old age, including degenerative diseases like Alzheimer’s and Parkinson’s. The hope is that the drug would not only allow people to live longer, but would also allow its users to maintain a relatively high level of health, making their extended years feel more like a gift than a burden.

With the goal of sustaining healthy human life to the age of 110 or even 120, the diabetes drug metformin has already met with success in animal trials, and now, the U.S. Food and Drug Administration has given the green light for human trials. Ideally, it would allow for people at the age of 70 to enjoy the health of 50-year-olds, an unprecedented feat in medicine.

“If you target an aging process and you slow down aging then you slow down all the diseases and pathology of aging as well,” said Professor Gordon Lithgow of the Buck Institute for Research on Aging in California, who serves as one of the study advisors. “That’s revolutionary,” he continued. “That’s never happened before.”

The drug, which is cheaply available for just $0.16 a day, works by boosting the number of oxygen molecules released into a cell, which in turn seems to benefit the robustness and longevity of the body’s basic building blocks. The proposed test will involve around 3,000 individuals between the ages of 70 and 80 who either have or are at risk for cancer, heart disease, and dementia. Scientists hope that metformin would not only be able to stop the onset of these diseases, but also lead to sustained life.

“I have been doing research into aging for 25 years and the idea that we would be talking about a clinical trial in humans for an anti-aging drug would have been though inconceivable,” Lithgow said. “But there is every reason to believe it’s possible. The future is taking the biology that we’ve now developed and applying it to humans. Twenty years ago aging was a biological mystery. Now we are starting to understand what is going on.”

Fish Oil in Diet Promotes Blood Cell Growth in Mice

Would this help us have more red blood cells to carry more oxygen to our brain? Do not attempt any experiment with this on yourself.
http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/52193?

Oxygen therapy in stroke: past, present, and future - Nov. 2006

Hey, it's only 8 years old. Has any stroke protocol been written up on this? Or does each patient need to ask their doctor if regular oxygen supplied in the first 24 hours is useful? I know of no place I could ask such a f*cking simple question.
http://www.ncbi.nlm.nih.gov/pubmed/18706016

Singhal AB¹.

Author information

Abstract

Oxygen is frequently administered to patients with suspected stroke. However, the role of oxygen therapy in ischemic stroke remains controversial in light of the failure of three clinical trials of hyperbaric oxygen therapy to show efficacy, and the fear of exacerbating oxygen free radical injury. The previous trials had several shortcomings, perhaps because they were designed on basis of anecdotal case reports and little preclinical data. Most animal studies concerning oxygen therapy in stroke have been conducted over the last 6 years. Emerging data suggests that hyperbaric and even normobaric oxygen therapy can be effective if used appropriately, and raises the tantalizing possibility that hyperoxia can be used to extend the narrow therapeutic time window for stroke thrombolysis. This article reviews the history, rationale, mechanisms of action and adverse effects of hyperoxia, the key results of previous hyperoxia studies, and the potential role of oxygen therapy in contemporary stroke treatment.

Or maybe you want to deliver it to yourself. Nah, that would be practicing medicine
Oxygen from Powder