Effect of hypoxic-ischemic time on reduction of hypoxic-ischemic brain injury by sevoflurane postconditioning in neonatal rats

You will have to ask your great stroke association to do followup studies on humans to see if this is a good hyperacute therapy. If your doctor and stroke hospital do no followup with this they are just proving their total incompetency about anything to do with stroke. Fire them.
http://pesquisa.bvsalud.org/enfermeria/resource/es/wpro-935304
Ying Xu; Ye Tian; Hang Xue; Feng Pan; Xingyue Li; Yating Yang; Ping Zhao.

Chinese Journal of Anesthesiology; 36(2): 207-210, 2016.

Artículo en Ch | WPRIM | ID: wpro-935304

Resumen

Objective To evaluate the effect of hypoxic-ischemic time on reduction of hypoxic-ischemic brain injury by sevoflurane postconditioning in neonatal rats.Methods Two hundred and ten 7-day-old Sprague-Dawley rats (105 male,105 female),weighing 13-17 g,were randomly divided into 7groups (n=30 each) using a random number table:sham operation group (group Sham),hypoxia-ischemia group (group HI),and sevoflurane postconditioning at different hypoxic-ischemic time point groups (P0,P3,P6,P 12 and P24 groups).Immediately after ligation of the left common carotid artery,and at 3,6,12 and 24 h after ligation,the rats inhaled the mixed gas containing 2％ sevoflurane for 30 min in P0,P3,P6,P13 and P24 groups,respectively.The fatality was recorded within 7 days after establishment of the model.At 7 days after establishment of the model,the rats were sacrificed,the brains were removed,and the right and left cerebral hemispheres were weighed separately,and the left/right cerebral hemisphere weight ratio was calculated.The hippocampal CA1 region and posterior cingulate gyrus were isolated,and the ratio of density of normal neurons in the left to the right was calculated.
Results Compared with group Sham,the left cerebral hemisphere weight,left/right cerebral hemisphere weight ratio,and ratio of density of normal neurons were significantly decreased,and the fatality rate was increased in the other six groups (P<0.05).Compared with group HI,the left cerebral hemisphere weight,left/right cerebral hemisphere weight ratio,and ratio of density of normal ncurons were significantly increased in P0,P3 and P6 groups (P<0.05),and no significant change was found in the parameters mentioned above in P12 and P24 groups (P>0.05).Compared with group P6,the left cerebral hemisphere weight,left/right cerebral hemisphere weight ratio,and ratio of density of normal neurons were significantly increased in P0 and P3 groups (P< 0.05).There was no significant difference in the parameters mentioned above between group P0 and group P3 (P>0.05).
Conclusion Sevoflurane postconditioning performed within 6 h of hypoxia-ischemia can reduce hypoxic-ischemic brain injury,and it provides no cerebral protection if exceeding 12 h.

Biblioteca responsable: WPRO

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Effects of Postconditioning on Neurogenesis and Angiogenesis During the Recovery Phase After Focal Cerebral Ischemia

Whatever the hell postconditioning is.
Earlier research explanation of it here:

Ischemic postconditioning as a novel avenue to protect against brain injury after stroke

The new one here:

Effects of Postconditioning on Neurogenesis and Angiogenesis During the Recovery Phase After Focal Cerebral Ischemia

1. Elga Esposito, PhD,
2. Kazuhide Hayakawa, PhD,
3. Takakuni Maki, MD, PhD,
4. Ken Arai, PhD and
5. Eng H. Lo, PhD

+ Author Affiliations

1. From the Departments of Neurology and Radiology, Massachusetts General Hospital, Harvard Medical School, Boston.

1. Correspondence to Eng H. Lo, PhD, or Elga Esposito, PhD, Massachusetts General Hospital, E Bldg 149, 13th St, Charlestown, MA 02129. E-mail lo@helix.mgh.harvard.edu or eesposito@partners.org

Abstract

Background and Purpose—Postconditioning may be a clinically feasible way to protect the brain after a stroke. However, its effects during the recovery phase post stroke remain to be fully elucidated. Here, we examine the hypothesis that ischemic postconditioning amplifies neurogenesis and angiogenesis during stroke recovery.

Methods—Male Sprague–Dawley rats were subjected to 100-minute transient middle cerebral artery occlusion (MCAO) or postconditioning (100-minute middle cerebral artery occlusion plus 10-minute reperfusion plus 10-minute reocclusion). After 2 weeks, infarct volumes, behavioral outcomes, and immunohistochemical markers of neurogenesis and angiogenesis were quantified.

Results—Postconditioning significantly reduced infarction and improved neurological outcomes. Concomitantly, brains subjected to postconditioning showed an increase in doublecortin/BrdU and collagen-IV/Ki67-positive cells.

Conclusions—These results suggest that therapeutic effects of postconditioning may involve the promotion of neurogenesis and angiogenic remodeling during the recovery phase after focal cerebral ischemia.

Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats

I don't think our doctors are going to agree to stopping blood flow several times after the clot is removed. But it is a fascinating idea.  I'll have to add reperfusion injury as another problem in the neuronal cascade of death.
http://www.nature.com/jcbfm/journal/v26/n9/full/9600348a.html

Heng Zhao^1,2, Robert M Sapolsky^1,2,3 and Gary K Steinberg^1,2

1. ¹Department of Neurosurgery, Stanford University, Stanford, California, USA
2. ²Department of Stanford Stroke Center, Stanford University, Stanford, California, USA
3. ³Department of Biological Sciences, Stanford University, Stanford, California, USA

Correspondence: Dr H Zhao, Department of Neurosurgery, Stanford University School of Medicine, 1201 Welch Rd, Rm P306, MSLS Bld, Stanford, California 94305-5327, USA. E-mail: hzhao@stanford.edu

Received 24 March 2006; Revised 25 April 2006; Accepted 3 May 2006; Published online 31 May 2006.

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Abstract

Cerebral ischemic preconditioning protects against stroke, but is clinically feasible only when the occurrence of stroke is predictable. Reperfusion plays a critical role in cerebral injury after stroke; we tested the hypothesis that interrupting reperfusion lessens ischemic injury. We found for the first time that such postconditioning with a series of mechanical interruptions of reperfusion significantly reduces ischemic damage. Focal ischemia was generated by permanent distal middle cerebral artery (MCA) occlusion plus transient bilateral common carotid artery (CCA) occlusion. After 30 secs of CCA reperfusion, ischemic postconditioning was performed by occluding CCAs for 10 secs, and then allowing for another two cycles of 30 secs of reperfusion and 10 secs of CCA occlusion. Infarct size was measured 2 days later. Cerebral blood flow (CBF) was measured in animals subjected to permanent MCA occlusion plus 15 mins of bilateral CCA occlusion, which demonstrates that postconditioning disturbed the early hyperemia immediately after reperfusion. Postconditioning dose dependently reduced infarct size in animals subjected to permanent MCA occlusion combined with 15, 30, and 60 mins of bilateral CCA occlusion, by reducing infarct size approximately 80%, 51%, and 17%, respectively. In addition, postconditioning blocked terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling-positive staining, a marker of apoptosis, in the penumbra 2 days after stroke. Furthermore, in situ superoxide detection using hydroethidine suggested that postconditioning attenuated superoxide products during early reperfusion after stroke. In conclusion, postconditioning reduced infarct size, most plausibly by blocking apoptosis and free radical generation. With further study it may eventually be clinically applicable for stroke treatment.

The neuroprotective actions of hypoxic preconditioning and postconditioning in a neonatal rat model of hypoxic ischemic brain injury

This is a fascinating idea, treat your recently oxygen starved brain with more reduced oxygen supply. Completely opposite of the HBOT theories.
http://www.ncbi.nlm.nih.gov/pubmed/23274537

Abstract

Perinatal hypoxic-ischemic (HI) brain injury remains a major contributing factor to newborn mortality and morbidity. Preconditioning with mild hypoxia has been shown to protect the brain against HI insults and it has recently been shown that mild hypoxia administered after a brain injury, termed 'postconditioning' can protect the adult mouse brain. Here, we have investigated the neuroprotective effects of hypoxic pre- and postconditioning in a neonatal rat model of HI brain injury. 7-day-old Sprague-Dawley rat pups underwent unilateral common carotid artery ligation in combination with 3h at 8% oxygen. Hypoxic treatments consisted of either 3h of 5.5% oxygen performed 24h prior to injury (preconditioning); or 1h of 8% oxygen 24h post-injury, performed once a day for 5 days (postconditioning). Brains were removed 1 week post-injury for histological analysis. HI caused an increase in lesion volume compared to controls and both hypoxic pre- and postconditioning reduced the degree of brain damage following HI injury. To specifically examine neuronal loss, NeuN immunohistochemistry and regional brain area analysis was performed. HI injury caused a loss in NeuN staining in all brain regions examined. Preconditioning with hypoxia resulted in a significant reduction in cortical, hippocampal and striatal neuronal loss, compared with HI alone. Hypoxic postconditioning resulted in a reduction in cortical and striatal neuronal loss, compared to HI alone. Our results further support the clinical potential for mild hypoxia in the treatment of brain injuries, either as a pre- or post-injury treatment strategy.