You'll just have to ask your doctor what remote ischemic postconditioning is. My google searches came up with no easy explanation.
Remote Ischemic Postconditioning vs. Physical Exercise After Stroke: an Alternative Rehabilitation Strategy?
Molecular Neurobiology (2021)
Abstract
There remain debates on neuroprotection and rehabilitation techniques for acute ischemic stroke patients. Therapeutic physical exercise following stroke has shown promise but is challenging to apply clinically. Ischemic conditioning, which has several clinical advantages, is a potential neuroprotective method for stroke rehabilitation that is less understood. In the present study, the rehabilitative properties and mechanisms of physical exercise and remote ischemic postconditioning (RIPostC) after stroke were compared and determined. A total of 248 adult male Sprague-Dawley rats were divided into five groups: (1) sham, (2) stroke, (3) stroke with intense treadmill exercise, (4) stroke with mild treadmill exercise, and (5) stroke with RIPostC. Focal ischemia was evaluated by infarct volume and neurological deficit. Long-term functional outcomes were represented through neurobehavioral function tests: adhesive removal, beam balance, forelimb placing, grid walk, rota-rod, and Morris water maze. To further understand the mechanisms underlying neurorehabilitation and verify the presence thereof, we measured mRNA and protein levels of neuroplasticity factors, synaptic proteins, angiogenesis factors, and regulation molecules, including HIF-1α, BDNF, TrkB, and CREB. The key role of HIF-1α was elucidated by using the inhibitor, YC-1. Both exercise intensities and RIPostC significantly decreased infarct volumes and neurological deficits and outperformed the stroke group in the neurobehavioral function tests. All treatment groups showed significant increases in mRNA and protein expression levels of the target molecules for neurogenesis, synaptogenesis, and angiogenesis, with intermittent further increases in the RIPostC group. HIF-1α inhibition nullified most beneficial effects and indicative molecule expressions, including HIF-1α, BDNF, TrkB, and CREB, in both procedures. RIPostC is equally, or superiorly, effective in inducing neuroprotection and rehabilitation compared to exercise in ischemic rats. HIF-1α likely plays an important role in the efficacy of neuroplasticity conditioning, possibly through HIF-1α/BDNF/TrkB/CREB regulation.
Introduction
Stroke is the fifth leading cause of death and the leading cause of disability worldwide [1]. Over the past two decades, the economic and disease burden of stroke has increased dramatically and is anticipated to continue growing due to aging populations and shifting dependency ratios [2]. Meanwhile, the development of neuroprotective and rehabilitative strategies remains a challenge in improving the quality of life in post-stroke patients after initial life-saving measures.
The effect of physical exercise in neuroprotection and rehabilitation following ischemic stroke has been extensively studied and is recommended for all post-stroke patients [3]. Physical exercise mitigates many detrimental consequences of stroke, including memory loss [4], neurological impairment [5], and motor function [6]. However, there is significant variability in the extent of neuroprotection conferred by exercise, depending on the time of initiation, the dosage, and the type of activity [7]. While there is ample recent evidence to support the ability of physical exercise to promote recovery through increased neuroplasticity, a key component of successful rehabilitation [8], a number of obstacles still remain in implementing post-stroke exercise in stroke rehabilitation. Stroke patients are generally refractory to physical activity and are likely to face challenges in complying with post-stroke exercise plans, especially in the earlier post-stroke period [9], which can impair rehabilitation potential during the most salient stages of disease progression. Given patients’ varying forms and extent of disability after a stroke, it also remains a challenge to research and implement a standardized treatment plan for stroke patients. Patients’ amenability to physical activity may vary depending on age, motivation, and other factors. Moreover, recent clinical trials of stroke patients undergoing early physical exercise did not show consistent rehabilitative benefits and instead revealed that very early exercise rehabilitation, such as within 24 h of the stroke, may worsen the post-stroke prognosis [10]. In order to bridge these challenges in the continuum of post-stroke rehabilitation and care, there is growing interest in alternative rehabilitation options, namely ischemic conditioning.
Ischemic conditioning leverages the neuroplastic and neuroprotective benefits of temporary and controlled ischemia for therapeutic benefit [11]. A variety of ischemic conditioning methods have been employed, including ischemic preconditioning (IPreC, exposure to moderate hypoxia prior to an ischemic event) and ischemic postconditioning (IPostC, exposure to moderate hypoxia after an ischemic event) [12]. IPostC has been shown to increase cerebral perfusion, prevent neuronal cell death, and improve cognitive function, notably in spatial learning and memory impairment, in ischemic brains [13,14,15,16]. Remote ischemic postconditioning (RIPostC) is a conditioning method that induces brief, focal hypoxia in the limbs using blood pressure cuffs [17]. It has been employed in a variety of clinical situations for diverse therapeutic goals [18]. RIPostC may confer neuroprotection through multiple mechanisms, including enhanced cerebral perfusion, formation of cerebral collaterals, and increased tolerance to cerebral ischemia [19, 20]. As a result, it has been shown to improve motor function recovery [21], reduce infarct size [22], and minimize cerebral injury by attenuating apoptosis [23, 24]. Furthermore, it is a passive therapeutic measure for the patient and its use is not dependent on his or her level of motivation or post-stroke disability. As an attractive option to augment or replace post-stroke physical exercise, ischemic conditioning may confer neurorehabilitation to stroke patients with high disease burdens. However, RIPostC is yet to be thoroughly studied in the setting of stroke rehabilitation.
The present study aimed to determine whether RIPostC following ischemic stroke can be an effective alternative or augmentative rehabilitation strategy to physical exercise. In order to comprehensively understand and compare the efficacy of exercise and ischemic conditioning, this study further elucidated the important molecular regulations of neurorehabilitative mechanisms. We measured various proteins and biochemical pathways known to be involved in rehabilitation of the ischemic brain in order to assess the benefit of RIPostC. To assess neuroplasticity, we measured neural microtubule proteins (Tau), growth associated protein 43 (GAP-43) and synaptic proteins (postsynaptic density protein 95 (PSD-95) and synaptophysin (SYN)); for angiogenesis, we measured vascular endothelial growth factor (VEGF), Angiopoietin-1 (Ang-1), and Angiopoietin-2 (Ang-2); and for neuroplasticity regulation, we measured brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), cAMP-response-element binding protein (CREB), and nerve growth factor (NGF). We further elucidated the key role of hypoxia-inducible factor 1α (HIF-1α) underlying the rehabilitative mechanism by using the inhibitor, YC-1.
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