Remote Ischemic Postconditioning for Ischemic Stroke

Zhao, Jingjing; Xiao, Hui; Zhao, Wenbo; Zhang, Xiao-Pei; Yu, Xiao Hong; Ye, Zeng Jie; Mo, Miao-Miao; Peng, Xueting; Wei, Lin

doi:10.4103/0366-6999.229892

Cited by 34 publications

(11 citation statements)

References 28 publications

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“…Total occlusion of blood flow was induced by two plastic strips around the proximal part of the hind limbs, and absence/presence of blood flow was verified by ultrasound with Doppler. 5-min periods of ischemia/reperfusion have been found cardio-and neuroprotective in adults (5,6). In accordance with this, we have previously found reduced brain Lac/NAA ratios in piglets treated with 5 min of RIPC compared to untreated controls (12).…”

Section: Remote Ischemic Postconditioningsupporting

confidence: 88%

“…The tissue protective mechanism of RIPC remains to be fully elucidated together with the optimal timing, number, and duration of remote ischemic cycles. In a review of RIPC for cardio and neuro protection, clinical studies used 5-min cycles of RIPC (5,6). RIPC has been proposed as a novel neuroprotective intervention for HIE and proven to be neuroprotective in both smaller and larger animal models (7).…”

Section: Introductionmentioning

confidence: 99%

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No Added Neuroprotective Effect of Remote Ischemic Postconditioning and Therapeutic Hypothermia After Mild Hypoxia-Ischemia in a Piglet Model

et al. 2020

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Introduction: Hypoxic ischemic encephalopathy (HIE) is a major cause of death and disability in children worldwide. Apart from supportive care, the only established treatment for HIE is therapeutic hypothermia (TH). As TH is only partly neuroprotective, there is a need for additional therapies. Intermittent periods of limb ischemia, called remote ischemic postconditioning (RIPC), have been shown to be neuroprotective after HIE in rats and piglets. However, it is unknown whether RIPC adds to the effect of TH. We tested the neuroprotective effect of RIPC with TH compared to TH alone using magnetic resonance imaging and spectroscopy (MRI/MRS) in a piglet HIE model. Methods: Thirty-two male and female piglets were subjected to 45-min global hypoxia-ischemia (HI). Twenty-six animals were randomized to TH or RIPC plus TH; six animals received supportive care only. TH was induced through whole-body cooling. RIPC was induced 1 h after HI by four cycles of 5 min of ischemia and 5 min of reperfusion in both hind limbs. Primary outcome was Lac/NAA ratio at 24 h measured by MRS. Secondary outcomes were NAA/Cr, diffusion-weighted imaging (DWI), arterial spin labeling, aEGG score, and blood oxygen dependent (BOLD) signal measured by MRI/MRS at 6, 12, and 24 h after the hypoxic-ischemic insult. Results: All groups were subjected to a comparable but mild insult. No difference was found between the two intervention groups in Lac/NAA ratio, NAA/Cr ratio, DWI, arterial spin labeling, or BOLD signal. NAA/Cr ratio at 24 h was higher in the two intervention groups compared to supportive care only. There was no difference in aEEG score between the three groups. Andelius et al. Remote Postconditioning and Neonatal Encephalopathy Conclusion: Treatment with RIPC resulted in no additional neuroprotection when combined with TH. However, insult severity was mild and only evaluated at 24 h after HI with a short MRS echo time. In future studies more subtle neurological effects may be detected with increased MRS echo time and post mortem investigations, such as brain histology. Thus, the possible neuroprotective effect of RIPC needs further evaluation.

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Section: Remote Ischemic Postconditioningsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

No Added Neuroprotective Effect of Remote Ischemic Postconditioning and Therapeutic Hypothermia After Mild Hypoxia-Ischemia in a Piglet Model

et al. 2020

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“…Clinical trials have been performed in adults 55 – 57 and in children 58 – 62 which suggest benefits from RIC protecting various organs including heart, lung, and kidney. In addition, a systematic review and meta-analysis evaluating randomized trials, found that compared with controls, RIC significantly reduced the recurrence of stroke or transient ischemic attacks 63 . However, the advantage of RIC on specific human organs remains controversial as large randomized controlled trials showed no improvement after myocardial infarction 64 or in relation to cardiac surgery 65 , 66 .…”

Section: Discussionmentioning

confidence: 99%

Remote ischemic conditioning counteracts the intestinal damage of necrotizing enterocolitis by improving intestinal microcirculation

Koike

Ganji

et al. 2020

Nat Commun

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Necrotizing enterocolitis (NEC) is a devastating disease of premature infants with high mortality rate, indicating the need for precision treatment. NEC is characterized by intestinal inflammation and ischemia, as well derangements in intestinal microcirculation. Remote ischemic conditioning (RIC) has emerged as a promising tool in protecting distant organs against ischemia-induced damage. However, the effectiveness of RIC against NEC is unknown. To address this gap, we aimed to determine the efficacy and mechanism of action of RIC in experimental NEC. NEC was induced in mouse pups between postnatal day (P) 5 and 9. RIC was applied through intermittent occlusion of hind limb blood flow. RIC, when administered in the early stages of disease progression, decreases intestinal injury and prolongs survival. The mechanism of action of RIC involves increasing intestinal perfusion through vasodilation mediated by nitric oxide and hydrogen sulfide. RIC is a viable and non-invasive treatment strategy for NEC.

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“…However, the interpretation of these results is limited by the small sample sizes and low quality of evidence. Another meta-analysis of RCTs published in 2018 suggested that remote ischemic postconditioning might offer cerebral protection for stroke patients suffering from or at risk of brain I/R injury and that there were no side effects (Zhao J.J. et al, 2018). However, most previous studies focused on patients younger than 80 years of age; there are few investigations about the safety and effectiveness of RLIC on stroke prevention and treatment in octo- and nonagenarians.…”

Section: Potential Interventionsmentioning

confidence: 99%

Potential Neuroprotective Treatment of Stroke: Targeting Excitotoxicity, Oxidative Stress, and Inflammation

et al. 2019

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Stroke is a major cause of death and adult disability. However, therapeutic options remain limited. Numerous pathways underlie acute responses of brain tissue to stroke. Early events following ischemic damage include reactive oxygen species (ROS)-mediated oxidative stress and glutamate-induced excitotoxicity, both of which contribute to rapid cell death within the infarct core. A subsequent cascade of inflammatory events escalates damage progression. This review explores potential neuroprotective strategies for targeting key steps in the cascade of ischemia–reperfusion (I/R) injury. NADPH oxidase (NOX) inhibitors and several drugs currently approved by the U.S. Food and Drug Administration including glucose-lowering agents, antibiotics, and immunomodulators, have shown promise in the treatment of stroke in both animal experiments and clinical trials. Ischemic conditioning, a phenomenon by which one or more cycles of a short period of sublethal ischemia to an organ or tissue protects against subsequent ischemic events in another organ, may be another potential neuroprotective strategy for the treatment of stroke by targeting key steps in the I/R injury cascade.

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Remote Ischemic Postconditioning for Ischemic Stroke

Cited by 34 publications

References 28 publications

No Added Neuroprotective Effect of Remote Ischemic Postconditioning and Therapeutic Hypothermia After Mild Hypoxia-Ischemia in a Piglet Model

No Added Neuroprotective Effect of Remote Ischemic Postconditioning and Therapeutic Hypothermia After Mild Hypoxia-Ischemia in a Piglet Model

Remote ischemic conditioning counteracts the intestinal damage of necrotizing enterocolitis by improving intestinal microcirculation

Potential Neuroprotective Treatment of Stroke: Targeting Excitotoxicity, Oxidative Stress, and Inflammation

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