Results 51 to 60 of about 8,004 (220)

Pharmacological postconditioning against myocardial infarction with a slow-releasing hydrogen sulfide donor, GYY4137 [PDF]

open access: yes, 2016
Exogenous hydrogen sulfide (H2S) protects against myocardial ischemia/reperfusion injury but the mechanism of action is unclear. The present study investigated the effect of GYY4137, a slow-releasing H2S donor, on myocardial infarction given specifically
Baxter, Gary F.   +4 more
core   +1 more source

Very short cycles of postconditioning have no protective effect against reperfusion injury. Experimental study in rats

open access: yesBrazilian Journal of Cardiovascular Surgery, 2014
Introduction: Ischemic postconditioning has been recognized as effective in the prevention of reperfusion injury in situations of ischemia and reperfusion in various organs and tissues. However, it remains unclear what would be the best way to accomplish
Ricardo Kenithi Nakamura   +7 more
doaj   +1 more source

Hyperglycemia raises the threshold of levosimendan- but not milrinone-induced postconditioning in rat hearts [PDF]

open access: yes, 2012
Background The authors examined whether milrinone and levosimendan could exert cardiac postconditioning effects in rats under normoglycemia and hyperglycemia, and whether the effects could be mediated by mitochondrial permeability transition pore (mPTP).
Shuhei Matsumoto   +6 more
core   +2 more sources

Function and mechanism of toll-like receptors in cerebral ischemic tolerance: from preconditioning to treatment [PDF]

open access: yes, 2015
Increasing evidence suggests that toll-like receptors (TLRs) play an important role in cerebral ischemia-reperfusion injury. The endogenous ligands released from ischemic neurons activate the TLR signaling pathway, resulting in the production of a large ...
Jing Chen   +5 more
core   +1 more source

Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia‐reperfusion injury

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Heart attack causes ischaemia–reperfusion injury in cardiomyocytes. Mitochondria generate reactive oxygen species (ROS), leading to oxidative stress. High levels of mitochondrial calcium (Ca2+) activate the mitochondrial permeability transition pore (mPTP), and excess ROS levels can lower the Ca2+ required to activate the mPTP ...
Emily Rozich   +5 more
wiley   +1 more source

Morphine and remifentanil-induced cardioprotection: its experimental and clinical outcomes [PDF]

open access: yesKorean Journal of Anesthesiology, 2011
During the past few decades, a large number of animal studies demonstrated that commonly used opioids could provide cardioprotection against ischemia-reperfusion (I/R) injury.
Jin Mo Kim, Young Ho Jang, Jun Kim
doaj   +1 more source

Remote pharmacological post-conditioning by intrathecal morphine: Cardiac protection from spinal opioid receptor activation [PDF]

open access: yes, 2010
Background: Intrathecal morphine pre-conditioning attenuates cardiac ischemia-reperfusion injury via activation of central opioid receptors. We hypothesized that intrathecal morphine also post-conditions the myocardium in the rat.
Irwin, MG   +4 more
core   +1 more source

HIF‐1α/Netrin‐4 Axis Mediates RIPC‐Induced Angiogenesis and Neurogenesis After Ischemic Stroke

open access: yesJournal of Cellular and Molecular Medicine, Volume 30, Issue 7, April 2026.
ABSTRACT Remote ischemic postconditioning (RIPC) confers neuroprotection in ischemic stroke partly via promoting angiogenesis and neurogenesis, but its precise molecular mechanisms remain unclear; here, we investigated the role of the secreted guidance protein Netrin‐4 (NTN4) and its upstream regulator hypoxia‐inducible factor 1α (HIF‐1α) in mediating ...
Zhaowei Feng   +9 more
wiley   +1 more source

Ischemic postconditioning fails to protect against neonatal cerebral stroke. [PDF]

open access: yesPLoS ONE, 2012
The lack of efficient neuroprotective strategies for neonatal stroke could be ascribed to pathogenic ischemic processes differentiating adults and neonates. We explored this hypothesis using a rat model of neonatal ischemia induced by permanent occlusion
Pierre-Louis Leger   +5 more
doaj   +1 more source

Actin-Cytoskeleton Drives Caveolae Signaling to Mitochondria during Postconditioning

open access: yesCells, 2023
Caveolae-associated signaling toward mitochondria contributes to the cardioprotective mechanisms against ischemia-reperfusion (I/R) injury induced by ischemic postconditioning.
Francisco Correa   +10 more
doaj   +1 more source

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