Limb remote ischemia per-conditioning protects the heart against ischemia–reperfusion injury through the opioid system in rats
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چکیده
منابع مشابه
The role of nitric oxide in the protective action of remote ischemic per-conditioning against ischemia/reperfusion-induced acute renal failure in rat
Objective(s): We investigated the role of nitric oxide (NO) in the protective effects of remote ischemic per-conditioning (rIPerC) on renal ischemia/reperfusion (I/R) injury in male rats. Materials and Methods: I/R treatment consisted of 45 min bilateral renal artery ischemia and 24 hr reperfusion interval. rIPerC was performed using four cycles of 2 min occlusions of the left femoral artery an...
متن کاملProtective role of remote ischemic per-conditioning in acute renal injury induced by ischemia reperfusion via TLR-4 and TNF-α signaling pathway in rats
sIntroduction: Acute kidney injury (AKI) induced by ischemia-reperfusion (I / R) of the kidney as an inflammatory process in which multiple inflammatory factors are involved. Recently, one of the modalities of inflammation in AKI is Remote Ischemic Per-Conditioning (RIPerC). Materials and Methods: In this study, bilateral renal artery and vein occlusion were done for 45 minute and reperfusion a...
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BACKGROUND Whether alterations in mitochondrial morphology affect the susceptibility of the heart to ischemia/reperfusion injury is unknown. We hypothesized that modulating mitochondrial morphology protects the heart against ischemia/reperfusion injury. METHODS AND RESULTS In response to ischemia, mitochondria in HL-1 cells (a cardiac-derived cell line) undergo fragmentation, a process that i...
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The small GTPase RhoA serves as a nodal point for signaling through hormones and mechanical stretch. However, the role of RhoA signaling in cardiac pathophysiology is poorly understood. To address this issue, we generated mice with cardiomyocyte-specific conditional expression of low levels of activated RhoA (CA-RhoA mice) and demonstrated that they exhibited no overt cardiomyopathy. When chall...
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Cardiac mammalian target of rapamycin (mTOR) is necessary and sufficient to prevent cardiac dysfunction in pathological hypertrophy. However, the role of cardiac mTOR in heart failure after ischemic injury remains undefined. To address this question, we used transgenic (Tg) mice with cardiac-specific overexpression of mTOR (mTOR-Tg mice) to study ischemia-reperfusion (I/R) injury in two animal ...
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ژورنال
عنوان ژورنال: Canadian Journal of Physiology and Pharmacology
سال: 2018
ISSN: 0008-4212,1205-7541
DOI: 10.1139/cjpp-2016-0585