Opioid-Induced Second Window of Cardioprotection
نویسندگان
چکیده
منابع مشابه
Opioid-induced second window of cardioprotection: potential role of mitochondrial KATP channels.
Opioids have been previously shown to confer short-term cardioprotection against a prolonged ischemic insult. Therefore, the present study was designed to determine whether opioids can induce a delayed or "second window" of cardioprotection and to assess the potential involvement of the mitochondrial KATP channel. All rats were subjected to 30 minutes of ischemia and 2 hours of reperfusion (I/R...
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“Preconditioning with ischemia” (PC) is the phenomenon whereby one or more episodes of brief ischemia paradoxically renders the myocardium resistant to a later, more sustained ischemic insult (1–3). The cardioprotection afforded by brief, transient ischemia is biphasic; a “first window” of protection is manifest within the initial 5 min to approximately 3 h of the PC stimulus, the hallmark of w...
متن کاملRole of Nitric-Oxide Synthase, Free Radicals, and Protein Kinase C in Opioid-Induced Cardioprotection
Opioids generate free radicals that mediate protection in isolated cultured cardiomyocytes. We hypothesize that the nature of these radicals is nitric oxide, and that nitric oxide activates the protein kinase C (PKC) isoform. Through this signal transduction pathway, opiates protect cardiomyocytes during hypoxia and reoxygenation. Cell viability was quantified in chick embryonic ventricular myo...
متن کاملDifferential activation of extracellular signal regulated kinase isoforms in preconditioning and opioid-induced cardioprotection.
Stimulation of the delta(1)-opioid receptor has been shown to trigger ischemic preconditioning (IPC). Additionally, myocardial ischemia/reperfusion induces the activation of extracellular signal-regulated kinase (ERK). Therefore, we examined the role of ERK in acute cardioprotection induced by delta(1)-opioid receptor stimulation or IPC. Infarct size (IS) was expressed as a percentage of the ar...
متن کاملRole of nitric-oxide synthase, free radicals, and protein kinase C delta in opioid-induced cardioprotection.
Opioids generate free radicals that mediate protection in isolated cultured cardiomyocytes. We hypothesize that the nature of these radicals is nitric oxide, and that nitric oxide activates the protein kinase C (PKC) delta isoform. Through this signal transduction pathway, opiates protect cardiomyocytes during hypoxia and reoxygenation. Cell viability was quantified in chick embryonic ventricul...
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ژورنال
عنوان ژورنال: Circulation Research
سال: 1999
ISSN: 0009-7330,1524-4571
DOI: 10.1161/01.res.84.7.846