Abstract
The present study was designed to investigate the effect of early and late administration of phenylephrine during ischemia against regional ischemia–reperfusion injuries in an isolated rat heart model. All animals were randomly divided into experimental groups: (I) IR (Ischemic/ reperfusion): the hearts underwent 35 min of regional ischemia followed by 60 min of reperfusion; (II) 5HD-IR-0: the hearts were perfused for 5 min with 5HD (5-hydroxydecanoate, specific mKATP channel blocker, 100 µM) at the onset of regional ischemia; (III) 5HD-IR-20: the hearts were perfused for 5 min with 5HD 20 min after regional ischemia; (IV) PE-IR-10: the hearts were perfused for 5 min with phenylephrine 10 min after regional ischemia; (V) PE-IR-30: the hearts were perfused for 5 min with phenylephrine (100 µM) 30 min after regional ischemia; (VI) PE-5HD-IR-10 group: the hearts were perfused for 5 min with 5HD at the onset of regional ischemia after which phenylephrine was administrated as in group IV; and (VII) PE-5HD-IR-30: the hearts were perfused for 5 min with 5HD 20 min after the ischemia and then phenylephrine was administrated as in group V. The hemodynamic parameters were recorded throughout the experiment. Ischemia-induced arrhythmias, myocardial infarct size (IS), creatin kinase-MB isoenzyme (CK-MB), plasma lactate dehydrogenase (LDH) activities, and coronary blood flow (CBF) were measured in all animals. Perfusion of phenylephrine 30 min after the regional ischemia curtailed the myocardial infarct size, reduced CK-MB, and improved cardiac function and CBF. Administration of 5HD 30 min after the ischemia abolished cardioprotective effects of phenylephrine in the late phase. These results suggest the involvement of mKATP in the mechanism of phenylephrine-induced late preconditioning.
Highlights
Brief periods of ischemia lead to reduced severity of cardiac injury following a second sustained period of ischemia
We examined the role of the mKATP channels in this form of myocardial protection
Since HR and LVDP may recover to different degrees, the rate pressure product was calculated through multiplying the heart rate by left ventricular developed pressure and presented as a reliable left ventricular function parameter for the isolated heart
Summary
Brief periods of ischemia lead to reduced severity of cardiac injury following a second sustained period of ischemia. This cardioprotective effect has been termed ischemic preconditioning (Tonkovic-Capin et al, 2002). Local preconditioning cannot be used in acute clinical settings such as acute myocardial infarction, ischemic stroke, or acute major vascular occlusion. It has become necessary to develop new techniques suitable for providing protection against unpredictable ischemic events. A shortcoming of both preconditioning and postconditioning is lengthened operative time, possibly even for duration of 15-20 min. A further negative aspect is that in the presence of atherosclerosis, these invasive techniques can lead to serious, life-threatening complications such as plaque rupture
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