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KMID : 1160620010060010043
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Preventive Nutrition and Food Science
2001 Volume.6 No. 1 p.43 ~ p.50
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Myocardial Function and Metabolic Energetics in Low Flow Ischemia and with β-Adrenergic Stimulation in Spontaneously Hypertensive Rat Hearts
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Kang Young-Hee
Kang Jung-Sook
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Abstract
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The effects of cardiac ischemia-reperfusion and β-adrenergic stimulation on metabolic function and energetics were investigated in Langendorff-perfused spontaneously hypertensive rat (SHR) hearts. Sarcoplasmic reticulum Ca^(2+)-dependent ATPase and cardiac lactate dehydrogenase (LDH) are additionally studied. The perfusion medium (1.0 mM Ca^(2+)) contained 5 mM glucose ( + 5 U/L insulin) and 2 mM pyruvate as substrates. Global ischemia was induced by reducing perfusion pressure of 100 to 40 ㎝H₂O, followed by 20 min reperfusion. Isoproterenol (ISO, 1 μM) was infused for 10 min. Coronary vascular resistance and myocardial oxygen consumption (MVO₂) of SHR were increased in parallel with enhanced venous lactate during ischemia and reperfusion compared to those of Sprague Dawley (SD) hearts. Although ischemia-induced increase in venous lactate and combined adenosine plus inosine was abolished, coronary vasodilation produced in SD during reperfusion. In SHR, depressed reactive hyperemia was associated with a fall in cardiac ATP and CrP/Pi ratio and a rise in intracellular lactate/pyruvate ratio. On the other hand, ISO produced coronary functional hyperemia and an increase in MVO₂. However, these responses were less than those in SHR hearts. The ATPase activity of SHR was attenuated in free Ca^(2+) concentrations used under basal condition and with ISO compared to that of SD. Venous lactate output and cardiac LDH activity were augmented in SHR as influenced by ISO. These results demonstrate that coronary reactive and functional hyperemia was depressed in SHR, which could be explained by alterations in the cytosolic phosphorylation potential and the cytosolic redox state manipulated by LDH, and by abnormal free calcium handling.
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KEYWORD
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ischemia, β-adrenergic stimulation, myocardial function, metabolic energetics, spontaneously hypertensive rat heart
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