Journal of Nutrition and Health

The Korean Nutrition Society (한국영양학회)
권호 표지

Substrate-Perfusion Studies on Coronary Circulation and Myocardial Energy Metabolism in Spontaneously Hypertensive Rat Hearts

발현성 고혈압쥐의 관상순환 기능과 심장근의 에너지 대사에 관한 생체외 에너지원의 관류 연구

  • 김은지 (한림대학교 자연과학대학 식품영양학과)
  • Published : 1995.03.01
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Abstract

The effects of energy-yielding substrates on coronary circulation, myocardial oxygen metabolism, and intramyocytic adenylates of perfused Wistar control rat(WC) and spontaneously hypertensive rat(SHR) hearts were examined under basal and $\beta$-adrenergic stimulation conditions. The perfusion medium (1.0mM Ca2+) contained 5mM glucose (+5U/l insulin) in combination with 5mM pyruvate, 5mM lacate, 5mM acetate, or 5mM octanoate as energy substrates. Hearts were perfused with each substrate buffer for 20min under basal conditions. Coronary functinal hyperemia was induced by infusing for 20min isoproterenol (ISO, 1uM), a $\beta$-receptor agonist. Cardiac adenylates, glycolytic intermediates, and coronary venous lactate were measured by using an enzymatic analysis technique. Under basal conditions, acetate and octanoate significantly increased coronary flow(CF) of WC in parallel with myocardial oxygen consumption. However, CF of SHR was partly attenuated by coronary vasoconstriction despite metabolic acidosis. In addition, pyruvate and lactate depressd ISO-induced coronary functional hyperemia in SHR. It should be noted that octanoate exhibited coronary dysfunction under ISO conditions. On the other hand, fat substrates depleted myocardial high energy phosphate pool and accumulated breakdown intermediates. In SHR with coronary vasoconstriction under basal conditions, and with depressed coronary functional hyperemia, high energy phosphates were greatly depleted. These results suggest that energy substrates in the myocardium and coronary smooth muscle alter remarkably coronary circulation, and that coronary circulatory function is associated with a reserve of high energy phosphates and a balance between breakdown and nono synthesis of energy phosphates. These findings could be explained by alterations in the cytosolic redox state manipulated by LDH and hence in the cytosolic phosphorylation potential, which might be involved in hypertension of SHR.

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References

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