Preservation of mitochondrial function during ischemia as a possible mechanism for cardioprotection of diltiazem against ischemia/reperfusion injury.

A possible mechanism for D-cis-diltiazem (diltiazem)-mediated improvement of the contractile function of ischemic/reperfused hearts was examined. Thirty-five-min ischemia/60-min reperfusion recovered little the left ventricular developed pressure (LVDP) and decreased myocardial high-energy phosphates (HEPs). Ischemia induced an accumulation of tissue Na+ content, an increase in cytochrome c in the cytosolic fraction, and a decrease in the oxygen consumption rate (OCR) in perfused hearts.

Effects of N-(2-mercaptopropionyl)-glycine on mitochondrial function in ischemic-reperfused heart.

Objective: A possible mechanism for N-(2-mercaptopropionyl)-glycine (MPG) underlying the improvement of contractile function and mitochondrial activity of ischemic-reperfused rat hearts was examined.

Methods: Isolated, perfused hearts were subjected to 35 min ischemia-60 min reperfusion. At the end of ischemia or reperfusion, myocardial Na(+) content and mitochondrial oxygen consumption rate (OCR) were examined.

Mitochondrial damage during ischemia determines post-ischemic contractile dysfunction in perfused rat heart.

Possible mechanisms underlying sodium overload-induced ischemia/reperfusion injury in perfused rat hearts were examined. Massive accumulation of myocardial Na(+) occurred during ischemia, suggesting cytosolic sodium overload in cardiac cells. Treatment of the pre-ischemic heart with 0.

Nicorandil preserves mitochondrial function during ischemia in perfused rat heart.

A possible mechanism for the action of nicorandil on the improvement of energy metabolism of ischemic/reperfused hearts was examined. Perfused rat hearts were subjected to 35-min ischemia/60-min reperfusion. The heart was treated with nicorandil at concentrations of 10 to 100 microM for the last 30-min of pre-ischemia.

Sodium accumulation during ischemia induces mitochondrial damage in perfused rat hearts.

Objective: The present study aimed to elucidate the involvement of sodium overload and following damage to mitochondria during ischemia in the genesis of ischemia/reperfusion injury of perfused rat hearts.

Methods: Isolated, perfused hearts were exposed to different durations (15-35 min) of ischemia followed by 60-min reperfusion. At the end of ischemia or reperfusion, myocardial sodium and calcium contents and myocardial high-energy phosphates were determined.

Protective effect of propranolol on mitochondrial function in the ischaemic heart.

1. The present study was aimed to determine whether propranolol improves contractile function of the ischaemic/reperfused heart through protection of the mitochondrial function during ischaemia. 2.