Mechanisms underlying myocardial stunning.
The effect of myocardial stunning on mitochondrial function was examined in rabbit hearts. After global normothermic ischemia followed by reperfusion, we previously found that mitochondrial high energy phosphate content was not significantly diminished. To determine whether myocardial stunning results from altered excitation-contraction coupling, we examined function and calcium uptake by sarcoplasmic reticulum (SR). Hearts were subjected to global ischemia under normothermic conditions. Ischemic hearts had significantly lower velocity of Ca2+ uptake by the SR (Vmax 36.3 +/- 1.94 nmol/min per mg vs 49.3 +/- 2.54 nmol/min per mg control) but velocity was restored by reperfusion. Similarly, myocardial ATP content was decreased during ischemia (4.5 +/- 1.23 mumol/g dry weight vs 13.6 +/- 0.98 mumol/g control) but returned to normal during reperfusion. Incubation of homogenates with 610 microM ryanodine did not alter the difference in Vmax between control, ischemic, or reperfused hearts, suggesting that ischemia affects SR Ca2+ pumping without affecting Ca2+ release. Recovery of calcium uptake during reperfusion also indicates that SR Ca2+ ATPase function is not the major cause of myocardial stunning. Potentiated contractions were studied in a Langendorff heart model, revealing that postrest potentiation (PRP) and peak paired-pulse potentiation (PPP) increase as a result of ischemia. On reperfusion, PPP also increased, but there was a decrease in PRP of left ventricular pressure (LVP) and LV dP/dt (PRP LV dP/dt = 127% preischemia vs 112% at 2 min postischemia), indicating than an impairment of an SR function other than Ca2+ ATPase occurs during myocardial stunning.
Flameng
W
W
Department of Cardiac Surgery, Centre of Experimental Surgery and Anaesthesiology, Katholieke Universiteit Leuven, Belgium.
D000255:Adenosine Triphosphate / Q000502:physiology; D000818:Animals; D015220:Calcium Channels / Q000502:physiology; D009202:Cardiomyopathies / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000502:physiology*; D017202:Myocardial Ischemia / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D011817:Rabbits; D012519:Sarcoplasmic Reticulum / Q000502:physiology
D015220:Calcium Channels; D000255:Adenosine Triphosphate