Mechanical and metabolic responses to extracorporeal regional hypoperfusion of the porcine heart.
Controversy exists as to whether hibernating myocardium is ischemic (with evidence of lactate production and ATP breakdown) during sustained coronary hypoperfusion or whether the oxygen supply is balanced by the oxygen requirements of contractile function. To investigate the mechanical and metabolic response to a moderate reduction in regional coronary blood flow, selective coronary perfusion was performed by a carotid-coronary shunt using a small roller pump circuit in six pigs. Flow was reduced for 45 minutes to 40% of base line followed by 2 hours reperfusion at normal blood flow. No hemodynamic changes occurred during flow reduction and reperfusion. Reduction of coronary blood flow to 40% resulted in a reduction in wall motion to 40.8 +/- 6.1% of base line. Two hours of reperfusion resulted in myocardial stunning shown by persistence of wall motion abnormalities (reduction to 64.6 +/- 6.0% of base line) without histologic and electron microscopic evidence of necrosis. The metabolic response to hypoperfusion varied from nil to substantial, measured as nucleotide catabolism and lactate production. We found no correlation between the base line normoxic contractile state and the magnitude of ischemic metabolite efflux. The efflux of lactate, inosine and uridine did not correlate with wall motion at each time during coronary flow reduction. Initial contractile recovery correlated with maximal lactate and uridine efflux during hypoperfusion. The results provide evidence that, in the in-vivo porcine myocardium, moderate coronary hypoperfusion can exist without metabolic evidence of ischemia.
Tukkie
R
R
Department of Experimental Surgery, Academic Medical Center, Amsterdam, The Netherlands.
Gründeman
P F
PF
de Jong
J W
JW
Klopper
P J
PJ
D000818:Animals; D001481:Basal Metabolism; D003326:Coronary Circulation / Q000502:physiology; D006321:Heart / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology; D007288:Inosine / Q000096:biosynthesis; D007773:Lactates / Q000096:biosynthesis; D008954:Models, Biological; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D015203:Reproducibility of Results; D013552:Swine; D014529:Uridine / Q000096:biosynthesis
D007773:Lactates; D007288:Inosine; D014529:Uridine