Reversible impairment of myocardial contractility due to hypercarbic acidosis in the isolated perfused rat heart.
METHODS
Striking increases in PCO2 of the myocardium have recently been documented during cardiac arrest. The purpose of the present study was to investigate selective effects of hypercarbia as distinct from acidosis on left ventricular contractile function and oxygen utilization. An isolated, spontaneously beating rat heart preparation was utilized. The perfusate was equilibrated with gases containing 5%, 10%, 20%, and 30% CO2. In a subset of experiments, the [H+] was adjusted independently of PCO2 by decreasing the concentration of HCO3-.


RESULTS
When the PCO2 of the perfusate was progressively increased from 36 to 146 torr (4.8 to 29.5 kPa), the left ventricular systolic pressure (LVSP) generated by the isolated heart and the maximum rate of pressure change in the left ventricle (dP/dt) were decreased to 20% of their control values. However, comparable acidosis in the absence of hypercarbia produced only minimal decreases in the LVSP or dP/dt such that contractility remained at greater than or equal to 88%. Increases in the perfusate PCO2 but not in the perfusate H+ were highly correlated with decreases in both myocardial contractility and oxygen consumption (r2 = .88).


CONCLUSIONS
Hypercarbia rather than acidosis accounts for decreased contractility and oxygen utilization in the isolated perfused rat heart.
Tang
W C
WC
Department of Medicine, University of Health Sciences, Chicago Medical School, North Chicago, IL 60064.
Weil
M H
MH
Gazmuri
R J
RJ
Bisera
J
J
Rackow
E C
EC
D000138:Acidosis / Q000378:metabolism / Q000503:physiopathology*; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism*; D066298:In Vitro Techniques; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains
D002245:Carbon Dioxide