Transmural inhomogeneity of extracellular [K+] and pH and myocardial energy metabolism in the isolated rat heart during acute global ischemia; dependence on gaseous environment.
We investigated in the isolated rat heart the influence of the gas surrounding the globally ischemic heart on transmural inhomogeneity of energy metabolism, extracellular K+ accumulation, and change of extracellular pH. Hearts were made ischemic in 100% N2 (N2-ischemia), 100% O2 (O2-ischemia) or 100% CO2 (CO2-ischemia). We measured: 1) Midmural, subepicardial, and epicardial changes of extracellular [K+] and pH during successive 6-min periods of global ischemia, and 2) content of creatinephosphate (CrP) in consecutive tissue sections of 100 microns, from the subepicardium after 10 min of ischemia. A) During O2-ischemia both extracellular [K+] and change of pH in the subepicardium are significantly less than in the midmyocardium. During N2-ischemia only minor differences exist in [K+] and pH between the subepicardium and the midmyocardium. During CO2-ischemia midmural and subepicardial [K+] are similar to those during N2-ischemia. The midmural change of pH resembles that during N2-ischemia; subepicardial change of pH, however, was slightly larger. Midmural changes in [K+] and pH were not influenced by the nature of the surrounding gas. B) After 10 min of O2-ischemia a gradient of tissue content of CrP extends from the epicardium (CrP about 30 mumoles/g dry weight) to a distance of about 1000 microns (CrP 1 mumoles/g dry weight). In N2- and CO2-ischemia a CrP gradient is absent; CrP is appreciably less than 1 mumoles/g dry weight at any distances from the epicardium. C) We conclude that diffusion of O2 into the myocardium and of CO2 from the myocardium affects transmural gradients of [K+], pH, and energy metabolism during ischemia. Local availability of O2 increases the capacity of the ischemic tissue to generate high energy phosphates and mitigates ischemia-induced changes of transsarcolemmal ion gradients.
Department of Cardiology and Experimental Cardiology, University of Amsterdam, The Netherlands.
A F
AF
Schaapherder
C A
CA
Schumacher
R
R
Coronel
J W
JW
Fiolet
D000136:Acid-Base Equilibrium / Q000502:physiology*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002245:Carbon Dioxide / Q000502:physiology*; D003327:Coronary Disease / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology*; D005110:Extracellular Space / Q000502:physiology*; D007473:Ion Channels / Q000502:physiology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology*; D010725:Phosphocreatine / Q000378:metabolism; D011188:Potassium / Q000502:physiology*; D051381:Rats
D007473:Ion Channels; D010725:Phosphocreatine; D002245:Carbon Dioxide; D000255:Adenosine Triphosphate; D011188:Potassium