A 31P-NMR study of the effects of reflow on the ischaemic rat heart.
(1) The recovery of perfused rat hearts experiencing various lengths of total global ischaemia was studied using 31P-NMR. Mechanical function was monitored by measuring left ventricular pressure. (2) Hearts exposed to a maximum of 14 min total global ischaemia regained stable contractile function on reperfusion. The concentration of phosphocreatine in these hearts rapidly exceeded its pre-ischaemic value while that of ATP rose very slowly. Pi fell on reflow to approximately its original level. These observations are interpreted as being the result of a rapid turnover of ATP stimulating phosphocreatine production by the mitochondrial isozyme of creatine kinase (ATP: creatine N-phosphotransferase, EC 2.7.3.2). (3) The recovery of intracellular pH on reperfusion does not depend upon the duration of ischaemia, nor on the pH or the percentage of ATP depletion at the end of the ischaemic period. This indicates that pH recovery is a flow-dependent phenomenon. (4) In non-recovering hearts, multiple Pi resonances are observed which arise from areas of differing myocardial pH. Phosphocreatine levels did not rise above 50% of their pre-ischaemic values. ATP levels remained depressed. This suggests that localized tissue necrosis only characterizes the failing situation.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006863:Hydrogen-Ion Concentration; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009200:Myocardial Contraction; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D010725:Phosphocreatine; D000255:Adenosine Triphosphate