Attenuation of myocardial acidosis by propranolol during ischaemic arrest and reperfusion: evidence with 31P nuclear magnetic resonance.
31P nuclear magnetic resonance (NMR) spectroscopy was used to ascertain whether propranolol could reduce the development of myocardial acidosis during periods of ischaemic arrest and were studied. Cardiac pH progressively declined during ischaemia from a normal 6.97 +/- 0.02 (n = 23) to 6.09 +/- 0.04 or 5.96 +/- 0.04, respectively. Normalisation of pH following reperfusion occurred only in the 35 min ischaemic hearts. Propranolol (1 mg. litre-1) given prior to arrest significantly reduced the magnitude of developing acidosis regardless of the length of ischaemia. Furthermore, it aided in the normalisation of intramyocardial pH upon reperfusion in both groups. Propranolol significantly reduced the magnitude of phosphocreatine (PCr  loss normally seen during ischaemic arrest alone, but it did not protect against depletion of ATP. Restoration of PCr reperfusion was virtually complete in all cases, while transient increases in ATP were seen only in those hearts protected by propranolol. In summary, this NMR study demonstrated the first direct evidence that a significant component of the myocardial acidosis caused by global ischaemia and arrest can be blocked by propranolol.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism*; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D010725:Phosphocreatine / Q000378:metabolism; D010758:Phosphorus; D011433:Propranolol / Q000494:pharmacology*
D010725:Phosphocreatine; D010758:Phosphorus; D000255:Adenosine Triphosphate; D011433:Propranolol