Cell sodium and the induction of myocardial injury after adrenaline

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Abstract
The metabolic and nonmetabolic components of reactive hyperaemia were separated by comparing the coronary blood flow response after total occlusion to that after perfusion of equal duration with deoxygenated blood at normal aortic pressure in 15 open chest dogs. The flow repayment after 10 and 15 s perfusions with deoxygenated blood was a third to a quarter of that following 10 and 15 s total occlusion (P = 0.0001) and also less than the calculated normoxic flow debt (0.96 ± 0.09 and 0.82 ± 0.16, respectively), indicating no overrepayment. The flow repayment after deoxygenated perfusion was not reduced by increasing the flow rate during the perfusion, suggesting that our results were not due to increased washout rates of vasodilator metabolites during the perfusion. We conclude that reactive hyperaemia following brief total occlusion differs significantly from hyperaemia following deoxygenated perfusion and that this difference is probably due to the mechanical effect of sudden changes in coronary flow and perfusion pressure accompanying occlusion-release and is independent of myocardial oxygen supply.