Sakai H, Yoshiyama M, Teragaki M, Takeuchi K, Takeda T, Ikata M, Ishikawa M, Miura I
First Department of Internal Medicine, Osaka City University Medical School, Japan.
Biochem Biophys Res Commun. 1988 Feb 15;150(3):1268-74. doi: 10.1016/0006-291x(88)90766-8.
To investigate mechanisms of development in ischemic myocardial injury, intracellular pH and high energy phosphates in perfused guinea-pig hearts were monitored by 31P-MRS. Intracellular ATP content decreased to 1.2% and 26.4% of control during 60 minutes global ischemia, respectively with and without preischemic administration of isoproterenol. Intracellular pH declined to 6.48 and 6.03 respectively. Postischemic cardiac function was severely impaired by isoproterenol. ATP breakdown had little influence on intracellular pH in ischemic hearts. It was verified that inotropic agents can progress ischemic myocardial injury, and that contractile recovery is more correlated with the residual ATP level than intracellular pH.