Circulation
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Comparative Study
Failure of superoxide dismutase to limit size of myocardial infarction after 40 minutes of ischemia and 4 days of reperfusion in dogs.
Reactive oxygen species such as the superoxide anion (. O2-) have recently been implicated as important agents involved in causing cell death in the setting of myocardial ischemia and reperfusion. When superoxide anion is involved in ischemic injury the administration of superoxide dismutase (SOD) may limit infarct size by reducing the level of superoxide anions in the myocardium. ⋯ Thus, SOD did not limit infarct size in this study. The results of the current study are consistent with our previous study in which allopurinol, a xanthine oxidase inhibitor, did not limit infarct size in this same experimental preparation. The results suggest that superoxide anions that are accessible to the infused SOD are not a major cause of myocyte death caused by 40 min of severe ischemia followed by reperfusion.
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Comparative Study
Disparity between ejection and end-systolic indexes of left ventricular contractility in mitral regurgitation.
To examine left ventricular function in mitral regurgitation (MR), we compared the ejection phase indexes of left ventricular contractility with maximal systolic elastance (Emax) in an experimental preparation of MR. In eight anesthetized open-chest dogs, pressure-volume loops were derived during afterload manipulation with methoxamine and nitroprusside from simultaneous left ventricular pressure and dimensional (sonomicrometry techniques) data before and after creation of MR. From these data maximal systolic elastance (Emax), the end-systolic pressure-volume relationship (ESPVR), and the end-systolic stress-volume relationship (ESSVR) were determined by linear regression analysis. ⋯ An inverse relationship was found between systolic elastance and end-diastolic volume in both control and MR states. When Emax, ESPVR, and ESSVR were normalized to end-diastolic volume, they were unchanged after MR. These results suggest that either there was a decline in left ventricular contractile state after MR, or that contractility was unchanged (if elastance is normalized for increased contractility, but occurred as a consequence of increased preload with no significant change in afterload.