Abstract
Using an isolated rat heart preparation (Langendorff perfusion, perfusion pressure 100 cm H2O) the response of the hypertrophied heart (spontaneous hypertensive rats lv/bw ratio 3.6 +/- 0.5) to global normothermic (30 min) and hypothermic (25 degrees C, 120 min) ischemic and cardioplegic arrest and reperfusion (30 min) was examined and compared with normal hearts (Wistar rats lv/bw ratio 2.0 +/- 0.3). St. Thomas solution and verapamil (2 mg/l Ringer solution) were used as cardioplegic agents. Before ischemia hypertrophied hearts had a significantly higher pressure-rate product, a lower myocardial perfusion/g myocardium and a lower myocardial ATP and adenine nucleotide content. Unmodified ischemia reduced myocardial function in the hypertrophied hearts to a greater degree than in normal hearts in both normo- and hypothermia. St. Thomas solution and verapamil protected significantly the myocardial function in the normal and hypertrophied heart after normothermic ischemia in a similar manner (60-70% of the initial value). In the hypertrophied ventricle ATP decay and adenine nucleotide loss was greater in verapamil than in St. Thomas solution treated hearts. In hypothermic ischemia only St. Thomas solution protected left ventricular function and adenine nucleotide loss in both normal and hypertrophied hearts. Verapamil was ineffective in the normal ventricle and protected left ventricular function but not the ATP and adenine nucleotide decay in the hypertrophied heart.
Published Version
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