Abstract
Experiments were designed to determine whether hyperkalemic crystalloid cardioplegic solution alters the hypoxic response of isolated segments of rabbit coronary arteries. Coronary arteries were suspended in organ chambers to measure isometric force. We measured the coronary perfusion pressure at a constant flow rate in isolated Langendorff-perfused hearts. Coronary arteries and hearts were preserved in warm (37 degrees C) physiologic solution or in cold (10 degrees C) crystalloid cardioplegic solution. In all groups of coronary arteries, the acetylcholine-induced relaxation before and after preservation was unchanged (n = 7). Hypoxia (15 mm Hg) caused an endothelium-dependent contraction, the amplitude of which did not change after cardioplegia. Conversely, in coronary arteries preserved in physiologic solution, hypoxic contraction amplitude decreased by 67% +/- 17%. In isolated hearts, hypoxic perfusion (15 mm Hg) induced a vasodilation. In all groups, the second hypoxic vasodilation was significantly greater (group 1, first hypoxic perfusion 2.8% +/- 2.8%, second hypoxic perfusion 18.2% +/- 7.1%; group 2, first hypoxic perfusion 6.8% +/- 1.5%, second hypoxic perfusion 29% +/- 9%). The crystalloid cardioplegic solution did not change the hypoxic response in isolated hearts and preserved the endothelium-dependent hypoxic contraction in coronary arteries.
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