Why the study?
Does potassium chloride arrest alter capillary bed distribution and erythrocyte orientation in dog myocardium?
Does potassium chloride arrest alter capillary bed distribution and erythrocyte orientation in dog myocardium?
Potassium chloride arrest in dog hearts alters myocardial capillary distribution, erythrocyte morphology, and weakens connective tissue, which worsens with longer arrest times.
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Should not yet change cardioplegia practice; hypothesis-generating for KCl arrest effects in canine myocardium.
Dog hearts were taken without loss of blood under 3 different conditions: (1) normally beating hearts, (2) hearts that were arrested by potassium chloride for varying lengths of time and (3) potassium chloride-arrested hearts that were reperfused with blood after varying lengths of time. In normal hearts counts of open capillaries containing erythrocytes showed a uniform distribution throughout the right myocardium and a gradient decreasing from the epicardium toward the endocardium in the left myocardium. Potassium chloride-arrested hearts showed a reverse gradient in the left myocardium. In normal hearts, erythrocytes are oriented in capillaries so that their flat sides lie against the nearest myocardial cell. In the arrested hearts, one sees few or no erythrocytes with this orientation. The erythrocytes in the arrested hearts are swollen, rounded, or packed in clumps in the capillaries. Arrested hearts exhibit a weakening of the connective tissue elements of the myocardium, evident upon fixation or on perfusion of the myocardium with blood. The weakening increases as the length of myocardial arrest increases.
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Reynolds et al. (1958) studied this question.
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