{'fraction_non_alphanumeric': 0.026485325697924122, 'fraction_numerical': 0.009305654974946313, 'mean_word_length': 5.819512195121951, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Ouabain-Induced Mechanical Toxicity: Aberrations in Left Ventricular Function, Calcium Concentration, and Ultrastructure

Abstract The isolated rabbit heart was employed to determine if the myocardial mechanical dysfunction (mechanical toxicity) produced by digitalis was accompanied by ultrastructural lesions and an excessive accumulation of calcium by the cardiac cell. Ouabain (1.2 or 2.4 μM) produced a transient increase and then a continuous decrease in the systolic pressure development by the isovolumic left ventricle. The end-diastolic pressure increased progressively during the time that the systolic pressure was diminishing. The ultrastructural abnormalities that were observed in the ouabain-treated hearts included swollen mitochondria, hypercontracted sarcomeres and, occasionally, myofibrillar disruption. The left ventricular cellular calcium concentration was increased (P < 0.05) in these mechanically toxic hearts and this increase correlated significantly (r = 0.65, P < 0.05) with the magnitude of the increase in end-diastolic pressure. Furthermore, a reduction in the perfusate calcium concentration did not attenuate the ouabain-stimulated uptake of calcium. The data suggest that the impaired mechanical performance and the ultrastructural aberrations that may develop in the digitalis-treated heart are related to an excessive uptake of calcium by the left ventricle.