Objective We investigated the relationship between the right cardiac system and increased pulmonary artery systolic pressure (PASP) in the elderly.Patients and Methods Echocardiography stable state data were available for 163 of 200 consecutive autopsied patients. Of these, PASP could be estimated by extrapolation from the maximum pressure gradient in tricuspid valve regurgitation from echocardiograms in 73 cases; however, 22 cases with secondary changes attributable to left cardiac insufficiency had to be excluded. We studied the remaining 51 patients in detail (16 men, 35 women, age 68-103 years; mean, 87.7±8.1). We investigated the following: echocardiographic and pathologic variables, age, sex, body mass index, the survival time (from echocardiography to autopsy), and the presence or absence of chronic pulmonary disease.Results
Free radicals have been implicated in myocardial reperfusion injury. Hydrogen peroxide (H(2)O(2)) is one possible source of reactive oxygen intermediates. We studied the formation and toxicity of H(2)O(2) in isolated myocytes during hypoxia-reoxygenation with the use of cerium. This method involves formation of an electron-dense precipitate when H(2)O(2) reacts with cerium chloride (CeCl(3)). Single myocytes were obtained from rat hearts by collagenase digestion. Isolated myocytes were reoxygenated for 15 min after 30 min of hypoxia. The cells were treated with digitonin to increase the permeability of the plasma membrane, and CeCl(3) was added to detect intracellular H(2)O(2) on electron microscopy. In the nonhypoxia control group, the ultrastructure of cells was well preserved, and no dense deposits were found in myocytes. In the hypoxia-reoxygenation group, precipitates, i.e., Ce-H(2)O(2) reaction products, were found inside and along swollen mitochondria, and cell viability was reduced to 72.3% of control. These results indicate that endogenous H(2)O(2) is generated by mitochondria and that its release into the cytosol may lead to myocyte death under pathological situations such as hypoxia-reoxygenation.
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