In experimental chronic pericarditis with effusion, edema formation is initiated by elevated venous pressure and impaired renal sodium excretion, preceding any decline in resting cardiac output or renal blood flow.
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Edema may begin with venous pressure rise before output falls; hypothesis-generating in animal pericarditis and requires human validation.
Recent studies of the mechanism of congestive heart failure have brought forth new data on the changes in cardiac output, central venous pres- sure, renal blood flow, and salt and water excre- tion, which have led to new interpretations of the pathogenesis of this syndrome (1-10). Several basic problems remain unsolved, however. Their resolution has been handicapped by the inability to reproduce chronic congestive heart failure in laboratory animals (11).
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Fishman et al. (1950) studied this question.
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