The American journal of medicine
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Increased left ventricular filling pressure and reduced cardiac output are two major hemodynamic deficits in pump failure. In patients with chronic heart failure, consequences of these hemodynamic deficits and diminished cardiac reserve are manifested initially during stress and eventually at rest. ⋯ These data suggest improved left ventricular performance with a combination of nitrates and hydralazine. Exercise hemodynamics improved in some patients, suggesting that such vasodilator therapy may be beneficial in chronic heart failure.
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Comparative Study
Hemodynamic responsiveness to short- and long-acting vasodilators in left ventricular failure.
Vasodilators acutely reduce afterload and improve hemodynamics in congestive heart failure. Intravenous nitroprusside reduces left ventricular filling pressure and increases cardiac output while modestly reducing blood pressure and not changing heart rate in patients with heart failure in whom this response is characteristic. Comparably reduced blood pressure during nitroprusside infusion in normal subjects or hypertensive patients without failure results in a decrease in cardiac output and tachycardia. ⋯ The quinazoline derivatives, trimazosin and prazosin, are also effective vasodilators, which act on both arteries and veins in patients with congestive heart failure. The hemodynamic response to vasodilators is influenced by the underlying hemodynamic status, as the change in cardiac output is directly related to base line ventricular filling pressure as well as systemic vascular resistance, and inversely related to the base line cardiac output. Response to vasodilators does not appear to be altered by age, diabetes, acute myocardial infarction or the cause of congestive myocardiopathy.
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A middle-aged man with lymphocytic lymphoma had numerous sea-blue histiocytes in his bone marrow, splenomegaly and thrombocytopenia. Thus, his illness mimicked that of patients with the primary syndrome of the sea-blue histiocyte. However, the paucity of sea-blue histiocytes in his spleen, the absence of neurologic disease, his age and the ultrastructure of his abnormal histiocytes were all evidence for the presence of the acquired syndrome. The pathogenesis of sea-blue histiocytosis and the relationship between acquired cases and the primary syndrome are discussed.
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Although the morphologist continues to describe cholestasis on the basis of precipitated bile seen on light microscopic sections of the liver or dilated canaliculi with loss of microvilli seen by electron microscopy, the physiologist can distinguish clearly between hyperbilirubinemia and cholestasis. Both bilirubin and bile acids are specifically removed from sinusoidal plasma by the normal hepatocyte and appear in bile in high concentration. Bilirubin conjugation and excretion appear to be governed by hepatocellular mechanisms that are, for the most part, separate from the conjugation and excretion of bile acids. ⋯ By contrast, cholestatic syndromes are characterized by marked bile acidemia with normal to slightly elevated bilirubin levels. Severe cholestasis, because of the marked reduction in bile flow, can however, engender jaundice. Further exploration of these excretory pathways will provide interesting new insights on the numerous cholestatic and hyperbilirubinemic syndromes that occur in nature.