Circulatory shock
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Any beneficial effects of prostaglandin synthesis inhibitors on systemic hemodynamic derangements during sepsis may be offset by the effect of these inhibitors to reduce renal blood flow. To determine the specific role of prostaglandins in maintaining renal perfusion during hyperdynamic live Escherichia coli bacteremia in rats, we used in vivo video-microscopy and optical doppler velocimetry to quantitate changes in renal microvascular blood flow, and to determine if endogenous prostaglandins participate in these responses. E. coli infusions constricted preglomerular arterioles and decreased renal microvascular blood flow in decerebrate animals without drug anesthesia but dilated pre- and postglomerular arterioles in urethane-anesthetized rats. Local inhibition of renal prostaglandin production with mefenamate after E. coli infusion caused renal arteriolar constriction in both groups and decreased renal blood flow to indicate that renal prostaglandin production is an important mechanism for maintenance of renal microvascular blood flow during high cardiac output sepsis.
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Adult respiratory distress syndrome has been described in patients following multiple trauma and hemorrhagic shock. Pure hemorrhagic shock in sheep does not lead to pulmonary dysfunction. To settle this seeming discrepancy, we hypothesized that an additional factor such as intraperitoneal blood was necessary to produce pulmonary dysfunction. ⋯ Blood hemoglobin decreased to 7.6 g/dl (P less than 0.0001) and platelets to 309,000/microliter (P less than 0.05). Pulmonary microvascular pressure fell to 6.7 torr (P less than 0.01) and pulmonary wedge pressure to 1.2 torr (P less than 0.005). These parameters were not altered by instillation of unclotted blood into the peritoneal cavity.(ABSTRACT TRUNCATED AT 250 WORDS)