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)
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Inhalation injury was produced in sheep that were chronically prepared for study. The injury was induced by insufflating them with smoke from burning cotton cloth. One group of animals was treated with the oxygen-free radical scavenger dimethylsulfoxide (DMSO) and heparin. ⋯ The treated groups showed much smaller responses to the inhalation insult. This was especially true in the animals that received the DMSO. These findings support the concept that oxygen free radicals are responsible for the pulmonary edema associated with inhalation injury.
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Hypertonic saline (ie, 7.5% NaCl) was injected intravenously (4 ml/kg bolus) to determine its effects in feline and murine models of hemorrhagic shock. Hypertonic NaCl transiently improved mean arterial blood pressure (MABP), superior mesenteric artery blood flow (SMAF), and cardiac output (CO) during the oligemic period. These effects lasted from 15 to 75 min. ⋯ Nevertheless, the plasma activity of a myocardial depressant factor (MDF) was significantly lower in shock cats and rats given hypertonic saline compared with the 0.9% NaCl groups (31 +/- 4 vs 54 +/- 7 U/ml, p less than 0.02, in cats; and 27 +/- 2 vs 51 +/- 7 U/ml, p less than 0.02, in rats). The beneficial effects of small-volume resuscitation with 7.5% NaCl during hemorrhagic shock in cats and rats are likely due to the transient hemodynamic improvement during the oligemic period rather than sustained improvement in splanchnic perfusion or in prevention of cellular injury during shock. Our results in two species (eg, cat and rat) suggest that small-volume resuscitation with 7.5% NaCl may be a useful initial treatment of hemorrhagic shock when supplemented by subsequent blood transfusion or perhaps some other appropriate pharmacologic intervention.