Circulatory shock
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In 16 anesthetized pigs the cardiovascular effects of prostaglandin E1 and methylprednisolone (MPS) during E. coli sepsis were studied. Gated blood pool scans and hemodynamic studies were simultaneously performed. A control group, group I (n = 4), received volume loading alone; groups II, III, and IV received (each n = 4) volume loading after intravenous administration of MPS, prostaglandin E1, and both MPS and prostaglandin E1, respectively. ⋯ The present study indicates that in a porcine model of E. coli septic shock with acute pulmonary hypertension, prostaglandin E1 and MPS treatment decrease pulmonary vascular resistance but also systemic vascular resistance. Prior to and during volume loading right ventricular ejection fraction increased in the prostaglandin E1 group. However, neither prostaglandin E1 nor MPS improved right ventricular performance and forward flow during volume loading.
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Previously, we have shown improved survival rate with colloid solutions of 2-4% concentration compared to 10% solutions or a colloid-free electrolyte solution, when given in volumes required to maintain the same intravascular volume expansion. This study examines the effect of increasing infusion volumes of Ringer's lactate (RL) and 3% albumin on survival time and blood volume expansion using the lethal intestinal ischemic shock model in rats. Shock was induced by exteriorization of the small intestine with added occlusion of the superior mesenteric vessels for 75 minutes. ⋯ No control animals survived 24 hours. Survival time was prolonged with both RL and 3% albumin infusions. The effect on survival time with albumin was obtained with approximately 25% of the fluid required for RL.
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Comparative Study
Prostacyclin and thromboxane A2 in septic shock: species differences.
Prostacyclin and thromboxane A2 have been implicated as mediators of septic shock. Correlations between the human prostanoid response to sepsis and experimental paradigms are poorly understood. The purpose of this study was to compare changes in plasma levels of prostaglandin 6-keto-F1 alpha (PGI) and thromboxane B2 (TxB) during septic shock in Sprague-Dawley rats, domestic pigs, mongrel dogs, and man. ⋯ In man, both PGI and TxB were significantly increased in severe sepsis, compared to normal controls, but only PGI was significantly higher in septic shock versus normotensive sepsis. Patterns of change in TxB/PGI ratios were similar for all species studied. Changes in PGI in the porcine septic experiments most closely paralleled those observed clinically.
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Radiolabeled microspheres were employed to measure the cerebrovascular response to severe anaphylactic-induced hypotension in pentobarbital-anesthetized dogs. A rapid drop in mean arterial pressure (MAP, 140 to below 50 mm Hg) coincided with total and regional cerebral blood flows (CBF) that were not significantly different from prechallenge values. While blood flow to the occipital region (highest measured region of the brain) was significantly greater than that of brainstem regions prior to and during the shock regimen, no major redistributional phenomena occurred to any cerebral region. ⋯ Similar to our previous findings, CBF was maintained to perfusion pressures of 39 +/- 4 mm Hg. The drop in cerebral vascular resistance during the severe hypotensive period was not associated with a significant decline in arterial PO2, or a significant increase in arterial PCO2, A-V PO2, or V-A PCO2. Our results suggest that the fall in cerebral vascular resistance during anaphylactic-induced hypotension would not be associated with a severely altered cerebral metabolism.