Circulatory shock
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Glucose-insulin-potassium infused (GIK) during endotoxin shock causes increased cardiac output (CO) accompanied by decreased systemic vascular resistance. We have studied the effects of GIK on the distribution of cardiac output with radioactive microspheres to see if this decrease in resistance is equally distributed over all organs. GIK resulted in increased CO and increased flow to heart, splanchnic bed, kidneys, adrenals, and skeletal muscle, but fractional flow to these organs did not change. ⋯ Myocardial and splanchnic oxygen consumption did not change significantly. Oxygen extraction also diminished in these areas after GIK. GIK did not influence serum lactate: In both groups lactate increased significantly.
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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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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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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.
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The hemodynamic and ultrastructural effects of lidocaine HCl pretreatment were assessed on anesthetized rats subjected to acute hemorrhagic shock. After 40 minutes of acute hemorrhagic shock (mean arterial pressure = 40 mmHg), significantly less fluid infusion was needed to return mean arterial pressure to 120 mmHg in lidocaine HCl treated animals as compared to the hemorrhagic shock-untreated group (p less than 0.05). Heart rate was significantly lower in lidocaine treated animals in the immediate post-shock period (p less than 0.05). ⋯ However, in the hemorrhagic shock-untreated group all arterial pressures were still significantly lower than their baseline values (p less than 0.05). Ultrastructural myocardial ischemic changes appeared to be less severe in the lidocaine HCl treated animals. Lidocaine HCl pretreatment improved the response to hemorrhagic shock and reinfusion in this model of hemorrhagic shock.