Circulatory shock
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Anesthetized spontaneously hypertensive rats (SHR) and normotensive WKY controls were subjected to either a constant pressure (CPH) (constant mean arterial pressure of 35 mmHg) or an incremental volume (IVH) hemorrhage protocol (successive 1-ml blood withdrawals separated by 20 minute compensatory periods). Diameters and pressures were measured in small (400-600 micron) intestinal mesenteric veins before and during hemorrhage. Before hemorrhage, vasodilator suffusion produced a significant venodilation in SHR but not in WKY. ⋯ During CPH, venous pressures in WKY were significantly higher than those in SHR. However, venous pressures in SHR and WKY were not significantly different during CPH with vasodilator suffusion. This study indicates that a decreased reserve capacity for compensatory venoconstriction may contribute to the reduced ability of SHR to tolerate hypotensive stress.
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The pathogenesis of burn shock syndrome involves the production of superoxide radicals which are first generated in the burned skin. They are responsible for an increase in vascular permeability with loss of plasma, which results in hemoconcentration and hypovolemia. The resulting systemic hypoperfusion leads to a generalized production of superoxide radicals and subsequent cellular damage. Prior administration of allopurinol or superoxide dismutase increases the survival rates of mice subjected to burn shock.
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Cellular membrane destabilization induced by endotoxin and endogenous inflammatory mediators contributes significantly to the progression of metabolic and hemodynamic dysfunction in endotoxemia. Owing to its membrane-stabilizing properties, lidocaine may prove beneficial in the treatment of endotoxic shock. Twelve 50-kg pigs were surgically fitted with jugular venous and carotid arterial catheters. ⋯ U-14C-glucose-derived glucose recycling was increased above the lidocaine group's preendotoxin control period and reached values twice those of the untreated pigs' endotoxin infusion period. Compared to their own control period and the untreated group's endotoxin infusion period, percentage lactate/glucose was decreased from 40 min on. Lidocaine treatment elicited modest improvements in systemic arterial blood pressure and reduced relative glucose utilization and gluconeogenesis, but in itself, was not a sufficient therapy for endotoxic shock in this model.
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The effects of temperature on naloxone treatment in canine hemorrhagic shock were examined in 24 dogs hemorrhaged to a mean arterial blood pressure of 35 mm Hg (ambient temperature, 21 degrees C). After two hours of hypotension, the blood reservoir was clamped with no return of shed blood. Dogs were divided into three groups: Control (n = 8) received normal saline (0.5 cc/kg/hr); naloxone-cold (n = 8) and -warm (n = 8) received naloxone (2 mg/kg bolus and 2 mg/kg/hr constant infusion). ⋯ In the warmer dogs, naloxone significantly improved hemodynamic function and myocardial perfusion as indicated by the increased mean arterial pressure, cardiac output, stroke volume, dP/dt, and coronary blood flow. Furthermore, naloxone reduced plasma beta-endorphin levels and corrected the metabolic derangements of shock in this group. Our data indicate hypothermia significantly diminished the beneficial effects of naloxone treatment in canine hemorrhagic shock.
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We compared the use of hypertonic salt solution (300 mEq Na/liter) with Ringer's lactate as an initial resuscitation fluid for the treatment of hemorrhagic shock. We monitored vascular pressures and cardiac output as well as microvascular function using chronic lymph fistulae in the lung and soft tissues to reflect transvascular fluid and protein flux. Seven unanesthetized sheep were bled to an aortic pressure of 50 mm Hg (2 hours) on two occasions 4-5 days apart, and were resuscitated initially with either lactated Ringer's (LR) or hypertonic saline (HS) to restore left atrial pressure to baseline. ⋯ The initial pulmonary hypertension seen with LR was eliminated with HS. Lymph flow in lung and soft tissue increased to a comparable degree in both groups, the increase being explained by the degree of plasma hypoproteinemia which was present. We conclude that HS increases cardiac output with less net fluid, decreases pulmonary vascular resistance, and does not result in more edema formation when compared with lactated Ringer's as an initial fluid for treatment of hemorrhagic shock.