Circulatory shock
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Thirty dogs underwent hemorrhage over a 60 minute period to a predetermined O2 debt of 60-120 mL O2/kg, quantified real-time by a Beckman metabolic cart; they were then resuscitated with 120% of the shed volume. The [total amino acids], [lactate], and [alanine]/[glutamine] rose during hemorrhage and resuscitation. Blood pressure, VO2, cardiac index, circulating amino acid pool, and systemic amino acid transport decreased during hemorrhage, but rose during resuscitation. ⋯ The O2 debt during hemorrhage was substantially better related to [lactate] compared to shed volume or blood pressure. The changes in [total amino acids] and [alanine]/[glutamine] and their relationship to O2 debt suggest a hemorrhagic-induced alteration in tissue amino acid kinetics. These data further suggest that using a metabolic substrate parameter such as O2 utilization is useful to stratify other cellular alterations such as amino acid uptake and release and lactic acidosis.
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The present work is a continuation of studies concerned with mathematical modelling and simulation of microvascular fluid and protein exchange following burn injuries [Bert et al.: Circulatory Shock 28: 199-219, 1989: Bowen et al.: Circulatory Shock 28: 221-233, 1989]. The model has been extended to include the effects of different types of fluid resuscitation on the circulatory and microvascular exchange systems. The model and a statistical fitting procedure were used to find the ranges of fitting parameter values that best describe the changes in interstitial fluid volume and protein mass as well as transcapillary protein extravasation for three sets of experiments (no resuscitation, resuscitation with Ringer's or resuscitation with plasma). Typical changes in mass exchange related parameters postburn that resulted in simulation predictions which were a good fit to the experimental data include: an increase in the large pore pathway for protein of 100 times in the injured skin and 5 times in non-injured skin and skeletal muscle, an increase in fluid filtration coefficients in injured skin of 10 times and an instantaneous decrease of 50% in the area available for exchange in injured skin at the time of the burn.
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Extracorporeal membrane oxygenation (ECMO) can provide total cardiopulmonary support via extrathoracic vascular cannulation. We evaluated the effects of ECMO in gram-negative septic shock in immature piglets subjected to fecal-Escherichia coli peritonitis. Group I, SEPSIS CONTROL (n = 10), had an intraperitoneal injection of E. coli but did not receive ECMO. ⋯ Conventional ventilatory therapy was unsuccessful in each. Systemic arterial blood pressure was significantly higher in ECMO CONTROL animals (P less than 0.01) as were leukocyte counts (P less than 0.01). In this model of gram-negative septic shock, ECMO did provide cardiopulmonary support but did not improve mortality.
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Monophosphoryl lipid A (MPL) is a nontoxic derivative of lipid A. In this study, the induction of tolerance by MPL to the hemodynamic effects of lethal endotoxemia was tested. Ten Sprague-Dawley rats were received either Salmonella minnesota MPL 0.5 mg/100 g intravenously (i.v.) or equivalent volume of diluent (control) i.v. on day zero. ⋯ Arterial lactate was 2.6 +/- 0.3 mmol/liter in controls and 1.3 +/- 0.2 mmol/liter in MPL animals at 6 hr (P less than 0.05). The controls died 7.5 +/- 1.3 hr after LPS administration, whereas all the MPL-pretreated animals survived. These data indicate that MPL induces tolerance to the acute hemodynamic effects of LPS and enhances survival from lethal endotoxemia.