[Impact of the combined application of elastic bandaging of the lower extremities and autohemotransfusion on biochemical indices of the blood and severity of endogenous intoxication in patients with concomitant cardiovascular insufficiency].

Venous congestion in abdominal inner organs in surgical diseases in patients with heart insufficiency may additionally impact biochemical indices of the blood and severity of endogenous intoxication (EI). Basing on the data obtained in the investigations, th was established, that the lower extremities bandaging promotes exit of the blood from depot, where it resides in a concentrated state in cellular and biochemical aspects. It promotes more effective accomplishment of hemodilution as well as reduction of the EI severity in taking of the autologous blood.

Lidocaine attenuates the hypotensive and inflammatory responses to endotoxemia in rabbits.

OBJECTIVE: To assess the effects of lidocaine on the hemodynamic and inflammatory responses to Escherichia coli endotoxemia in rabbits. DESIGN: Prospective, randomized, controlled experimental study. SETTING: University laboratory. SUBJECTS: Twenty-seven female Japanese rabbits, anesthetized with urethane and ventilated mechanically. INTERVENTIONS: Animals were randomly assigned to one of three groups: a) endotoxemic control group (n = 9), receiving intravenous Escherichia coli endotoxin (0.5 mg/kg bolus) via the mesenteric vein; b) laparotomy control group (n = 9), treated identically to the endotoxemic control group, except for substitution of 0.9% saline for endotoxin; and c) lidocaine-treated group (n = 9), treated identically to the endotoxemic controls and additionally, intravenous lidocaine (3 mg/kg bolus, followed by infusion at 2 mg/kg/hr) was administered immediately after endotoxin MEASUREMENTS AND MAIN RESULTS: We compared hemodynamics, blood gases, and microscopic findings of lung tissue obtained at necropsy in each group. Laparotomy alone had a minimal effect on the parameters and findings. Endotoxin injection decreased mean systolic arterial pressure from 135 +/- 6 (SD) to 95 +/- 25 mm Hg (p < .05) and increased the mean base deficit from -1.2 +/- 1.8 to -14.4 +/- 4.2 mmol/L (p < .05), and caused the infiltration of neutrophils into the lungs. Lidocaine administration abolished the hypotension and attenuated the increase the base deficit to -9.5 +/- 2.1 mmol/L (p < .05) and the cellular infiltration in comparison with endotoxemic controls. CONCLUSIONS: Lidocaine attenuated the hemodynamic and inflammatory responses to endotoxemia in rabbits. Findings suggest that lidocaine administration may prevent the development of hypotension and metabolic acidosis during endotoxemia.

Endogenously opsonized particles divert prostanoid action from lethal to protective in models of experimental endotoxemia.

We report that, in rats, the lethal consequences of high-dose endotoxin challenge are exacerbated by the intravascular administration of prostaglandin E1 but attenuated by the intravascular administration of endocytosable particles. This protection is mediated by opsonins. Nonopsonizable particles were unable to provide protection unless first pseudoopsonized with antibody directed against the CR3 (CD11b/CD18) phagocyte receptor. We show that endogenously opsonized particles can act in concert with prostaglandin E1 (putatively by elevation of neutrophil intracellular cAMP and the resultant downregulation of CR3) to completely rescue animals from the lethal late-stage sequelae of experimental endotoxemia. These data illustrate that the interaction of particles with cellular receptors can transform the overall systemic response to prostaglandin E1 from pro- to antiinflammatory. This suggests a role for multiple receptor engagement events in defining the systemic prostaglandin response and offers a rationale for developing new therapeutic modalities in the treatment of sepsis and other inflammatory diseases.

[The participation of the renin-angiotensin-aldosterone system in the pathogenesis of acute kidney failure in endotoxemia]. / Uchastie renin-angiotenzin-al 'dosteronovoi sistemy v patogeneze ostroi nedostatochnosti pochek pri éndotoksemii.

It was found in acute experiments on white rats that injection of Salmonella typhimurium lipopolysaccharide activates renin-angiotensin-aldosterone system (RAAS) and causes oligohydruria form of acute renal failure (ARF). Enalapril, angiotensin-converting enzyme, being injected simultaneously with endotoxin, increases diuresis, glomerular filtration rate, electrolytes excretion and reabsorption by proximal tubules, decreases proteinuria and blood nitrogen-down to the normal. Thus, RAAS takes part in endotoxemia ARF induction and enalapril has protective effect.

Influence of omega-3 fatty acids on splanchnic blood flow and lactate metabolism in an endotoxemic rat model.

Alteration in regional blood flow is important in the pathogenesis of organ failure during endotoxemia and sepsis. In particular, intestinal ischemia is thought to enhance the translocation of bacteria into the systemic circulation. We used radioactive microspheres to measure the influence of two intravenous (IV) dietary fats (vegetable oil containing high levels of omega-6 fatty acids, and fish oil containing high levels of omega-3 fatty acids) on regional blood flow during low-dose Escherichia coli endotoxin infusion (0.1 mg/100 g body weight [BW]) in a rat model. Despite absence of changes in the cardiac output, blood flow rates to the small and large intestines, stomach, and pancreas, and also to the skin and skeletal muscle were significantly reduced after 18 hours of endotoxin infusion in the rats fed standard vegetable oil. Short-term IV feeding during a period of 40 hours with an isonitrogenous, isocaloric nutrient solution containing fish oil as the only lipid source normalized intestinal perfusion and increased blood flow to the liver and spleen. Low-dose endotoxin infusion also resulted in significant increases in glucose, lactate, and pyruvate concentrations. In comparison to standard vegetable fat emulsion, fish oil significantly reduced these parameters. A second experiment was conducted to measure lactate kinetics. Based on the dilution of U-14C-lactate, fish oil feeding was associated with higher lactate clearance than standard vegetable oil feeding during the endotoxin infusion. We conclude that short-term IV feeding with fish oil improves intestinal perfusion and portal blood flow, improves glucose tolerance, and increases lactate clearance in a low-dose endotoxin rat model.