Articles: sepsis.
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Critical care medicine · Mar 1994
Hematocrit modifies the circulatory control of systemic and myocardial oxygen utilization in septic sheep.
To describe the relationship between hematocrit and oxygen utilization before and after the onset of a hyperdynamic septic state. ⋯ The normal circulatory compensation to anemia in hyperdynamic sepsis includes increases in cardiac index and whole-body oxygen extraction, although greater reliance is likely placed on the use of systemic flow reserve to maintain tissue oxygen uptake in septic vs. healthy study conditions. Furthermore, increased reliance on myocardial oxygen extraction in sepsis suggests that the normal flow-reserve supporting myocardial oxygen availability may be limited in this syndrome.
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This study assessed the hepatic acute phase response and cellular Ca2+ regulation in septic animals and in hepatoma cell lines in vitro. Sepsis was induced in male Sprague-Dawley rats by implanting in their abdominal cavities fecal pellets impregnated with live Escherichia coli and Bacteroides fragilis. 8 h after implantations, rats were treated with diltiazem (1.2 mg/kg) or superoxide dismutase (SOD) (5 x 10(3) units/kg). After 24 h, plasma acute phase proteins (APP) were determined by immunoelectrophoresis, and hepatic APP-mRNAs by Northern blot hybridization. ⋯ Because diltiazem was previously shown to prevent sepsis-related disturbances in hepatic cellular Ca2+ regulation, its mediation of decrease in APP, systemic/metabolic response, and mortality may be effected through modifications in cellular Ca2+ regulation. The data from hepatoma cells show an attenuation of the AAP can result from direct effects of a calcium blocker. However, whether the blocker primarily modifies cellular Ca2+ regulation and secondarily effects APP gene expression, or directly effects gene expression remains unknown.
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Acute renal failure (ARF) is often a component of multiple organ system failure in critically ill patients. Sepsis (i.e. systemic bacterial infection) is a major factor in the aetiology of ARF and this is primarily caused by sepsis-induced cardiovascular and pulmonary failure. ⋯ However, ARF in the course of sepsis or endotoxaemia may not be solely due systemic or renal haemodynamic changes, since humoral and cellular reactions may also have an adverse effect on renal function. This review will address the haemodynamic and non-haemodynamic factors and their interaction in the development of ARF during sepsis.