Critical care medicine
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Critical care medicine · May 1994
Protecting the gut and the liver in the critically ill: effects of dopexamine.
To measure the clinical effects of dopexamine on systemic and splanchnic perfusion in critically ill patients. ⋯ Dopexamine improves gastric intramucosal pH, and thus, splanchnic oxygenation. This improvement in gastric intramucosal pH appears to be independent of dopexamine's systemic effects.
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Critical care medicine · May 1994
Comparative StudyIncreased plasma concentrations of soluble tumor necrosis factor receptors in sepsis syndrome: correlation with plasma creatinine values.
Tumor necrosis factor (TNF) is an important mediator in the complex pathophysiology of sepsis syndrome. Although a positive correlation with mortality rate has been demonstrated, TNF has not been found consistently in sepsis. Since prolonged increases in soluble TNF receptor concentrations were demonstrated after endotoxin and TNF administration, we investigated whether the measurement of TNF receptor concentrations could provide a better indicator of disease than plasma TNF and interleukin (IL)-6 concentrations. ⋯ In the population studied, plasma-soluble TNF receptor concentrations correlated with outcome as well as with plasma creatinine concentrations. The data presented suggest that increased plasma-soluble TNF receptor concentrations in patients with sepsis syndrome are merely the result of renal failure complicating sepsis, and are similarly correlated with mortality rate.
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Critical care medicine · May 1994
Ventilatory response to high caloric loads in critically ill patients.
To assess the effect of high caloric loads on CO2 metabolism and ventilation. ⋯ Increased CO2 production, exhaled minute ventilation, and deadspace ventilation values in the overfed group and the lack of difference between alveolar ventilation, PaCO2, and measured energy expenditure, along with correlations between CO2 production and alveolar ventilation suggest that carbohydrate loads increase CO2 production which drives alveolar ventilation, thus preventing hypercapnia. When alveolar ventilation does not increase (and PaCO2 increases) or when the spontaneous breathing rate increases to augment alveolar ventilation, the clinical response of increasing mechanical ventilation may increase deadspace ventilation.