Critical care medicine
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Critical care medicine · Aug 1997
Clinical TrialInsights into the increased oxygen demand during chest physiotherapy.
To determine the mechanism responsible for the increase in oxygen consumption (VO2) during chest physical therapy. Specifically, to examine the hypothesis that muscular activity is the major contributor to the increase in oxygen demand. ⋯ The increase in metabolic demand during chest physiotherapy is the result of increased muscular activity as evidenced by the suppression of VO2 following the administration of the muscle relaxant and the observation that turning a patient into the lateral decubitus position produces similar increases in VO2. The increases in blood pressure and cardiac output are due to another mechanism, most likely enhanced sympathetic output. The increase in physiologic activity produced by chest physiotherapy is thus secondary to both exercise-like and stress-like responses.
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Critical care medicine · Aug 1997
Apoptosis in lymphoid and parenchymal cells during sepsis: findings in normal and T- and B-cell-deficient mice.
To determine if apoptosis (programmed cell death) occurs systemically in lymphoid and parenchymal cells during sepsis. To examine the potential role of T and B cells in the apoptotic process using knockout mice deficient in mature T and B lymphocytes. ⋯ Apoptosis is an important mechanism of cell death in lymphocytes and parenchymal cells in sepsis and occurs systemically in many organs. Apoptosis may be an important cause of immunologic suppression in sepsis by inducing widespread lymphocyte depletion. Alternately, apoptosis may be beneficial to host survival by down-regulating the inflammatory response which accompanies sepsis. The degree to which parenchymal cell apoptosis is contributing to multiple organ failure cannot be determined from the present study. Findings in Rag-1 mice demonstrate that mature T and B cells and their secretory products are not necessary for apoptosis to occur during sepsis and that apoptotic cell death is not restricted to T or B cells. Apoptosis may be a key regulator of the balance between the pro- and anti-inflammatory process.
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Critical care medicine · Aug 1997
Comparative StudyEffects of hypoxemia and reoxygenation with 21% or 100% oxygen in newborn piglets: extracellular hypoxanthine in cerebral cortex and femoral muscle.
To determine whether reoxygenation with an FIO2 of 0.21 (21% oxygen) is preferable to an FIO2 of 1.0 (100% oxygen) in normalizing brain and muscle hypoxia in the newborn. ⋯ Significantly higher extracellular concentrations of hypoxanthine were found in the cerebral cortex during the initial period of reoxygenation with 100% oxygen compared with 21% oxygen. Hypoxanthine is a marker of hypoxia, and reflects the intracellular energy status. These results therefore suggest a possibly more severe impairment of energy metabolism in the cerebral cortex or an increased blood-brain barrier damage during reoxygenation with 100% oxygen compared with 21% oxygen in this newborn piglet hypoxia model.
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Critical care medicine · Aug 1997
Behavior of nitric oxide infused at constant flow rates directly into a breathing circuit during controlled mechanical ventilation.
This study was designed to test the hypothesis that the practice of infusing nitric oxide at constant flow rates directly into breathing circuits with intermittent (pulsatile) flow can lead to streaming and tidal pooling of the nitric oxide. This study was also designed to show the extent to which streaming and tidal pooling of nitric oxide affect nitric oxide delivery. ⋯ Estimates of nitric oxide delivery using a constant flow rate of nitric oxide infused directly into a breathing circuit during controlled mechanical ventilation can be confounded by streaming and tidal propagation of nitric oxide pools. Improved reproducibility of reported dose-response relationships is likely to be achieved through further study of nitric oxide behavior within the breathing circuits. Reduced toxicity associated with nitric oxide inhalation may also be achieved through a better understanding of this nitric oxide behavior.
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Critical care medicine · Aug 1997
Case Reports Clinical Trial Controlled Clinical TrialVasopressin pressor hypersensitivity in vasodilatory septic shock.