Journal of critical care
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Journal of critical care · Dec 1996
Exhaled nitric oxide as a marker for serum nitric oxide concentration in acute endotoxemia.
The main aim of this study was to assess the correlation between exhaled nitric oxide (NO) and serum NO concentrations during the course of endotoxemia. We also assessed whether or not the inducible isoform of NO synthase is responsible for the increase in NO production in endotoxemia animals. ⋯ These results suggest that exhaled NO accurately reflects changes in arterial serum NO concentration and that the source of enhanced NO release in acute endotoxemia is not the iNOS isoform.
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Journal of critical care · Dec 1996
Clinical TrialEffect of passive range of motion on intracranial pressure in neurosurgical patients.
A prospective patient study was done to evaluate the effect of passive range of motion (PROM) on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in neurosurgical patients. ⋯ PROM results in no significant changes in ICP or CPP in stable, neurosurgical patients in the absence of intracranial hypertension.
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Journal of critical care · Dec 1996
Reversal of muscle fatigue in intact rabbits by intravenous potassium chloride.
Skeletal muscle fatigue has been associated with potassium efflux from the myocytes, resulting in endogenous increases in blood potassium concentration ([K+]). Conversely, exogenous increases in extracellular [K+] potentiates contraction in isolated muscle preparations. The mechanisms responsible for these contradictory effects of [K+] on skeletal muscle function are unknown. Moreover, little is known about the effect of exogenous increases in [K+] on force generation by intact animals, given potassium's deleterious effect on cardiac function. ⋯ Exogenous increases in blood [K+] potentiate skeletal muscle contraction in intact animals and reverse low-frequency twitch fatigue. A possible mechanism may be the maintenance of intracellular [K+] by hindering K+ efflux from skeletal muscle cells.
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Journal of critical care · Dec 1996
The effects of high dose NG-nitro-L-arginine-methyl ester on myocardial blood flow and left ventricular function in dogs.
Nitric oxide (NO) synthase inhibition has been reported to cause elevation in mean arterial pressure (MAP) and a decrease in cardiac index (CI), the cause of which is not completely understood. It has been shown that increased concentrations of NO synthase inhibitors cause a further drop in cardiac output without a corresponding increase in arterial pressure, prompting the conclusion that NO inhibition results in direct myocardial depression. However, myocardial ischemia was not completely ruled out as a cause for myocardial dysfunction in these studies. The purpose of this study was to examine the effects of 30 mg/kg of the NO synthase inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) to those of 300 mg/kg and assess the effects on coronary ischemia and myocardial function. ⋯ L-NAME at 30 mg/kg caused a rise in MAP and systemic vascular resistance; however, it had no effect on ventricular function. High dose NO synthase inhibition causes myocardial depression not related to increased afterload, coronary vasoconstriction, or myocardial ischemia.
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The increase of cardiac output (CO) in sepsis must be matched by an increase in venous return. Our goal was to determine which of the determinants of venous return are responsible in volume-loaded and nonvolume-loaded pigs with endotoxemia. The determinants include stressed volume, venous compliance (Cv), venous resistance (RVR) and right atrial pressure (Pra). We also tested the effect of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine-methyl ester (L-NAME) after the hemodynamics with endotoxin stabilized. ⋯ Changes in vascular tone during endotoxemia are dependent on volume status. The increased cardiac output in volume-treated septic animals occurred because of an increase in stressed volume due to the volume given in combination with a dilated vasculature. L-NAME restored arterial tone but decreased CO because of a rise in RVR and decrease in cardiac function.