33 research outputs found

    Effects of ketamine, thiopental sodium and propofol on muscle contractures in rat diaphragm in vitro

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    PubMed ID: 1742205The effects of commonly used intravenous anaesthetic agents ketamine, thiopental sodium and propofol on the caffeine-alone or halothane-plus-caffeine-induced muscle contractures were investigated to determine safety for use in patients susceptible to malignant hyperthermia (MH). The muscle strips from rat diaphragm were exposed to one of these anaesthetic agents prior to challenge with caffeine 8 mmol/l alone or halothane 3% plus caffeine 8 mmol/l together. None of the three agents induced contractures when added alone. Ketamine 100 µmol/l and thiopental sodium 300 µmol/l augmented neither caffeine-alone nor caffeine-with-halothane contractures significantly and these two agents appear to be safe for use in MH-susceptible patients. In contrast, propofol 150 µmol/l augmented these contractile responses significantly and may not be recommended for use in patients known to be susceptible to this anaesthetic complication

    Effects of ketamine, thiopental sodium and propofol on muscle contractures in rat diaphragm in vitro.

    No full text
    The effects of commonly used intravenous anaesthetic agents ketamine, thiopental sodium and propofol on the caffeine-alone or halothane-plus-caffeine-induced muscle contractures were investigated to determine safety for use in patients susceptible to malignant hyperthermia (MH). The muscle strips from rat diaphragm were exposed to one of these anaesthetic agents prior to challenge with caffeine 8 mmol/l alone or halothane 3% plus caffeine 8 mmol/l together. None of the three agents induced contractures when added alone. Ketamine 100 mumol/l and thiopental sodium 300 mumol/l augmented neither caffeine-alone nor caffeine-with-halothane contractures significantly and these two agents appear to be safe for use in MH-susceptible patients. In contrast, propofol 150 mumol/l augmented these contractile responses significantly and may not be recommended for use in patients known to be susceptible to this anaesthetic complication

    Effects of MK-886, a leukotriene biosynthesis inhibitor, in a rabbit model of endotoxic shock

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    WOS: 000074468700011PubMed ID: 9696411Leukotrienes are one of the biological mediators that play a role in endotoxic shock. In this study, we investigated the effects of a leukotriene biosynthesis inhibitor, MK-886, in a rabbit model of endotoxic shock. Lipopolysaccharide (Escherichia coli serotype 055:B5) infusion (1 mg kg(-1) h(-1)) to rabbits caused a biphasic decline in arterial blood pressure and decreased the vasoresponsiveness to phenylephrine, potassium chloride, sodium nitroprusside and acetylcholine in abdominal aortic rings. Oral administration of MK-886 (3-(1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl(-2,2-dimethylpropanoic acid) (5 mg/kg) 3 h prior to lipopolysaccharide infusion significantly inhibited the decline in arterial blood pressure and enhanced the responsiveness to phenylephrine and acetylcholine, whereas the changes in sodium nitroprusside and potassium chloride responses were not significant. However, the pD(2) (-log EC50) values for sodium nitroprusside in this group were higher than those of the group that received lipopolysaccharide alone. Neither the administration of the vehicle alone to endotoxemic rabbits, nor MK-886 administration to control animals, caused significant changes. These data suggest that MK-886 attenuates the hypotension and partially reverses the impaired vascular responsiveness observed in endotoxic shock. (C) 1998 Elsevier Science B.V. All rights reserved

    Direct vasodilator effect of propofol on isolated rabbit vessels [PROPOFOLUN IZOLE TAVSAN DAMARLARINDA DIREKT VAZODILATOR ETKISI]

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    It has been demonstrated that propofol produces hypotension partially by its direct endothelium-independent vasodilatory effect on vascular smooth muscle. The present study was performed to investigate the role of local autocoid mediators on the direct vasodilator effect of propofol on isolated rabbit vessels. It was observed that propofol decreased basal tone of coronary vessels in Langendorff isolated rabbit heart, concentration, dependently and induced a concentration-dependent relaxation in the endothelium-denuded, isolated rabbit thoracic aorta precontracted with 5-hydroxytryptamine (5-HT), histamine, phenylephrine, PGF2? or KCl. But the difference between the concentrations inducing 50% relaxation was found to be statistically insignificant (p>0.05). Some aortic rings were contracted with 5-HT, histamine, phenylephrine and PGF2? and concentration-response curves were obtained. It was observed that when propofol was added prior to contractile agent, only the curve for 5-HT was shifted to right with a significant decrease in the maximum response. It was concluded that vasodilation induced by propofol might be mediated by a decrease in intracellular Ca++ effect and possibly, the blocking effect of propofol on the 5-HT receptors of vascular smooth muscle might play an additional role in this vasodilation
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