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Effect of halothane on synthesis and secretion of liver proteins

T1 - Effects of halothane anesthesia on vasoconstrictor response to N(G)- nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, in sheep

N2 - Administration of the oxidant lipid peroxide tertiary butyl hydroperoxide (t-bu-OOH) in the isolated rabbit lung leads to acute pulmonary vasoconstriction, which is caused by the synthesis of thromboxane. The inhalation anesthetics, halothane, nitrous oxide, and cyclopropane, markedly enhance t-bu-OOH-induced pulmonary vasoconstriction and thromboxane production. The effects of the intravenous (iv) barbiturates thiopental and pentobarbital on t-bu-OOH-induced vasoconstriction were studied. Thiopental completely and pentobarbital partially blocked t-bu-OOH-induced vasoconstriction. Thiopental inhibited t-bu-OOH-induced synthesis of thromboxane and prostacyclin but pentobarbital did not. This inhibitory action of thiopental may be due to its antioxidant properties because similar inhibition has been observed of t-bu-OOH-induced thromboxane production with the antioxidants, vitamin E, or butylated hydroxylanisole. Thiopental and pentobarbital also inhibited the vasoconstriction induced by a thromboxane analog, epoxymethano prostaglandin H2 (U46619). Finally, both barbiturates partially inhibited the pulmonary vasoconstriction caused by potassium chloride, which requires calcium entry, but they did not inhibit the constriction caused by angiotensin II, which does not require calcium entry. These results suggest that pentobarbital and thiopental may block pulmonary vasoconstriction by inhibiting calcium entry.

New synthesis of (+)-(S)-halothane | Request PDF

Synthesis of New Synthons for Organofluorine …

| A new synthesis of non-racemic halothane (1-bromo-1-chloro-2,2,2-trifluoroethane) is reported

Administration of the oxidant lipid peroxide tertiary butyl hydroperoxide (t-bu-OOH) in the isolated rabbit lung leads to acute pulmonary vasoconstriction, which is caused by the synthesis of thromboxane. The inhalation anesthetics, halothane, nitrous oxide, and cyclopropane, markedly enhance t-bu-OOH-induced pulmonary vasoconstriction and thromboxane production. The effects of the intravenous (iv) barbiturates thiopental and pentobarbital on t-bu-OOH-induced vasoconstriction were studied. Thiopental completely and pentobarbital partially blocked t-bu-OOH-induced vasoconstriction. Thiopental inhibited t-bu-OOH-induced synthesis of thromboxane and prostacyclin but pentobarbital did not. This inhibitory action of thiopental may be due to its antioxidant properties because similar inhibition has been observed of t-bu-OOH-induced thromboxane production with the antioxidants, vitamin E, or butylated hydroxylanisole. Thiopental and pentobarbital also inhibited the vasoconstriction induced by a thromboxane analog, epoxymethano prostaglandin H2 (U46619). Finally, both barbiturates partially inhibited the pulmonary vasoconstriction caused by potassium chloride, which requires calcium entry, but they did not inhibit the constriction caused by angiotensin II, which does not require calcium entry. These results suggest that pentobarbital and thiopental may block pulmonary vasoconstriction by inhibiting calcium entry.

This study tests the hypothesis that halothane-induced inhibition of the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) pathway significantly contributes to cardiovascular performance and thus reduces the vasoconstrictor response to NO synthesis inhibitors in vivo. We determined the effects of the administration of the NO synthesis inhibitor N(G)-nitro- L-arginine methyl ester (L-NAME) in chronically instrumented, halothane- anesthetized sheep and in awake control animals. Six sheep underwent halothane anesthesia (1.5 vol%) with mechanical ventilation. Five sheep were studied in the awake state with spontaneous breathing. Both groups received a bolus of L-NAME (25 mg/kg), followed 4 h later by L-arginine (300 mg/kg) to reverse the effects of L-NAME. L-NAME administration caused a significant increase in pulmonary and systemic vascular resistance (P

Synthesis of fluorine compounds using zinc complex of halothane

AB - The two most critical variables necessary to initiate halothane induced liver injury are induction of the hepatic biotransformation enzyme system and a reduced inspired oxygen concentration, which results in an increased rate of halothane biotransformation by the reductive, hepatotoxic pathway. Additional evidence implicating halothane bioactivation as a causative factor is indicated by the inhibition of the lesion by pretreatment of rats with inhibitors of drug metabolism. At present the hypoxic model does not completely correlate with the reported clinical cases of fulminating liver injury following halothane anesthesia. The lesion that develops in rat liver rapidly repairs and does not progress to liver failure. Also, female rats appear resistant. The latter problem has been partially resolved by pretreatment of female rats with testosterone a hormone necessary for maximal microsomal cytochrome P-450 mediated reactions in both male and female rats. Some progress has also been made at prolonging the duration of liver injury by inhibition of liver repair processes with inhibitors of protein synthesis. However, it should be stressed that only a small percentage of animals would be expected to develop progressive liver failure and that only a small number have been studied longer than 2 days post exposure. Perhaps the most exciting finding is the inhibition of lesion development by post-anesthetic treatment with sulfhydryl containing compounds. Cystamine, cysteine and N-acetylcysteine produced nearly complete inhibition when administered 4 hours after end of anesthesia and afford partial protection 8 hours post anesthesia.

Inhibition of Synthesis of Lung Proteins by Halothane

The commercial synthesis of halothane starts from , which is reactedwith in the presence of at 130°C toform 2-chloro-1,1,1-trifluoroethane. This is then reacted with at 450°C to producehalothane.

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Effects of halothane on protein synthesis and …


It is also an important reagent in organic synthesis

AB - This study tests the hypothesis that halothane-induced inhibition of the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) pathway significantly contributes to cardiovascular performance and thus reduces the vasoconstrictor response to NO synthesis inhibitors in vivo. We determined the effects of the administration of the NO synthesis inhibitor N(G)-nitro- L-arginine methyl ester (L-NAME) in chronically instrumented, halothane- anesthetized sheep and in awake control animals. Six sheep underwent halothane anesthesia (1.5 vol%) with mechanical ventilation. Five sheep were studied in the awake state with spontaneous breathing. Both groups received a bolus of L-NAME (25 mg/kg), followed 4 h later by L-arginine (300 mg/kg) to reverse the effects of L-NAME. L-NAME administration caused a significant increase in pulmonary and systemic vascular resistance (P

Synthesis and Metabolism of Halothane-1-14C - Nature

AB - Administration of the oxidant lipid peroxide tertiary butyl hydroperoxide (t-bu-OOH) in the isolated rabbit lung leads to acute pulmonary vasoconstriction, which is caused by the synthesis of thromboxane. The inhalation anesthetics, halothane, nitrous oxide, and cyclopropane, markedly enhance t-bu-OOH-induced pulmonary vasoconstriction and thromboxane production. The effects of the intravenous (iv) barbiturates thiopental and pentobarbital on t-bu-OOH-induced vasoconstriction were studied. Thiopental completely and pentobarbital partially blocked t-bu-OOH-induced vasoconstriction. Thiopental inhibited t-bu-OOH-induced synthesis of thromboxane and prostacyclin but pentobarbital did not. This inhibitory action of thiopental may be due to its antioxidant properties because similar inhibition has been observed of t-bu-OOH-induced thromboxane production with the antioxidants, vitamin E, or butylated hydroxylanisole. Thiopental and pentobarbital also inhibited the vasoconstriction induced by a thromboxane analog, epoxymethano prostaglandin H2 (U46619). Finally, both barbiturates partially inhibited the pulmonary vasoconstriction caused by potassium chloride, which requires calcium entry, but they did not inhibit the constriction caused by angiotensin II, which does not require calcium entry. These results suggest that pentobarbital and thiopental may block pulmonary vasoconstriction by inhibiting calcium entry.

Synthesis and Metabolism of Halothane-1-14C

N2 - This study tests the hypothesis that halothane-induced inhibition of the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) pathway significantly contributes to cardiovascular performance and thus reduces the vasoconstrictor response to NO synthesis inhibitors in vivo. We determined the effects of the administration of the NO synthesis inhibitor N(G)-nitro- L-arginine methyl ester (L-NAME) in chronically instrumented, halothane- anesthetized sheep and in awake control animals. Six sheep underwent halothane anesthesia (1.5 vol%) with mechanical ventilation. Five sheep were studied in the awake state with spontaneous breathing. Both groups received a bolus of L-NAME (25 mg/kg), followed 4 h later by L-arginine (300 mg/kg) to reverse the effects of L-NAME. L-NAME administration caused a significant increase in pulmonary and systemic vascular resistance (P

It can be used to start or maintain anaesthesia

N2 - The two most critical variables necessary to initiate halothane induced liver injury are induction of the hepatic biotransformation enzyme system and a reduced inspired oxygen concentration, which results in an increased rate of halothane biotransformation by the reductive, hepatotoxic pathway. Additional evidence implicating halothane bioactivation as a causative factor is indicated by the inhibition of the lesion by pretreatment of rats with inhibitors of drug metabolism. At present the hypoxic model does not completely correlate with the reported clinical cases of fulminating liver injury following halothane anesthesia. The lesion that develops in rat liver rapidly repairs and does not progress to liver failure. Also, female rats appear resistant. The latter problem has been partially resolved by pretreatment of female rats with testosterone a hormone necessary for maximal microsomal cytochrome P-450 mediated reactions in both male and female rats. Some progress has also been made at prolonging the duration of liver injury by inhibition of liver repair processes with inhibitors of protein synthesis. However, it should be stressed that only a small percentage of animals would be expected to develop progressive liver failure and that only a small number have been studied longer than 2 days post exposure. Perhaps the most exciting finding is the inhibition of lesion development by post-anesthetic treatment with sulfhydryl containing compounds. Cystamine, cysteine and N-acetylcysteine produced nearly complete inhibition when administered 4 hours after end of anesthesia and afford partial protection 8 hours post anesthesia.

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