PubMed · 6369259
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L Carter. Snatching the thyroid.. https://pubmed.ncbi.nlm.nih.gov/6369259/
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Anesthetic agents are often administered in the presence of ethyl alcohol, both in research and in the clinical setting. The authors tested the hypothesis that anesthetic agents may affect cerebrovascular responses to ethanol. A closed cranial window preparation in the rat was used to compare the response of pial arterioles to topically applied ethanol (0.01% to 1% vol/vol) in the presence of alpha-chloralose/urethane (50 and 600 mg/kg, respectively) or halothane (0.5% to 1%) anesthesia. Heart rate, mean arterial blood pressure, and blood gas levels were maintained stable and within the physiological range throughout each experiment. Ethanol induced significant vasoconstriction in alpha-chloralose/urethane-anesthetized animals (multivariate analysis of variance (MANOVA), p = 0.039); conversely, ethanol induced significant vasodilation of the pial arterioles in halothane-anesthetized animals (MANOVA, p = 0.017). These responses were significantly different from one another (MANOVA, p = 0.001). Thus, the choice of anesthetic agent alters the cerebrovascular response to ethanol, and care should be taken to ascertain the influence of anesthesia in both research and clinical settings.
The effects of sevoflurane on the coronary circulation were investigated in the instrumented dogs with or without coronary stenosis. A-V block was produced by injection of formalin into A-V node to control heart rate at 120 beats.min-1 by pacing and mean systemic blood pressure was held constant at 65 mmHg with the pressurized blood reservoir. Left anterior descending coronary artery was cannulated with stainless steel tube supplied from the femoral artery. Total coronary flow was measured with an electromagnetic flow probe and the regional myocardial blood flow was calculated using color microsphere technique. Coronary resistance was reduced with the increasing end-tidal concentrations of sevoflurane up to 1.2 MAC. An adjustable screw clamp was used to reduce the coronary flow down to 50% of control value. Inner/outer ratio of regional myocardial blood flow decreased with stenosis, but was unaffected with 1.2 MAC of sevoflurane. We concluded that 1.2 MAC of sevoflurane was not strong enough to dilate the coronary artery to produce the transmural steal phenomenon in the dog with coronary stenosis. Further investigations are needed to clarify how hemodynamic factors influence the transmural steal phenomenon in myocardium.
The effects of several general anaesthetics on the responses evoked by the excitatory amino acid agonists N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) were investigated in mouse cortical wedges placed in a two compartment bath and superfused with a nominally Mg(2+)-free Krebs solution. Chloroform (3-6 mM) and halothane (1-3 mM) preferentially antagonized AMPA responses; thiopental (0.1-0.4 mM), diethyl ether (10-30 mM) and isoflurane (1-3 mM) antagonized both AMPA or NMDA responses while ketamine antagonized NMDA responses in a highly selective way. The antagonism of the excitatory amino acid responses exerted by the anaesthetics was non competitive in nature. The inhibition of excitatory amino acid receptor function may be one of the mechanisms whereby general anaesthesia is produced.