Anesthesia and analgesia
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Anesthesia and analgesia · Dec 2002
Duration of preoperative fast correlates with arterial blood pressure response to halothane in infants.
In this study, we sought to determine whether the duration of preoperative fasting affects the decrease in blood pressure observed in infants and children during halothane anesthesia. Two-hundred-fifty pediatric patients were divided into 5 age groups: term neonates (n = 50), 1-6 mo (n = 50), 6-24 mo (n = 50), 2-6 yr (n = 50), and 6-12 yr (n = 50). After anesthetic induction with halothane, end-tidal halothane was maintained at 2 minimum alveolar anesthetic concentration (MAC) for 10 min to allow myocardial uptake. Patients were grouped by duration of preoperative fast (0-4 h, 4-8 h, 8-12 h, and >12 h). Changes in heart rate and systolic (SAP) and mean (MAP) arterial blood pressure from preinduction to 2 MAC were compared among fasting groups within each age group. In the 1- to 6-mo age group, the changes in SAP and MAP were significantly greater in infants fasting 8-12 h than in those fasting 0-4 h (SAP, -51 mm Hg versus -31 mm Hg, respectively; MAP, -48 mm Hg versus -32 mm Hg; P < 0.05). No statistically significant differences were noted in the older age groups. The results of this study demonstrate that prolonged preoperative fasting is associated with a greater decrease in blood pressure in infants. This exacerbation of the already significant hemodynamic depression observed in infants during halothane anesthesia underscores the importance of adherence to published fasting guidelines. ⋯ We studied changes in blood pressure during halothane anesthesia in infants and children and found that blood pressure decreased to a greater extent in infants who fasted for longer than 8 h before surgery. This exacerbation of the already significant hemodynamic depression observed in infants during halothane anesthesia underscores the importance of adherence to published fasting guidelines.
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Anesthesia and analgesia · Dec 2002
Acetylcholine receptors and thresholds for convulsions from flurothyl and 1,2-dichlorohexafluorocyclobutane.
There are acetylcholine receptors throughout the central nervous system, and they may mediate some forms and aspects of convulsive activity. Most high-affinity binding sites on nicotinic acetylcholine receptors for nicotine, cytisine, and epibatidine in the brain contain the beta2 subunit of the receptor. Transitional inhaled compounds (compounds less potent than predicted from their lipophilicity and the Meyer-Overton hypothesis) and nonimmobilizers (compounds that do not produce immobility despite a lipophilicity that suggests anesthetic qualities as predicted from the Meyer-Overton hypothesis) can produce convulsions. The nonimmobilizer flurothyl [di-(2,2,2,-trifluoroethyl)ether] blocks the action of gamma-aminobutyric acid on gamma-aminobutyric acid(A) receptors, whereas the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (2N, also called F6) does not. 2N can block the action of acetylcholine on nicotinic acetylcholine receptors. We examined the relative capacities of these compounds to cause convulsions in mice having and lacking the beta2 subunit of the acetylcholine receptor. The partial pressure causing convulsions in half the mice (the 50% effective concentration [EC(50)]) was the same as in control mice. For the knockout mice, the EC(50) for flurothyl was 0.00170 +/- 0.00030 atm (mean +/- SD), and for 2N, it was 0.0345 +/- 0.0041 atm. For the control mice, the respective values were 0.00172 +/- 0.00057 atm and 0.0341 +/- 0.0048 atm. The ratio of the 2N to flurothyl EC(50) values was 20.8 +/- 3.5 for the knockout mice and 21.7 +/- 7.0 for the control mice. These results do not support the notion that acetylcholine receptors are important mediators of the capacity of 2N or flurothyl to cause convulsions. However, we also found that both nonimmobilizers inhibit rat alpha4beta2 neuronal nicotinic acetylcholine receptors at EC(50) partial pressures (0.00091 atm and 0.062 atm for flurothyl and 2N, respectively) that approximate those that produce convulsions (0.0015 atm and 0.04 atm). ⋯ The results from the present study provide conflicting data concerning the notion that acetylcholine receptors mediate the capacity of nonimmobilizers to produce convulsions.