Anesthesia and analgesia
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Anesthesia and analgesia · Feb 1998
Comment Letter Case ReportsA suspected malignant hyperthermia episode during desflurane anesthesia.
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Anesthesia and analgesia · Jan 1998
Prolonged inhaled NO attenuates hypoxic, but not monocrotaline-induced, pulmonary vascular remodeling in rats.
In concentrations of 10-20 ppm, inhaled nitric oxide (NO) decreases pulmonary artery pressure and attenuates vascular remodeling in pulmonary hypertensive rats. Because NO is potentially toxic, it is important to know whether lower concentrations attenuate vascular remodeling produced by different etiologies. Therefore, we determined the effects of prolonged, small-dose inhaled NO administration on hypoxic and monocrotaline (MCT)-induced pulmonary vascular remodeling. Rats were subjected to normoxia, hypoxia (normobaric 10% oxygen), or hypoxia plus NO in concentrations of 50 ppb, 200 ppb, 2 ppm, 20 ppm, and 100 ppm for 3 wk. A second group of normoxic rats was given MCT (60 mg/kg intraperitoneally) alone or in the presence of 2, 20, and 100 ppm of NO. Subsequently, pulmonary artery smooth muscle thickness and the number of muscular arteries (percentage of total arteries) were determined. Right ventricular hypertrophy was determined by right to left ventricle plus septum weight ratio (RV/LV + S). Pulmonary artery smooth muscle thickness and the percent muscular arteries were increased by hypoxia and MCT. The hypoxic increase in thickness was attenuated by all concentrations of NO, with 100 ppm being greatest, whereas NO had no effect on MCT rats. NO attenuated the increase in percent muscular arteries in hypoxic but not MCT rats. The RV/LV + S was increased by hypoxia and MCT compared with normoxia. Hypoxia-induced RV hypertrophy was decreased by all concentrations of inhaled NO, although attenuation with 50 ppb was less than with 200 ppb, 20 ppm, and 100 ppm. In MCT rats 2 and 100 ppm NO increased RV hypertrophy, whereas 20 ppm had no effect. In conclusion, inhaled NO in concentrations as low as 50 ppb attenuates the pulmonary vascular remodeling and RV hypertrophy secondary to hypoxia. In contrast, concentrations as high as 100 ppm do not attenuate MCT-induced pulmonary remodeling. These results demonstrate that extremely low concentrations of NO may attenuate remodeling but that the effectiveness is dependent on the mechanism inducing pulmonary remodeling. ⋯ The authors determined whether inhaled NO, a selective pulmonary vasodilator, attenuates pulmonary vascular remodeling caused by two models of pulmonary hypertension: chronic hypoxia and monocrotaline injection. Analysis of pulmonary vascular morphology suggests that very low concentrations of NO effectively attenuate hypoxic remodeling but that NO is not effective in monocrotaline-induced pulmonary remodeling.
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Anesthesia and analgesia · Jan 1998
Randomized Controlled Trial Clinical TrialThe pharmacodynamics of mivacurium preceded by atracurium or cisatracurium in children.
We evaluated whether mivacurium maintains its short duration of effect when preceded by atracurium or cisatracurium in 45 children during propofol/alfentanil/N2O/O2 anesthesia. Neuromuscular response was recorded by using an adductor pollicis electromyogram (EMG). Children were randomized to receive two doses of atracurium (350 micrograms/kg and 70 micrograms/kg in Group AM), cisatracurium (64 micrograms/kg and 10 micrograms/kg in Group CM), or mivacurium (200 micrograms/kg and 100 micrograms/kg in Group MM), followed by a final dose of mivacurium 100 micrograms/kg. The second and third doses of the muscle relaxants were administered at 25% EMG recovery. After the final dose of mivacurium, the times to 95% of EMG recovery in groups AM, CM, and MM were (median with 10-90 percentile range) 33.0 (28.0-40.0) min, 30.7 (26.0-40.3) min, and 10.3 (8.0-14.0) min, respectively (P < 0.0001). The recovery times to a train-of-four ratio of 0.70 were 30.3 (24.7-37.0) min, 28.0 (24.7-37.7) min, and 10.3 (8.0-13.7) min for groups AM, CM, and MM, respectively (P < 0.0001). Thus, the duration of effect of mivacurium was prolonged by 200% if preceded by either atracurium or cisatracurium. ⋯ We compared the pharmacodynamics of mivacurium given alone or preceded by atracurium or cisatracurium in children. The duration of effects of mivacurium was prolonged by 200% if preceded by either atracurium or cisatracurium. This implies that mivacurium has a short duration of effect only when given as a single relaxant.
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Anesthesia and analgesia · Jan 1998
The inhibitory effects of thiopental, midazolam, and ketamine on human neutrophil functions.
We investigated the effect of thiopental, midazolam, and ketamine (at clinically relevant concentrations and at 0.1 and 10 times these concentrations) on several aspects of human neutrophil functions. The three intravenous (i.v.) anesthetics significantly decreased chemotaxis, phagocytosis, and reactive oxygen species (ROS) (O2-, H2O2, OH) production of neutrophils in a dose-dependent manner. At clinically relevant concentrations, thiopental and midazolam significantly depressed these neutrophil functions. However, ketamine at the clinical plasma concentration did not impair chemotaxis or ROS production, except phagocytosis. In contrast, the three anesthetics had no effect on the levels of ROS production by a cell-free ROS generating system. In addition, intracellular calcium concentrations in neutrophils stimulated by N-formyl-L-methionyl-L-leucil-L-phenylalanine were dose-dependently decreased in the presence of each of the three anesthetics. The suppression of an increase in intracellular calcium concentrations may be responsible for the inhibition of neutrophil functions by the i.v. anesthetics. ⋯ Neutrophils play an important role in the antibacterial host defense system and autotissue injury. We found that thiopental and midazolam (but not ketamine), at clinically relevant concentrations, impaired the neutrophil functions.