Anesthesia and analgesia
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Anesthesia and analgesia · Mar 1998
Diabetes mellitus and difficult laryngoscopy in renal and pancreatic transplant patients.
Limited mobility of the cervical spine or temperomandibular joint may contribute to increased difficulty of laryngoscopy in patients who have severe diabetes mellitus. The frequency of difficult laryngoscopy in diabetics undergoing renal and/or pancreatic transplants has been reported to be as high as 32%. We retrospectively reviewed the anesthetic records of all adult patients who underwent renal and/or pancreatic transplant and endotracheal intubation from January 1, 1985 to October 31, 1995. Characteristics specifically reviewed included the presence of diabetes mellitus, type of organ donor, age, gender, body mass index, previous difficult laryngoscopy, known characteristics potentially related to difficult laryngoscopy, and degree of difficulty with laryngoscopy. Laryngoscopy was graded as easy, minimally to moderately difficult, and moderately to extremely difficult to perform. Factors associated with any degree of difficult intubation were univariately assessed by using Fisher's exact test. Of 725 patients, 15 (2.1%) were identified as having difficult laryngoscopies, although all underwent successful endotracheal intubations. Factors associated with difficult laryngoscopy were diabetes mellitus (P = 0.002) and characteristics known to be related to difficult laryngoscopy (P = 0.02). These findings confirm an increase in the frequency of difficult laryngoscopy in diabetic patients undergoing renal and/or pancreatic transplant, although no laryngoscopies were rated as moderately to extremely difficult. We conclude that the frequency of difficult laryngoscopy in these diabetic patients is much lower than previous reports have suggested. ⋯ Previous studies have suggested that airway management of many diabetic patients may be difficult. Our medical record review of patients with severe diabetes undergoing organ transplants showed that extraordinary techniques were not required to successfully manage their airways.
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Anesthesia and analgesia · Mar 1998
The infusion rate of mivacurium and its spontaneous neuromuscular recovery in magnesium-treated parturients.
Magnesium (Mg) enhances the activity of nondepolarizing neuromuscular blocking drugs. However, no interaction between mivacurium and magnesium has been described. Therefore, we sought to determine the effect of the influence of Mg on the infusion rate of mivacurium and its spontaneous recovery. We studied 24 parturients who had undergone cesarean section under general anesthesia. Those who had been given MgSO4 for the treatment of preeclampsia were assigned to the Mg group (n = 12), and the other normal parturients were assigned to the NonMg group (n = 12). In both groups, the train-of-four (TOF) response to stimuli of the ulnar nerve was measured at intervals of 15 s. Anesthesia was induced with thiopental and succinylcholine. In both groups, a bolus dose of mivacurium 0.06 mg/kg was administered when the first twitch of TOF (T1) reached 100% after the succinylcholine injection. When the electromyographic response after mivacurium had recovered to approximately 5%-10% of the baseline, a continuous infusion of mivacurium was given to maintain 93%-97% neuromuscular blockade. The plasma concentration of Mg in blood of the Mg group was 4.0 1.0 mEq/L, higher than that (1.4 mEq/L) of the NonMg group (P < 0.01). The infusion rates of mivacurium of Mg and NonMg groups were 1.6 and 5.4 mEq x kg(-1) x min(-1), respectively. In addition, the recovery indexes of the Mg and NonMg groups were 12.9 and 4.3 min, respectively. We conclude that a smaller dose of mivacurium should be infused to patients receiving Mg. ⋯ Magnesium, used as a standard therapy for severe toxemia, may act to enhance muscle relaxants such as mivacurium, a short-acting drug used in general anesthesia. Among women undergoing a cesarean section who were given a magnesium pretreatment, the infusion rate of mivacurium required to obtain relaxation was lower than that among women who did not receive pretreatment.
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Anesthesia and analgesia · Mar 1998
Epithelial dependence of the bronchodilatory effect of sevoflurane and desflurane in rat distal bronchi.
The bronchial epithelium releases substances that enhance bronchodilation in response to certain bronchodilators. We examined the hypothesis that the bronchodilatory effect of desflurane and sevoflurane depends on the epithelium in rat distal bronchial segments. Wistar rat subsegmental bronchial segments (diameter approximately 100 microm) were dissected. After preconstriction with 5-hydroxytryptamine, each segment was exposed to increasing concentrations of desflurane 0%-12% or sevoflurane 0%-4.8% under four conditions: after epithelial rubbing, after pretreatment with the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine (L-NNA), after pretreatment with the cyclooxygenase inhibitor indomethacin, or with no preintervention (control). Changes in bronchial diameter were monitored using an in vitro video detection system. Both desflurane and sevoflurane produced concentration-dependent bronchodilation (P < 0.001 for either anesthetic; 54% +/- 8% [mean +/- SD] dilation for 12% desflurane and 48% +/- 14% dilation for 4.8% sevoflurane). For both anesthetics, bronchodilation was significantly attenuated by epithelial rubbing (15% +/- 4% dilation for 12% desflurane and 13% +/- 10% dilation for 4.8% sevoflurane; P < 0.001 each), by pretreatment with indomethacin (12% +/- 3% dilation for 12% desflurane and 9% +/- 5% dilation for 4.8% sevoflurane; P < 0.001 each), and by L-NNA (24% +/- 8% dilation for 12% desflurane, P < 0.001; and 17% +/- 10% dilation for 4.8% sevoflurane, P < 0.01). Desflurane- and sevoflurane-mediated bronchodilation depends at least partially on the epithelium, and may involve both a prostanoid and NO in rat distal bronchi. ⋯ Bronchodilation by the volatile anesthetics desflurane and sevoflurane is at least partially epithelium-dependent and may be attenuated in diseases affecting the epithelium, such as asthma.
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Anesthesia and analgesia · Mar 1998
Mild hypothermia can attenuate nitroglycerin-induced vasodilation of pial arterioles in the cat.
The purpose of the present study was to investigate the effect of mild hypothermia on nitroglycerin-induced vasodilation of cerebral vessels. The cranial window technique, combined with microscopic video recording, was used in an experiment involving 26 cats anesthetized with isoflurane. Animals were randomly assigned to either a normothermic or a mildly hypothermic group (33 degrees C). We administered three different concentrations of nitroglycerin (10[-6], 10[-5], 10[-4] M) under the window and measured the diameter of small (< 100 microm) and large (100-200 microm) pial arterioles. In the normothermic group (n = 13), nitroglycerin produced a significant dilation of both small and large arterioles in a dose-dependent manner. In the hypothermic group (n = 13), a significant dilation of arterioles was observed only after topical application of nitroglycerin at a concentration of 10(-4) M. The percent increase in diameter of small and large arterioles was less in the hypothermic group than the normothermic group. Our in vivo study demonstrates that topically applied nitroglycerin produces a dose-dependent dilation of pial arterioles in normothermic cats anesthetized with isoflurane, but the reduction of temperature to 33 degrees C significantly attenuates nitroglycerin-induced vasodilation of pial arterioles. ⋯ Although nitroglycerin may be used in hypothermic patients, the effect of mild hypothermia on nitroglycerin-induced vasodilation of cerebral vessels is unknown. In this study, we investigated the effects of nitroglycerin on pial arteriolar diameter in normothermic and hyperthermic cats. Hypothermia was found to attenuate nitroglycerin-induced vasodilation.
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Anesthesia and analgesia · Mar 1998
Propofol sedation produces dose-dependent suppression of lidocaine-induced seizures in rats.
The association of propofol with excitatory motor activity, such as myoclonic jerking and opisthotonus, in humans and in animals suggests that it may aggravate clinical seizure activity in some circumstances, although evidence suggests that under other circumstances, propofol inhibits seizure activity. In the current study, we assessed the effect of sedating doses of propofol on lidocaine-induced seizure activity in spontaneously breathing rats receiving no other anesthetics. Adult Sprague-Dawley male rats, 300-400 g, were divided into a control group and three experimental groups representing three graded levels of propofol sedation. The control rats then received a lidocaine infusion at the rate of 150 mg x kg(-1) x h(-1), resulting in a slow, progressive increase in systemic lidocaine concentrations. At the onset of electroencephalographic (EEG) seizure activity, arterial lidocaine concentrations were obtained. The treated rats received propofol according to three different dose schedules: Dose 1 = 10 mg x kg(-1) x h(-1) after a 2.5-mg/kg bolus; Dose 2 = 20 mg x kg(-1) x h(-1) after a 5-mg/kg bolus; Dose 3 = 40 mg x kg(-1) x h(-1) after a 10-mg/kg bolus. After 30 min, a steady level of sedation, dependent on the dose of propofol, was achieved. The lidocaine infusion was then started, and systemic lidocaine levels were obtained at the onset of EEG seizure activity. The lidocaine was continued until the onset of death by cardiac arrest. Plasma lidocaine was measured by gas chromatography. Analysis of variance and Dunnett's t-test were used for comparisons with the control values. Continuous propofol sedation increased the seizure dose of lidocaine from 37.7 +/- 3.5 mg/kg (mean +/- SEM) to 52.5 +/- 2.6 mg/kg (Dose 1, P < 0.05) and 67.9 +/- 8.6 mg/kg (Dose 2, P < 0.05), and completely abolished lidocaine seizures at Dose 3. The lethal dose of lidocaine, 89.4 +/- 10.5 mg/kg control versus 108.7 +/- 10.3 mg/kg (Dose 1), 98.3 +/- 10.1 mg/kg (Dose 2), and 93.5 +/- 10.4 mg/kg (Dose 3) did not differ among groups. The lidocaine levels at seizure threshold were increased in the propofol-treated rats: 16.9 +/- 0.5 microg/mL control versus 19.2 +/- 0.7 microg/mL (Dose 1, P = not significant) and 23.7 +/- 1.8 microg/mL (Dose 2, P < 0.05). Continuous propofol sedation in spontaneously breathing rats receiving no other anesthetics exerts a protective effect against lidocaine-induced seizures in a monotonic, dose-dependent fashion. The cardiac arrest dose of lidocaine is unaffected by propofol under these conditions. ⋯ The i.v. anesthetic drug propofol, given to rats to produce sedation, was found to suppress seizure activity caused by overdosage of the local anesthetic lidocaine.