Anesthesia and analgesia
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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
The effect of electroconvulsive treatment on thermal hyperalgesia and mechanical allodynia in a rat model of peripheral neuropathy.
We tested the ability of electroconvulsive treatment (ECT) to block thermal hyperalgesia and mechanical allodynia in rats with peripheral neuropathy. Repeated ECT (six times daily) significantly reduced thermal hyperalgesia 48 h after the end of the final treatment but had no significant effects on mechanical allodynia. Single ECT had no significant effect on thermal hyperalgesia or mechanical allodynia. Neither single nor repeated ECT had any significant effect on the withdrawal response of sham-operated paws and untreated rats to thermal and mechanical stimuli. The anti-thermal hyperalgesic effect of repeated ECT was reversed by the previous administration of nifedipine (L-type Ca2+ channel blocker). We conclude that, due to effects on the voltage dependent calcium channel, ECT modified one of the pain behaviors induced by nerve injury. ECT may be of use in the treatment of human neuropathic pain. ⋯ We showed that repeated electroconvulsive treatment reduced pain responses to heat stimulation after sciatic nerve injury in rats. This study implies a possible therapeutic effect of electroconvulsive treatment on neuropathic pain.
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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.
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Anesthesia and analgesia · Mar 1998
Gastric mucosal oxygen delivery decreases during cardiopulmonary bypass despite constant systemic oxygen delivery.
Previous studies report a decrease in gastric mucosal oxygen delivery during cardiopulmonary bypass (CPB). However, in these studies, CPB was associated with a reduction in systemic oxygen delivery (DO2). Conceivably, this decrease in DO2 could have contributed to the observed decrease in gastric mucosal oxygen delivery. Thus, in the present study, we assessed the effects of the maintenance of DO2 (at pre-CPB values) during hypothermic (30-32 degrees C) CPB on the gastric mucosal red blood cell flux (GMRBC flux) using laser Doppler flowmetry. In 11 patients requiring cardiac surgery, the pump flow rate during CPB was initially set at 2.4 L x min(-1) x m(-2) and was adjusted to maintain DO2 at pre-CPB values (flow 2.5-2.7 L x min[-1] x m[-2]). Despite a constant DO2, the GMRBC flux was decreased during CPB. These decreases averaged 50% +/- 16% after 10 min, 50% +/- 18% after 20 min, 49% +/- 21% after 30 min, and 49% +/- 19% after 40 min of CPB. The rewarming period was associated with an increase in GMRBC flux. Thus, maintaining systemic DO2 during CPB seems to be an ineffective strategy to improve gastric mucosal oxygen delivery. ⋯ In the present study, we tested the hypothesis that gastric mucosal red blood cell flux assessed by laser Doppler flowmetry could be improved by maintaining baseline systemic flow and oxygen delivery during hypothermic cardiopulmonary bypass. Despite this strategy, gastric mucosal red blood cell flux decreased by 50% during hypothermic cardiopulmonary bypass.