Anesthesia and analgesia
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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
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.