Effects of maternal enflurane exposure on NR2B expression in the hippocampus of their offspring

This work aims to study the pathogenesis of learning and memory impairment in offspring rats resulting from maternal enflurane anesthesia by focusing on the expression of the N-methyl-d-aspartic acid receptor subunit 2B (NR2B) in the hippocampus of the offspring. Thirty female Sprague-Dawley rats were randomly divided into three groups: control (C group), 4 h enflurane exposure (E1 group), and 8 h enflurane exposure (E2 group) groups. Eight to ten days after the initiation of pregnancy, rats from the E1 and E2 groups were allowed to inhale 1.7% enflurane in 2 L/min oxygen for 4 h and 8 h, respectively. Rats from the C group were allowed to inhale 2 L/min of oxygen only. The Morris water maze was used to assay the learning and memory function of the offspring on postnatal days 20 and 30. RT-PCR and immunohistochemistry assays were then used to measure the mRNA levels and protein expression of NR2B, respectively. Relative to offspring rats from the C group, those from the E1 and E2 groups exhibited longer escape latencies, lesser number of crossings over the platform, and less time spent in the target quadrant in the spatial exploration test (P < 0.05). In addition, the mRNA and protein expression levels of NR2B in the hippocampus of offspring rats in the E1 and E2 groups were down-regulated (P < 0.05). No significant differences between the E1 and E2 groups were observed (P > 0.05) in terms of mRNA levels and protein expression of NR2B. The cognitive function of the offspring is impaired when maternal rats are exposed to enflurane during early pregnancy. A possible mechanism of this effect is related to the down-regulation of NR2B expression.

No potentiation of fentanyl by use of transdermal buprenorphine in patients undergoing fast-track anesthesia for open-heart surgery

Simultaneous use of opioids with a different pharmacological profile during anesthesia may lead to unexpected prolongation of effects. In addition, long-term use of transdermal buprenorphine may result in a reduced sensitivity to opioid anesthesia. In a prospective study, possible overlap of opioid effects and vigilance was determined in a group of patients (n = 22) using a buprenorphine patch for at least two months for treatment of chronic pain, and undergoing fentanyl-based fast-track enflurane anesthesia for open-heart surgery. The patients using buprenorphine were compared with a control group (n = 21) undergoing similar open-heart procedures with no opioid other than fentanyl on board. Aside from time to extubation, total dose of fentanyl, postoperative blood gases, and vigilance assessment score were used to determine possible overlap of opioid effects and/or development of opioid tolerance in the buprenorphine group compared to the control group. Both groups had similar operation and anesthesia times and comparable doses of fentanyl (0.69 mg ± 0.23 vs. 0.67 mg ± 0.16 SD). There was no significant difference in postoperative arterial blood gases (PaO2 136 ± 48 torr vs. 128 ± 35 torr SD; PCO2 43.3 ± 3.3 torr vs. 41.9 ± 1.2 torr SD), time until extubation (27 ± 22 min vs. 33 ± 24 min), and postanesthetic vigilance and recovery score (6.8 ± 1.0 vs. 7.5 ± 0.8, arbitrary units) between the two groups. Because of adaptive mechanisms and the development of tolerance in patients using buprenorphine, respiratory depression or sedation does not project into the postoperative period. The significant (p < 0.05) lower incidence of nausea and emesis in patients with transdermal buprenorphine owes to the development of tolerance to these opioid-related side effects.

Effects of Halothane and Enflurane Anesthesia on Sympathetic β-adrenoreceptor–mediated Pulmonary Vasodilation in Chronically Instrumented Dogs

Background The authors previously reported that the pulmonary vasodilator response to the sympathetic beta-adrenoreceptor agonist isoproterenol is potentiated during isoflurane anesthesia compared with the conscious state. In the present in vivo study, the authors tested the hypothesis that halothane and enflurane anesthesia also enhance sympathetic beta adrenoreceptor-mediated pulmonary vasodilation. The authors also used the membrane-permeable analog of cyclic adenosine monophosphate (cAMP), dibutyryl cAMP, to help delineate the site in the signaling pathway for an anesthesia-induced effect on beta adrenoreceptor-mediated pulmonary vasodilation. Methods Mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow (LPQ) relationship. LPQ plots were measured on separate days in the conscious, halothane-, and enflurane-anesthetized states at baseline, after preconstriction with the thromboxane analog U46619, and during the cumulative intravenous administration of isoproterenol. LPQ plots were also measured in conscious, halothane-, and isoflurane-anesthetized dogs after U46619 preconstriction and during the cumulative intravenous administration of dibutyryl cAMP. Results Compared with the conscious state, neither halothane nor enflurane had an effect on the baseline LPQ relationship. The magnitude of the pulmonary vasodilator response to isoproterenol was potentiated during halothane anesthesia but unchanged during enflurane anesthesia. The pulmonary vasodilator response to dibutyryl cAMP was not altered during either halothane or isoflurane anesthesia compared with the conscious state. Conclusions These results indicate that inhalational anesthetic agents can exert differential effects on the pulmonary vasodilator response to sympathetic beta-adrenoreceptor activation. The potentiated vasodilator response observed during halothane and isoflurane anesthesia is the result of effects proximal to cAMP accumulation in the beta-adrenoreceptor signaling pathway.