Remifentanil reversibly abolished phrenic long term facilitation in rats subjected to acute intermittent hypoxia.

The aim was to investigate whether intravenous infusion of remifentanil would depress phrenic long term facilitation (pLTF) evoked by acute intermittent hypoxia (AIH) in adult, male, urethane anaesthetized Sprague-Dawley rats, bilaterally vagotomized, paralyzed and mechanically ventilated. The experimental group received a remifentanil infusion (0.5 µg/kg/min i.v., n=12), whereas the control group (n=6) received saline. Rats were exposed to AIH protocol. Phrenic nerve amplitude (PNA), burst frequency (f) and breathing rhythm parameters (Ti, Te, Ttot) were analyzed during 5 hypoxias and at 15, 30, and 60 minutes after the final hypoxia, and compared to baseline values. At the end of the experiment, the infusion of remifentanil was stopped and phrenic nerve activity was compared to baseline values prior to remifentanil infusion. In the control group, peak phrenic nerve activity (pPNA) significantly increased at 60 min (T60, increase by 138.8±28.3%, p=0.006) after the last hypoxic episode compared to baseline values, i.e. pLTF was induced. In remifentanil treated rats, there were no significant changes in peak phrenic nerve activity at T60 compared to baseline values (decrease by 5.3±16.5%, p>0.05), i.e. pLTF was abolished. Fifteen minutes following cessation of remifentanil infusion, pPNA increased by 93.2±40.2% (p<0.05) and remained increased compared to pre-remifentanil-infusion values for more than 30 minutes, i.e. pLTF could be observed after cessation of the remifentanil infusion. In conclusion, the short acting µ-opioid receptor agonist, remifentanil, reversibly abolished phrenic long term facilitation in urethane anesthetized rats.

Propofol abolished the phrenic long-term facilitation in rats.

The aim was to investigate the effect of propofol anesthesia on the phrenic long-term facilitation (pLTF) in rats. We hypothesized that pLTF would be abolished during propofol-compared with urethane anesthesia. Fourteen adult, male, anesthetized, vagotomized, paralyzed, and mechanically ventilated Sprague-Dawley rats (seven per group), were exposed to the acute intermittent hypoxia (AIH) protocol. Peak phrenic nerve activity (PNA), burst frequency (f), and breathing rhythm parameters (Ti, Te, Ttot) were analyzed during the first hypoxia (TH1), as well as at 15 (T15), 30 (T30), and 60min (T60) after the final hypoxic episode, and compared to the baseline values. In propofol-anesthetized rats no significant changes of PNA were recorded after the last hypoxic episode, i.e. no pLTF was induced. There was a significant increase of PNA (59.4+/-6.6%, P<0.001) in urethane-anesthetized group at T60. AIH did not elicit significant changes in f, Ti, Te, Ttot in either group at T15, T30, and T60. The pLTF, elicited by AIH, was induced in the urethane-anesthetized rats. On the contrary, pLTF was abolished in the propofol-anesthetized rats.

The acute hypoxic ventilatory response under halothane, isoflurane, and sevoflurane anaesthesia in rats.

The relative order of potency of anaesthetic agents on the hypoxic ventilatory response has been tested in humans, but animal data are sparse. We examined the effects of 1.4, 1.6, 1.8, and 2.0 MAC halothane, isoflurane, and sevoflurane on phrenic nerve activity in euoxia (baseline) and during acute normocapnic hypoxia (inspired oxygen fraction 0.09) in adult male Sprague-Dawley rats. With halothane, all animals became apnoeic even in euoxia, and the hypoxic response was completely abolished at all anaesthetic levels. With isoflurane, 5 of 14 animals exhibited phrenic nerve activity in euoxia at 1.4 MAC and demonstrated a hypoxic response (302% of baseline activity), but all became apnoeic and lost the hypoxic response at higher doses. With sevoflurane, phrenic nerve activity and a hypoxic response was preserved in at least some animals at all doses (i.e. even the highest dose of 2.0 MAC). Similar to the rank order of potency previously observed in humans, the relative order of potency of depression of the hypoxic ventilatory response in rats was halothane (most depressive) > isoflurane > sevoflurane (p = 0.01 for differences between agents).

Rocuronium attenuates oculocardiac reflex during squint surgery in children anesthetized with halothane and nitrous oxide.

BACKGROUND: The oculocardiac reflex (OCR) may be activated during squint surgery. The aim of this study was to test whether rocuronium 0.4 mg kg(-1) could reduce the frequency of OCR, and also whether a single dose of succinylcholine 1 mg kg(-1) could affect the frequency of OCR during anesthesia with halothane in a nitrous oxide/oxygen mixture. METHODS: A total of 161 ASA I children, 3-10 years old, undergoing elective surgery of the medial rectus muscle (MRM) were randomly assigned to three groups. Group R (n = 51), received 0.4 mg kg(-1) of rocuronium intravenously before endotracheal intubation. Group S (n = 58) received 1 mg kg(-1) of succinylcholine. Group C (controls, n = 52) received no relaxant. Oculocardiac reflex was defined as a reduction in heart rate (HR) > or = 15% and/or the appearance of any other arrhythmias, during manipulation of the MRM. Analysis of variance (anova), chi-squared, Kruskal-Wallis, and Student's t-tests were used for statistical analysis; P< 0.05 was considered statistically significant. RESULTS: In group R, OCR occurred in 15/51 (29%) of children, in group S in 31/58 (53%), and in group C in 23/52 (44%) (chi2 = 6.46, P = 0.049). In group R, the incidence of arrhythmias such as nodal rhythms, supraventricular and ventricular premature beats was 6%, compared with 22% in group S and 19% in group C (chi2 = 6.01, P = 0.040). However, there was no reduction in the occurrence of bradycardia (chi2 = 0.16, P = 0.924). CONCLUSION: Rocuronium reduced the frequency of OCR, mainly by reducing the incidence of supraventricular and ventricular premature beats.