engleski

The influence of anesthetics on inspiratory phase parameters in rats

In mammals, generation of respiratory rhythm is dominated by preBötzinger neurons located in the ventral medulla. PreBötzinger neurons drive inspiratory activity, generating breathing pattern. The choice of anesthetics has an important role in respiratory control research, since they influence breathing and its variability. Opioids and volatile anesthetics depress rhythmogenic function of the PreBötzinger inspiratory neurons, resulting in alteration of respiratory rhythm parameters. Moreover, anesthetics exhibit a depression of central respiratory drive and abolish phrenic long term facilitation (pLTF), a form of respiratory plasticity that manifests as a long lasting increase of phrenic nerve activity elicited by acute intermittent hypoxia. We aimed to investigate effects of urethane, sevoflurane, isoflurane, and remifentanil on inspiratory phase parameters during the baseline conditions, hypoxic challenge, and 60 minutes post hypoxia. Adult, male, bilaterally vagotomized, paralyzed, and mechanically ventilated Sprague Dawley rats were exposed to acute intermittent hypoxia protocol, consisting of 5 3-minute hypoxic episodes at 9% O2, separated by 3-minute recovery periods at 50% O2. Control group was anesthetized with urethane, one group with sevoflurane, one with isoflurane, and one with remifentanil. Inspiratory phase parameters including peak phrenic nerve activity (pPNA) and inspiratory peak area (PA) were analyzed during baseline (T0), first hypoxia (TH1), and 60 minutes post hypoxia (T60). Hypoxia elicited increases of pPNA and PA at TH1 compared to T0 in all groups (in urethane group by 705.9±176.8%, P=0.001, and 535.0±168.0%, P=0.005 ; in sevoflurane group by 273.7±81.7%, P=0.016, and 222.2±53.9%, P=0.014 ; in isoflurane group by 225.5±156.4%, P>0.05, and 368.3±295.8%, P>0.05 ; in remifentanil group by 312.8±97.6%, P=0.03, and 424.7±238.8%, P>0.05, respectively). In urethane group pPNA and PA significantly increased at T60 compared to T0 (by 146.42±32.6%, P=0.001, and 200.4±58.7%, P=0.005, respectively), indicating pLTF. There were no significant differences in pPNA and PA at T60 compared to T0 in sevoflurane, isoflurane and remifentanil groups. Our results confirmed that sevoflurane, isoflurane, and remifentanil compared to urethane anesthesia did not significantly alter inspiratory phase parameters at 60 minutes after the last hypoxic episode in rats.

anesthetics; inspiratory phase; rats; hypoxia

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