Mutolo D, Bongianni F, Corda M, Fontana G A, Pantaleo T
Dipartimento di Scienze Fisiologiche, Università degli Studi di Firenze, Italy.
Am J Physiol. 1995 Jul;269(1 Pt 2):R113-23. doi: 10.1152/ajpregu.1995.269.1.R113.
Poststimulatory depression in respiratory activity induced by superior laryngeal nerve (SLN) stimulation was quantitatively investigated in 20 adult cats. The role played in this phenomenon by endogenous opioids was studied using the opiate antagonist naloxone. The effects of hypercapnia on the same phenomenon were also investigated for comparison. Experiments were performed on cats anesthetized with pentobarbitone or alpha-chloralose, vagotomized, paralyzed, and artificially ventilated with 100% O2. Some animals were also carotid sinus denervated. Respiratory output was monitored as integrated phrenic nerve activity. SLN stimulation produced apnea, which outlasted the stimulation period; when respiration resumed, it was markedly depressed as revealed mainly by a decrease in phrenic minute output, respiratory frequency, and rate of rise of inspiratory activity. Phrenic output recovered gradually to control levels following an exponential time course. These effects varied as a function of the duration of SLN stimulation. Naloxone administration (0.8 mg/kg iv) significantly reduced the duration of poststimulatory apnea and attenuated the depression of phrenic minute output of the first recovery breath as a result of changes in peak phrenic activity; it also accelerated the time course of recovery. Hypercapnia did not affect the duration of poststimulatory apnea, but attenuated the initial poststimulatory depression because of changes in respiratory frequency; the rate of recovery was reduced. The results provide characterization of poststimulatory respiratory depression of laryngeal origin in the adult cat and suggest a role of endogenous opioids in its genesis or modulation.
在20只成年猫中，对由喉上神经（SLN）刺激诱发的呼吸活动的刺激后抑制进行了定量研究。使用阿片拮抗剂纳洛酮研究了内源性阿片类物质在这一现象中所起的作用。为作比较，还研究了高碳酸血症对同一现象的影响。实验在戊巴比妥或α-氯醛糖麻醉、迷走神经切断、麻痹并用100%氧气进行人工通气的猫身上进行。一些动物还进行了颈动脉窦去神经支配。以膈神经活动积分作为呼吸输出的监测指标。SLN刺激产生呼吸暂停，其持续时间超过刺激期；当呼吸恢复时，呼吸明显受到抑制，主要表现为膈神经每分钟输出量、呼吸频率和吸气活动上升速率的下降。膈神经输出量按照指数时间进程逐渐恢复到对照水平。这些效应随SLN刺激持续时间而变化。静脉注射纳洛酮（0.8 mg/kg）可显著缩短刺激后呼吸暂停的持续时间，并由于膈神经活动峰值的变化而减轻第一次恢复呼吸时膈神经每分钟输出量的抑制；它还加速了恢复的时间进程。高碳酸血症不影响刺激后呼吸暂停的持续时间，但由于呼吸频率的变化而减轻了刺激后的初始抑制；恢复速率降低。这些结果描述了成年猫中喉源性刺激后呼吸抑制的特征，并提示内源性阿片类物质在其发生或调节中起作用。
