Haouzi P, Beyaert C, Gille J P, Chalon B, Marchal F
Faculté de Médecine de Nancy, Institut National de la Santé et de laRecherche Médicale Unite 14, Vandoeuvre-lès-Nancy, France.
Am J Physiol. 1997 Feb;272(2 Pt 2):R586-92. doi: 10.1152/ajpregu.1997.272.2.R586.
This study was carried out on seven chloralose-anesthetized sheep and was designed to investigate the role of muscular afferent fiber stimulation on the duration of reflex apnea triggered by laryngeal stimulation (LS). In six animals, injection of distilled water onto the laryngeal mucosa provoked a 15.7 +/- 1.0 s (mean +/- SE) apnea associated with a rise in systemic blood pressure (+7 +/- 0.8 Torr). Electrically induced contractions (EIC) of the hindlimb muscles doubled the metabolic rate and ventilation and reduced the duration of the apnea produced by LS to 7.4 +/- 1.0 s (P < 0.01). Apnea duration was still reduced during the first minute after the cessation of EIC (7.2 +/- 1.1 s, P < 0.01) but returned to control after a 5-min recovery period (16.7 +/- 1.6 s). The apnea triggered by LS was also reduced during EIC when the venous return was impeded by occluding the inferior vena cava (5.2 +/- 1.1 s, P < 0.01), despite a profound hypocapnia (20.7 +/- 0.3 Torr). The duration of apnea was not significantly affected (14.2 +/- 1.4 s) by breathing a 6% CO2-14% O2 in N2 gas mixture that roughly mimicked the alveolar gas composition when the apnea turned off. These results suggest that chemical drive has a negligible role in the fast reinitiation of breathing after LS during muscular stimulation. Stimulation of muscle afferent fibers does, however, appear to be a potent source of ventilatory reflexes capable of counteracting the inhibition of breathing resulting from laryngeal stimulation. Conversely, it is postulated that any reduction in somatic afferent traffic during this type of reflex apnea, including that resulting from the LS-induced systemic vasoconstriction, may delay the termination of apnea.
本研究以7只氯醛糖麻醉的绵羊为对象,旨在探讨刺激肌肉传入纤维对喉刺激(LS)引发的反射性呼吸暂停持续时间的作用。在6只动物中,向喉黏膜注射蒸馏水引发了15.7±1.0秒(平均值±标准误)的呼吸暂停,同时伴有全身血压升高(+7±0.8托)。后肢肌肉的电诱发收缩(EIC)使代谢率和通气量增加了一倍,并将LS引起的呼吸暂停持续时间缩短至7.4±1.0秒(P<0.01)。在EIC停止后的第一分钟内,呼吸暂停持续时间仍缩短(7.2±1.1秒,P<0.01),但在5分钟的恢复期后恢复至对照水平(16.7±1.6秒)。当下腔静脉被阻断导致静脉回流受阻时,EIC期间LS引发的呼吸暂停也缩短(5.2±1.1秒,P<0.01),尽管存在严重的低碳酸血症(20.7±0.3托)。当呼吸大致模拟呼吸暂停结束时肺泡气体成分的6%CO2-14%O2氮气混合气体时,呼吸暂停持续时间未受到显著影响(14.2±1.4秒)。这些结果表明,在肌肉刺激期间,化学驱动在LS后呼吸快速重新启动中的作用可忽略不计。然而,刺激肌肉传入纤维似乎是一种强大的通气反射源,能够抵消喉刺激引起的呼吸抑制。相反,据推测,在这种反射性呼吸暂停期间,包括由LS引起的全身血管收缩导致的躯体传入流量的任何减少,都可能延迟呼吸暂停的终止。