Yu J, Wang Y, Soukhova G, Collins L C, Falcone J C
Department of Medicine, University of Louisville, Louisville, Kentucky 40292, USA.
J Appl Physiol (1985). 2001 Mar;90(3):857-64. doi: 10.1152/jappl.2001.90.3.857.
Recently, a vagally mediated excitatory lung reflex (ELR) causing neural hyperpnea and tachypnea was identified. Because ventilation is regulated through both inspiratory and expiratory processes, we investigated the effects of the ELR on these two processes simultaneously. In anesthetized, open-chest, and artificially ventilated rabbits, we recorded phrenic nerve activity and abdominal muscle activity to assess the breathing pattern when the ELR was evoked by directly injecting hypertonic saline (8.1%, 0.1 ml) into lung parenchyma. Activation of the ELR stimulated inspiratory activity, which was exhibited by increasing amplitude, burst rate, and duty cycle of the phrenic activity (by 22 +/- 4, 33 +/- 9, and 57 +/- 11%, respectively; n = 13; P < 0.001), but suppressed expiratory muscle activity. The expiratory muscle became silent in most cases. On average, the amplitude of expiratory muscle activity decreased by 88 +/- 5% (P < 0.002). The suppression reached the peak at 6.9 +/- 1 s and lasted for 200 s (median). Injection of H(2)O(2) into the lung parenchyma produced similar responses. By suppressing expiration, the ELR produces a shift in the workload from expiratory muscle to inspiratory muscle. Therefore, we conclude that the ELR may contribute to inspiratory muscle fatigue, not only by directly increasing the inspiratory activity but also by suppressing expiratory activity.
最近，一种引起神经性呼吸急促和呼吸过速的迷走神经介导的兴奋性肺反射（ELR）被发现。由于通气是通过吸气和呼气过程来调节的，我们同时研究了ELR对这两个过程的影响。在麻醉、开胸并进行人工通气的兔子身上，我们记录膈神经活动和腹部肌肉活动，以评估通过向肺实质直接注射高渗盐水（8.1%，0.1 ml）诱发ELR时的呼吸模式。ELR的激活刺激了吸气活动，表现为膈神经活动的幅度、爆发频率和占空比增加（分别增加22±4%、33±9%和57±11%；n = 13；P < 0.001），但抑制了呼气肌活动。在大多数情况下，呼气肌变得静止。平均而言，呼气肌活动的幅度下降了88±5%（P < 0.002）。抑制在6.9±1 s达到峰值，并持续200 s（中位数）。向肺实质注射H₂O₂产生了类似的反应。通过抑制呼气，ELR使工作负荷从呼气肌转移到吸气肌。因此，我们得出结论，ELR可能不仅通过直接增加吸气活动，还通过抑制呼气活动导致吸气肌疲劳。
