低氧和高碳酸血症信号通路之间的相互作用,在小鼠中尚未系统地确定同时发生的低氧高二氧化碳气体攻击(HH-C)期间和之后发生的通气变化。在未麻醉的雄性C57BL6小鼠中的这项研究解决了以下假设:缺氧(HX)和高碳酸血症(HC)信号传导事件显示出一系列相互作用,表明周围和中枢呼吸机制的协调。我们评估了低氧引起的通气反应(HX-C,10%,O2,90%N2),高碳酸血症(HC-C,5%CO2,21%,O2,90%N2)和HH-C(10%O2,5%,CO2,85%N2)挑战,以确定HH-C挑战引起的通气反应是否只是HX-C和HC-C引起的反应的累加,或者是否存在其他互动模式。HH-C引起的响应是潮气量的累加,分钟通气和呼气时间,在其他人中。HH-C引起的响应是HX-C和HC-C响应的低加性(即,通过简单添加HX-C和HC-C反应)呼吸频率,HH-C反应低于预期,吸气时间和松弛时间,在其他人中。此外,呼气末暂停在HX-C期间增加,但在HC-C期间下降,和HH-C,因此表明HC-C反应影响同时给予的HX-C反应。返回室内空气的反应对于潮气量和每分钟通风是附加的,其中,而它们对于呼吸频率来说是低加性的,吸气时间,峰值吸气流量,呼吸暂停,吸气和呼气驱动和排斥指数。这些数据显示HX-C和HH-C信号传导途径在加性和经常是次加性过程中彼此相互作用。
Interactions between hypoxic and hypercapnic signaling pathways, expressed as ventilatory changes occurring during and following a simultaneous hypoxic-hypercapnic gas challenge (HH-C) have not been determined systematically in mice. This study in unanesthetized male C57BL6 mice addressed the hypothesis that hypoxic (HX) and hypercapnic (HC) signaling events display an array of interactions indicative of coordination by peripheral and central respiratory mechanisms. We evaluated the ventilatory responses elicited by hypoxic (HX-C, 10%, O2, 90% N2), hypercapnic (HC-C, 5% CO2, 21%, O2, 90% N2), and HH-C (10% O2, 5%, CO2, 85% N2) challenges to determine whether ventilatory responses elicited by HH-C were simply additive of responses elicited by HX-C and HC-C, or whether other patterns of interactions existed. Responses elicited by HH-C were additive for tidal volume, minute ventilation and expiratory time, among others. Responses elicited by HH-C were hypoadditive of the HX-C and HC-C responses (i.e., HH-C responses were less than expected by simple addition of HX-C and HC-C responses) for frequency of breathing, inspiratory time and relaxation time, among others. In addition, end-expiratory pause increased during HX-C, but decreased during HC-C and HH-C, therefore showing that HC-C responses influenced the HX-C responses when given simultaneously. Return to room-air responses was additive for tidal volume and minute ventilation, among others, whereas they were hypoadditive for frequency of breathing, inspiratory time, peak inspiratory flow, apneic pause, inspiratory and expiratory drives, and rejection index. These data show that HX-C and HH-C signaling pathways interact with one another in additive and often hypoadditive processes.NEW & NOTEWORTHY We present data showing that the ventilatory responses elicited by a hypoxic gas challenge in male C57BL6 mice are markedly altered by coexposure to hypercapnic gas challenge with hypercapnic responses often dominating the hypoxic responses. These data suggest that hypercapnic signaling processes activated within brainstem regions, such as the retrotrapezoid nuclei, may directly modulate the signaling processes within the nuclei tractus solitarius resulting from hypoxic-induced increase in carotid body chemoreceptor input to these nuclei.