St John W M, Knuth K V
J Appl Physiol Respir Environ Exerc Physiol. 1981 May;50(5):984-93. doi: 10.1152/jappl.1981.50.5.984.
The purpose of this investigation was to compare the respiratory pattern of gasping with eupnea and apneusis. Decerebrate, cerebellectomized, vagotomized, paralyzed and ventilated cats were used. The ventilatory pattern, assessed by phrenic nerve activity, was reversibly altered from eupnea to apneusis or gasping by use of a cooling-for, thermode positioned inm the rostral pons or through the pontomedullary junction, respectively. Irreversible apneusis or gasping resulted from brain stem lesions or freezing at appropriate loci. Analysis of phrenic activity revealed that the rates of onset and rise of the gasp were much greater than those of the eupneic or apneustic inspiration. Moreover, in contrast to eupnea or apneusis, neither the frequency nor the intensity of gasps was altered by hypercapnia, hypocapnia, or carotid chemoreceptor stimulation by sodium cyanide. Although hypoxia caused an increase in gasping frequency, this response was transient and not dependent on carotid chemoreceptor mechanisms. These results provide no support for the concept that common mechanisms localized in medulla, underlie the neurogenesis of all automatic ventilatory patterns.
本研究的目的是比较喘息呼吸模式与平稳呼吸及长吸式呼吸。实验使用了去大脑、小脑切除、迷走神经切断、麻痹并通气的猫。通过膈神经活动评估的通气模式，分别通过将置于脑桥前部或经脑桥延髓交界处的冷却电极加热，可逆地从平稳呼吸改变为长吸式呼吸或喘息呼吸。脑干损伤或在适当部位冷冻会导致不可逆的长吸式呼吸或喘息呼吸。膈神经活动分析表明，喘息的起始速率和上升速率远大于平稳呼吸或长吸式呼吸吸气的速率。此外，与平稳呼吸或长吸式呼吸不同，高碳酸血症、低碳酸血症或氰化钠刺激颈动脉化学感受器均不会改变喘息的频率或强度。虽然低氧会导致喘息频率增加，但这种反应是短暂的，且不依赖于颈动脉化学感受器机制。这些结果并不支持延髓中存在共同机制是所有自动通气模式神经发生基础的观点。
