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绵羊热喘时的呼吸功能

Respiratory function during thermal tachypnoea in sheep.

作者信息

Hales J R, Webster M E

出版信息

J Physiol. 1967 May;190(2):241-60. doi: 10.1113/jphysiol.1967.sp008205.

Abstract
  1. Four Merino wethers were exposed to dry bulb temperatures ranging from approximately 20 to 60 degrees C, and the concurrent changes in respiratory frequency, tidal volume, respiratory minute volume, alveolar ventilation, dead space ventilation, carbon dioxide output, rectal temperature, and arterial and mixed venous blood, CO(2) content, CO(2) partial pressure and pH were established.2. The respiratory response to heat exposure showed two phases. Respiratory minute volume was initially increased by a rise in the respiratory frequency, while tidal volume decreased. After more prolonged exposure there was a second phase in which respiratory minute volume was further increased by an increase in the tidal volume; respiratory frequency was now slower than in the first phase but was still well above control values.3. The increase in respiratory minute volume during the first phase of the response was restricted almost entirely to the respiratory dead space; changes in blood CO(2) and pH were slight. In the second phase, respiratory minute volume showed a much greater increase, and a change of alveolar ventilation to about 5 times the control level resulted in severe respiratory alkalosis.4. Contrary to findings in cattle, the slower, deeper form of respiration could be elicited even with rectal temperature in the normal range. This change in respiration appears to be the result of either peripheral thermoreceptor function or mechanical demands of the respiratory system. The neglect of control of acid-base balance during the second phase indicates the existence of a dominant thermal stimulus or modification of respiratory control mechanisms.
摘要
  1. 选用4只美利奴种阉羊,使其暴露于干球温度范围约为20至60摄氏度的环境中,同时测定其呼吸频率、潮气量、每分通气量、肺泡通气量、死腔通气量、二氧化碳排出量、直肠温度以及动脉血和混合静脉血中的二氧化碳含量、二氧化碳分压和pH值的变化情况。

  2. 热暴露引起的呼吸反应呈现两个阶段。最初,每分通气量因呼吸频率增加而升高,潮气量则下降。在持续暴露更长时间后,进入第二阶段,此时每分通气量因潮气量增加而进一步升高;呼吸频率比第一阶段慢,但仍远高于对照值。

  3. 反应第一阶段每分通气量的增加几乎完全局限于呼吸死腔;血液中二氧化碳和pH值的变化轻微。在第二阶段,每分通气量增加幅度更大,肺泡通气量增加至对照水平的约5倍,导致严重的呼吸性碱中毒。

  4. 与牛的研究结果相反,即使直肠温度处于正常范围,也能引发较慢且较深的呼吸形式。这种呼吸变化似乎是外周温度感受器功能或呼吸系统机械需求的结果。第二阶段对酸碱平衡控制的忽视表明存在占主导地位的热刺激或呼吸控制机制的改变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5b9/1365290/5032401315bb/jphysiol01124-0005-a.jpg

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