Mechanisms of Maintaining a Normal Arterial P(subscript O2) during Acute Increase in Ventilation-Perfusion Inequality

肺通氣血流比值急速改變對動脈血氧分壓的影響機制

李不偏(B. P. Lee) ； 姜壽德(S. T. Chiang) ； 林玉鐘(Y. C. Lin)

《The Chinese Journal of Physiology》 26卷1期 (1983/06) Pp. 31-48

摘要

肺內通氣血流比値急速改變(V(下標 A)/Q Inequality)，為影響氣體交換的主要原因之一。但狗在V(下標 A)/Q Inequality時，仍能維持正常的動脈血氧分壓(PaO2)。本研究以六隻α-Chloralose麻醉的狗，為實驗動物，藉傾斜手術台，將狗體Tilting，來誘使V(下標 A)/Q Inequality。肺內通氣血流比値(V(下標 A)/Q)在水平仰臥(Supine)時約為0.88±0.09，當狗體被Tilting至頭向上75度時，其比値為Supine時的2.7倍。全肺通氣血流比値(Overall V(下標 A)/Q)係由所測得的心搏出量(Cardiac Output, Q)，每分鐘呼吸量(V(下標 E))及無效腔對潮氣容積(V(下標 D)/V(下標 T))比値等計算而得。當狗被Tiliting時所誘發的肺通氣功能過高(Hyper-Ventilation)，可由其肺泡通氣量(V(下標 A))及肺泡二氧化碳分壓(P(下標 A)CO2)間之負相關，及由肺泡通氣量(V(下標 A))和V(下標 A)/Q比値間之正相關看出端倪。此顯示了當V(下標 A)/Q比値急速增加，對氣體交換的影響，可藉由肺通氣功能過高和肺內血流重新分佈來代償。因V(下標 A)/Q比値不正常地增加，誘使肺通氣功能過高，可能有①缺氧症(Hypoxia)②腦血流供應量降低(Cerebral blood supply)③心肺血流量減少(Cardiopulmonary blood volume)等機制牽涉在內。當狗體被Tilting時，以Hyperoxygenation及阻止Carotid hypotention方法實驗之，則肺通氣功能過高現象雖有減少但並不完全消除。從靜脈急速灌注血液，用來補償狗體因被Tilting所引起的下半肢體血液，緩慢流入胸腔內，則可降低肺通氣功能過高現象。因此原發生缺氧(Initial hypoxia)，腦部血流量降低(Cerebral hypotension)及胸腔內血流量減少(thoracic hypovolemia)係促使V(下標 A)/Q比値變大及誘發肺通氣功能過高的原因。藉肺通氣功能過高，來代償因V(下標 A)/Q Inequality所造成的不良氣體交換，則動脈血氧分壓得能維持正常。本研究成果係接受國科會補助計劃編號NSC-71-0412-B010-11。

並列摘要

Ventilation-perfusion inequality is one of the major factors affecting pulmonary gas exchange. However, dogs maintain their arterial P(subscript O2)perfectly despite acute elevation of V(subscript A)/Q ratio. In this study, V(subscript A)/Q changes were induced by rapid passive head-up tilt in 6 anesthetized dogs. Passive tilting from supine to 75° in 15° increments achieved elevation of V(subscript A)/Q from 1.23 to 2.7 times the supine levels. Overall V(subscript A)/Q was computed from the measurement of cardiac output(Q), minute ventilation(V(subscript E)), and dead space to tidal volume ratio(V(subscript D)/V(subscript T)).Hyperventilation during tilting was clearly indicated by an inverse relationship between V(subscript A)and P(subscript ACO2). Furthermore, a positive correlation existed between V(subscript A)and V(subscript A)/Q ratio indicating the deteriorating effect of increased V(subscript A)/Q was compensated for by the hyperventilation. We investigated the possible involvement of 1)hypoxia,2)cerebral blood supply,and 3)cardiopulmonaryblood volume in the V(subscript A)/Q abnormality induced hyperventilation. Hyperoxygenation and prevention of carotid hypotention during tilting diminished but did not abolish the hyperventilatory response. Rapid infusion of blood intravenously thus compensating for central blood loss to the lower body during tilting also reduced the hyperventilatory response. It is, therefore, concluded that initial hypoxia and cerebral hypotension as well as thoracic hypovolemia during tilting all contributed to the cause of V(subscript A)/Q abnormality induced hyperventilation which is responsible for maintaining a normal P(subscript aO2)during increased V(subscript A)/Q.

並列關鍵字

Arterial P(subscript O2) ； Cardiac output ； Gas exchange ； Alveolar hyperventilation ； Hypoxia ； Hypovolemia ； Cerebral ischemia