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Right Ventricular Pressure and Ventilatory Responses to Pulmonary Gas Embolism

肺氣栓塞症所誘發的右心室壓對呼吸的影響

摘要


本實驗之目的,在探討於發生肺氣栓塞症(Plumonary gas embolism-PGE)時,所誘發的右心室壓(P(下标 RV))對呼吸頻率(f)的影響。造成PGE的方法,係將定量定速的空氣,從氯醛糖(α-chloralose)麻醉中狗的股靜脈內注入,當P(下标 RV)因PGE而改變時,記錄並分析其呼吸模式,以觀察P(下标 RV)對f的控制機轉。PGE促成P(下标 RV)上升,主要係由於肺血管阻力的增加。發生PGE後的第二分鐘,呼吸頻率增高,主要是藉由呼氣時間的減少,吸氣時間(TI)的減少並不顯著,但PGE使TI在整個呼吸週期中(T(下标 TOT))所佔比例(TI/T(下标 TOT))則呈顯著增加。f常伴隨著P(下标 RV)的改變而變。除PGE外,P(下标 RV)也會因肺動脈的阻塞,或因肺動脈血流量的增加而上升,而f則隨之也上升。另外如給予組織氨對抗劑(histamine antagonist),beta-腎上素激性抑制劑及興奮劑(beta-adrenergic blockade and stimulant)等,而使P(下标 RV)改變,f也隨之改變。前述反應會隨頸部迷走神經切斷而消失。這些結果暗示,在PGE時,呼吸頻率的增加,其部分原因係PGE誘使P(下标 RV)上升的結果,且因P(下标 RV)的增高而導致向心性迷走神經活動性增加所引起。

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並列摘要


This study was designed to test the hypothesis that changes in right ventricular pressure (P(subscript RV)) are responsible in part for the altered breathing frequency (f) during pulmonary gas embolism (PGE). PGE was induced by infusing air into the femoral vein of alpha-chloralose anesthetized dogs. Respiratory flow pattern was recorded and analyzed in relation to P(subscript RV) changes induced resulting from PGE. The rise of P(subscript RV), whether induced by PGE, by pulmonary artery occlusion, or by acute elevation of pulmonary arterial blood flow, was consistently associated with increased f. Breathing frequency rose principally through reduction of expiratory duration (T(subscript E)). The inspiratory duration (T(subscript I)) was shortened somewhat and the fractional inspiratory cycle, T(subscript I)/(T(subscript E)+T(subscript I)), increased. The relationships between P(subscript RV) and f were altered by changes of P(subscript RV) resulting from the administration of histamine antagonist, by beta-adrenergic blockade, beta-adrenergic stimulation, and by changing pulmonary arterial blood flow. The responses did not occur after bilateral cervical vagotomy. These results demonstrate that f during PGE is partially regulated in response to changes in P(subscript RV) and is mediated through the vagal afferent.

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