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The Effects ofα2-Adrenergic Agonism with Clonidine on the Pulmonary and Collateral Resistances in the Canine Lung Challenged with Histamine

Clonidine對于組織胺激發試驗引起肺及側枝阻力增加之效應

摘要


本實驗利用麻醉狗探討甲2型腎上線素接受器擬型劑Clonidine對於組織胺引起肺與側枝阻力增加之效應。在整體肺中,靜脈注射組織胺引起肺之吸氣阻力及呼氣阻力均明顯上升,預先給予clonidine(靜脈注射0.05mg/kg)後,注射組織胺引發之肺阻力上升幅度明顯受抑制,但在clonidine之前給予yohimbine(靜脈注射0.15mg/kg)則完全消除clonidine之抗組織胺效果。周邊之側枝阻力利用氣管鏡楔嵌技術加以測量,在封阻而獨立灌注氣流之次葉小支氣管中,局部給予噴霧式組織胺同樣引起側枝阻力明顯增加,但是clonidine並無顯著抗組織胺效果,而Isoproterenol(靜脈注射0.02mg/kg)大大減弱組織胺激發側枝阻力上升之幅度。本實驗之結果顯示:組織胺激發呼吸道收縮之效果,在整體肺中可以被甲2型接受器擬型劑clonidine所抑制,但在周邊小支氣管中(側枝系統),組織胺之效果則為乙2擬型劑Isoproterenol所對抗。

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並列摘要


Kao, S.J., C.Y. Shen, D. Wang and H.I. Chen: The effects of α2-adrenergic agonism with clonidine on the pulmonary and collateral resistances in the canine lung challenged with histamine. Chinese J. Physiol. 32(1): 21-30, 1989. In anesthetized dogs, we studied the effects of colonidine on the changes in pulmonary collateral resistance in response to histamine challenge. In the whole lung, an intravenous histamine increased the inspiratory (Ri), and expiratory (Re) resistance by 142±12%, and 229±30% over the control, respectively. Pretreatment with clonidine (0.05mg/kg, iv) significantly attenuated the increases to 76±16% (Ri), and 114±22% (Re) (p <0.05). However, the responses to histamine were restored after an addition of yohimbine (0.15mg/kg, iv) before clonidine. A bronchoscope wedge technique was used to measure the collateral resistance (Rcs) in the lung periphery. Histamine was administered in aerosolized form to a wedged sublobar segment. The local histamine challenge significantly increased Rcs. Pretreatment with clonidine did not discernibly affect the histamine-induced increase in Rcs. On the other hand, pretreatment with isoproterenol (0.02mg/kg, iv) remarkably attenuated the Rcs response to histamine. The results indicate that α2-adrenergic agonism with clonidine inhibits the brochoconstriction induced by histamine. α-antagonism with yohimbine abolishes the antiasthmatic effect of clonidine. In the lung periphery, the Rcs response to histamine is not altered by α2, but by β2 adrenergic agonism with isoproterenol.

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