INFLUENCE OF ACETYLCHOLINE ON THE PULMONARY ARTERIAL PRESSURE
INFLUENCE OF ACETYLCHOLINE ON THE PULMONARY ARTERIAL PRESSURE
复制标题
乙酰胆碱对肺动脉压的影响
DOI:
10.1136/hrt.19.2.272
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发表时间:
1957
影响因子:
--
通讯作者:
P. Harris
中科院分区:
文献类型:
--
作者:
P. Harris
It is still a matter for debate whether active variation in the calibre of the vessels of the pulmonary circulation can be caused by physiological or pharmacological stimuli. In most observations, the agents used to test the pulmonary circulation are known to have an effect also on the systemic circulation and often on the cardiac output. Under these circumstances the pulmonary arterial pressure is liable to be influenced by factors other than local alterations in the calibre of the vessels of the lesser circulation. In an attempt to circumvent these difficulties, it was decided to study the effects of acetylcholine on the pressures in the pulmonary circulation in a group of patients. Ellis and Weiss (1932) demonstrated the destruction of acetylcholine in the blood stream in man by the lack of cumulative action during its prolonged intravenous infusion. They and also Carmichael and Fraser (1933) observed flushing of the head and upper part of the body when acetylcholine was injected in sufficient dosage into a vein, while intra-arterial injection caused a regional dilatation of arteries and arterioles but no general effects. Since acetylcholine is destroyed so rapidly in the blood stream, it might be possible to inject it into the pulmonary artery in such a dose that it was inactivated before reaching the systemic circulation (Tiffenau and Beauvallet, 1944). In this way it was hoped that any vasomotor effect of the drug would be confined to the pulmonary circulation. In animals, the action of acetylcholine is most evident in the systemic circulation, where it causes widespread arterial vasodilatation irrespective of whether these vessels are supplied by the sympathetic or parasympathetic systems (Hunt and Taveau, 1906; Dale, 1914; Hunt, 1917a and 1917b). Reports of the activity of the drug in the pulmonary circulation, however, have been conflicting (Hunt, 1917a; Daly, 1932 and 1933; von Euler, 1932; Franklin, 1932; Gaddum and Holtz, 1933; Johnson et al., 1937; Hamilton et al., 1939; Petrovskaia, 1939; Foggie, 1940; Friedberg et al., 1943; von Euler and Liljestrand, 1946; Dirken and Heemstra, 1948).