On the mechanism of the effect of acetylcholine on the pulmonary circulation
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It was shown in experiments on dogs that during the circulation through the pulmonary vascular system of acetylcholine added to the blood no recordable pressure changes were noted in the pulmonary circulation. Pressor reaction began in 4–11 seconds after the administration into the pulmonary artery. Injection of acetylcholine into the left ventricle and aorta also leads to the pressor reaction in the pulmonary circulation; this occurs earlier than when the substance is injected into the femoral vein or directly into the pulmonary artery (in 4 seconds). Besides, pressor reaction is more marked in administration of acetylcholine into the left ventricle and aorta than in injection into the venous part of the systemic circulation. Pressure reduction in the pulmonary artery, preceding its rise, is directly connected with the inhibition of the cardiac activity and is also well reproduced with acetylcholine administered into the pulmonary artery and the left ventricle of the heart.
Thus, acetylcholine does not provoke direct changes in the hemodynamics of the pulmonary circulation, and, evidently, does not influence the tone of the pulmonary vessels.
Period of reaction development in the pulmonary circulation and the same type of reaction occurring in acetylcholine administration into the venous and the arterial portion of the circulation lead to the conclusion that the hemodynamic effects the pulmonary circulation reflect the hemodynamic shifts in the systemic circulation.
KeywordsPulmonary Artery Left Ventricle Acetylcholine Systemic Circulation Vascular System
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- 1.M. M. Lenkevich, Farmakol. i Toksikol.13, 4, 19 (1950).Google Scholar
- 2.A. I. Khomazyuk, in: Questions of Cardiovascular System Pathology [in Russian] (Kiev, 1959) p. 277.Google Scholar
- 3.H. G. Borst, E. Berglund, and M. McGregor, J. Clin. Invest.36, 669 (1957).Google Scholar
- 4.A. F. Cournand, Am. Heart J.54, 172 (1957).Google Scholar
- 5.R. Daley, Brit. Med. J.2, 249 (1957).Google Scholar
- 6.I. de B. Daly, Physiol. Rev.13, 149 (1933).Google Scholar
- 7.I. de B. Daly, et al., Quart. J. Exper. Physiol.27, 123 (1938).Google Scholar
- 8.I. de B. Daly and M. de B. Daly, J. Physiol.137, 427 (1957).Google Scholar
- 9.U. S. Euler and G. Liljestrand, Acta. Physiol. Scandinav.12, 301 (1946).Google Scholar
- 10.L. Friedberg, L. N. Katz, and F. S. Steinitz, J. Pharmacol. and Exper. Therap.77, 80 (1943).Google Scholar
- 11.J. H. Gaddum and P. Holtz, J. Physiol.77, 139 (1933).Google Scholar
- 12.V. Johnson, et al., Am. J. Physiol.120, 624 (1937).Google Scholar
- 13.P. Harris, Brit. Heart J.19, 272 (1957).Google Scholar
- 14.P. Harris, et al., Proc. Soc. Exper. Biol. and Med.93, 77 (1956).Google Scholar
- 15.S. Rodbard, Am. J. Med.15, 356 (1953).Google Scholar
- 16.J. C. Rose, Proc. Soc. Exper. Biol. and Med.94, 734 (1957).Google Scholar
- 17.D. J. Smith and J. W. Coxe, Am. J. Physiol.167, 732 (1951).Google Scholar
- 18.P. Wood, et al., Brit. Heart J.19, 279 (1957).Google Scholar