The peculiarities of pulmonary macro- and microhemodynamics changes after treatment with agonists and blockers of cholinoceptors

Cover Page


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

Background. The pulmonary arterial and venous vessels are innervated by parasympathetic cholinergic nerves. However, the studies, performed on the isolated rings of pulmonary vessels, can not give answer to the question about the role of cholinergic mechanisms in the changes of pulmonary circulation in full measure.

Aim. The comparative analysis of the changes of the pulmonary macro- and microhemodynamics after acetylcholine, atropine, pentamine and nitroglycerine treatment.

Materials and methods. The study was carried out on the anesthetized rabbits in the condition of intact circulation with the measurement of the pulmonary artery pressure and flow, venae cavae flows, cardiac output, and also on isolated perfused lungs in situ with stabilized pulmonary flow with measurement of the perfused pulmonary artery pressure, capillary hydrostatic pressure, capillary filtration coefficient and calculation of the pulmonary vascular resistance, pre- and postcapillary resistances.

Results. In the conditions of intact circulation after acetylcholine, pentamine and nitroglycerine treatment the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance did not change as a result of decreasing of pulmonary artery flow and left atrial pressure due to diminution of venous return and venae cavaе flows. On perfused isolated lungs acetylcholine caused the increasing of pulmonary artery pressure, capillary hydrostatic pressure, pulmonary vascular resistance, pre- and postcapillary resistance and capillary filtration coefficient. After M-blocker atropine treatment the indicated above parameters of pulmonary microcirculation increased, on the contrary, after N-blocker pentamine treatment they decreased. Nitroglycerine infusion caused less decreasing of the parameters of pulmonary microcirculation in comparison with effects of pentamine, but capillary filtration coefficient decreased to a greater extent. These data indicate that nitroglycerine decreases endothelial permeability of pulmonary microvessels.

Conclusion. After activation or blockade of cholinergic mechanisms in the condition of intact circulation the calculated parameter of pulmonary vascular resistance is depended from the ratio of the pulmonary artery pressure and flow and left atrial pressure, which are determined by the venous return. The different character of the changes of pulmonary microcirculatory parameters after M-blocker atropine and N-blocker pentamine treatment is evidence of reciprocal relations of M- and N-cholinoceptors in the nervous regulation of the pulmonary microcirculatory bed.

Full Text

Restricted Access

About the authors

Vadim I. Evlakhov

Institute of the Experimental Medicine; Pavlov First Saint Petersburg State Medical University

Author for correspondence.
Email: viespbru@mail.ru
ORCID iD: 0000-0002-2521-8140
SPIN-code: 9072-4077

Doctor of Medical Sciences, Head of the Laboratory of the Physiology of Visceral Systems named acad. K.M. Bykov; Docent of the Department of Normal Physiology

Russian Federation, Saint Petersburg

Ilya Z. Poyassov

Institute of the Experimental Medicine; Saint Petersburg State University of Aerospace Instrumentation

Email: ilpoar@yandex.ru
SPIN-code: 7285-0493

Doctor of Biological Sciences, Senior Research Fellow of the Laboratory of the Physiology of Visceral Systems named acad. K.M. Bykov; Professor of the Department of the Medical Electronics

Russian Federation, Saint Petersburg

Tatiana P. Berezina

Institute of the Experimental Medicine; Saint Petersburg State University of Aerospace Instrumentation

Email: retaber@mail.ru
ORCID iD: 0000-0003-0647-2458

Candidate of Biological Sciences, Research Fellow of the Laboratory of the Physiology of Visceral Systems named acad. K.M. Bykov

Russian Federation, Saint Petersburg

References

  1. Евлахов В.И., Поясов И.З. Физиология легочных венозных сосудов // Российский физиологический журнал им. И.М. Сеченова. – 2018. – Т. 104. – № 10. – С. 1135–1151. [Evlakhov VI, Poyassov IZ. The physiology of pulmonary venous vessels. Russian Journal of Physiology. 2018;104(10):1135–1151. (In Russ.)]. https://doi.org/10.7868/S0869813918100027.
  2. Vaillancourt M, Chia P, Sarji S, et al. Autonomic nervous system involvement in pulmonary arterial hypertension. Respir Res. 2017;18(1):201–216. https://doi.org/10.1186/s12931-017-0679-6.
  3. Ding X, Murray PA. Regulation of pulmonary venous tone in response to muscarinic receptor activation. Am J Physiol Lung Cell Mol Physiol. 2005;288(1):L131–140. https://doi.org/10.1152/ajplung.00230.2004.
  4. Ding X, Murray PA. Acetylcholine activates protein kinase C-α in pulmonary venous smooth muscle. Anesthesiology. 2007;106(3):507–514. https://doi.org/10.1097/00000542-200703000-00015.
  5. Walch L, Gascard JP, Dulmet E, et al. Evidence for a M(1) muscarinic receptor on the endothelium of human pulmonary veins. Br J Pharmacol. 2000;130(1):73–78. https://doi.org/10.1038/sj.bjp.0703301.
  6. Orii R, Sugawara Y, Sawamura S, Yamada Y. M3-muscarinic receptors mediate acetylcholine-induced pulmonary vasodilation in pulmonary hypertension. Biosci Trends. 2010;4(5):260–266.
  7. Park S, Bivona BJ, Harrison-Bernard LM. Lack of contribution of nitric oxide synthase to cholinergic vasodilation in murine renal afferent arterioles. Am J Physiol Renal Physiol. 2018;314(6):F1197–F1204. https://doi.org/10.1152/ajprenal.00433.2017.
  8. Chiba T, Sakuma K, Komatsu T, et al. Physiological role of nitric oxide for regulation of arterial stiffness in anesthetized rabbits. J Pharmacol Sci. 2019;139(1):42–45. https://doi.org/10.1016/j.jphs.2018.11.003.
  9. Saternos HC, Almarghalani DA, Gibson HM, et al. Distribution and function of the muscarinic receptor subtypes in the cardiovascular system. Physiol Genomics. 2018;50(1):1–9. https://doi.org/10.1152/physiolgenomics.00062.2017.
  10. Cooke JP. Imaging vascular nicotine receptors: A new window onto vascular disease. JACC Cardiovasc Imaging. 2012;5(5):537–539. https://doi.org/10.1016/j.jcmg.2012. 03.004.
  11. Li DJ, Huang F, Ni M, et al. α7 Nicotinic acetylcholine receptor relieves angiotensin II-induced senescence in vascular smooth muscle cells by raising nicotinamide adenine dinucleotide-dependent SIRT1 activity. Arterioscler Thromb Vasc Biol. 2016;36(8):1566–1476. https://doi.org/10.1161/atvbaha.116.307157.
  12. Евлахов В.И., Поясов И.З., Шайдаков Е.В. Гемодинамика в легких при экспериментальной тромбоэмболии легочной артерии на фоне блокады альфа-адренорецепторов // Российский физиологический журнал им. И.М. Сеченова. – 2016. – Т. 102. – № 7. – С. 815–824. [Evlakhov VI, Poyassov IZ, Shaidakov EV. The pulmonary hemodynamics changes in case of experimental acute pulmonary embolism after blockade of alpha-adrenoceptors. Russian Journal of Physiology. 2016;102(7):815–824. (In Russ.)]
  13. Evlakhov VI, Poyassov IZ. Changes in pulmonary hemodynamics induced by experimental myocardial ischemia in nitroglycerin- or acetylcholine-treated rabbits. Bull Exp Biol Med. 2014;157(4):443–446. https://doi.org/10.1007/s10517-014-2586-x.
  14. Машковский М.Д. Лекарственные средства. – 16-е изд. – М.: Новая волна, 2012. [Mashkovski MD. Lecarstvennie sredstva. 16th ed. Moscow: Novaya volna; 2012. (In Russ.)]
  15. Евлахов В.И., Поясов И.З., Шайдаков Е.В. Роль реакций венозных сосудов легких в изменениях легочной гемодинамики при экспериментальной тромбоэмболии легочной артерии // Российский физиологический журнал им. И.М. Сеченова. – 2017. – Т. 103. – № 7. – С. 778–788. [Evlakhov VI, Poyassov IZ, Shaidakov EV. The role of the venous vessels reactions in the pulmonary hemodynamics changes following experimental pulmonary thromboembolism. Russian Journal of Physiology. 2017;103(7):778–788. (In Russ.)]
  16. Евлахов В.И., Поясов И.З., Шайдаков Е.В. Гемодинамика в легких при экспериментальной тромбоэмболии легочной артерии на фоне блокады альфа-адренорецепторов // Российский физиологический журнал им. И.М. Сеченова. – 2016. – Т. 102. – № 7. – С. 815–824. [Evlakhov VI, Poyassov IZ, Shaidakov EV. The pulmonary hemodynamics changes in case of experimental acute pulmonary embolism after blockade of alpha-adrenoceptors. Russian Journal of Physiology. 2016;102(7):815–824. (In Russ.)]
  17. Евлахов В.И., Поясов И.З. Гемодинамические механизмы изменений давления и кровотока в легочной артерии при применении депрессорных вазоактивных веществ // Российский физиологический журнал им. И.М. Сеченова. – 2011. – Т. 97. – № 1. – С. 24–34. [Evlakhov VI, Poyassov IZ. Hemodynamic mechanisms of the pulmonary artery pressure and blood flow changes following vasoactive depressor drugs injection. Russian Journal of Physiology. 2011;97(1):24–34. (In Russ.)]
  18. Tkachenko BI, Evlakhov VI, Poyassov IZ. Hemodynamic mechanisms of reduction of venous return and pulmonary circulation during experimental myocardial ischemia. Bull Exp Biol Med. 2009;147(1):31–35. https://doi.org/10.1007/s10517-009-0455-9.
  19. Magder S. Volume and its relationship to cardiac output and venous return. Crit Care. 2016;20(1):271. https://doi.org/10.1186/s13054-016-1438-7.
  20. Morris RI, Sobotka PA, Balmforth PK, et al. Iliocaval venous obstruction, cardiac preload reserve and exercise limitation. J Cardiovasc Transl Res. 2020;13(4):531–539. https://doi.org/10.1007/s12265-020-09963-w.
  21. Лосев Н.А., Евлахов В.И., Шалковская Л.Н. Реципрокный характер взаимодействия мускариновых и никотиновых холинергических механизмов в регуляции системной гемодинамики // Медицинский академический журнал. – 2011. – Т. 11. – № 2. – С. 33–41. [Losev NA, Evlakhov VI, Shalkovskaya LN. The reciprocal character of the muscarinic and nicotinic cholinergic mechanisms interaction in the systemic hemodynamics regulation. Medical Academic Journal. 2011;11(2):33–41. (In Russ.)]
  22. Schmeck J, Konrad C, Schöffel S, et al. Interaction of acetylcholine and endothelin-1 in the modulation of pulmonary arterial pressure. Crit Care. 2000;28(12):3869–3875. https://doi.org/10.1097/00003246-200012000-00022.
  23. Kobayashi K, Horikami D, Omori K, et al. Thromboxane A2 exacerbates acute lung injury via promoting edema formation. Sci Rep. 2016;6:32109. https://doi.org/10.1038/srep32109.
  24. Comellas AP, Briva A. Role of endothelin-1 in acute lung injury. Transl Res. 2009;153(6):263–271. https://doi.org/10.1016/j.trsl.2009.02.007.
  25. Evlakhov VI, Poyassov IZ, Ovsyannikov VI. Pulmonary microcirculation in experimental model of pulmonary thromboembolism under conditions of α-adrenoceptor blockade. Bull Exp Biol Med. 2019;166(3):313–316. https://doi.org/10.1007/s10517-019-04340-3.
  26. Egan TM, Hoffmann SC, Sevala M, et al. Nitroglycerin reperfusion reduces ischemia-reperfusion injury in non-heart-beating donor lungs. J Heart Lung Transplant. 2006;25(1):110–119. https://doi.org/10.1016/j.healun.2005. 02.013.
  27. López-Rivera F, Cintrón Martínez HRC, La Torre CC, et al. Treatment of hypertensive cardiogenic edema with intravenous high-dose nitroglycerin in a patient presenting with signs of respiratory failure: A case report and review of the literature. Am J Case Rep. 2019;20:83–90. https://doi.org/10.12659/AJCR.913250.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2021 Evlakhov V.I., Poyassov I.Z., Berezina T.P.

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: серия ПИ № ФС 77 - 74760 от 29.12.2018 г.