Influence of splanchnic intravascular volume changes on cardiac output during muscarinic receptor stimulation in the anaesthetized dog.

Journal Article (Journal Article)

The direct influence of systemic muscarinic receptor stimulation on total splanchnic intravascular volume and the splanchnic organs responsible for the total splanchnic volume change associated with muscarinic receptor stimulation in the animal with an intact circulation are unknown. Furthermore, the subsequent effect of these volume changes on cardiac output is not known. Thus, acetylcholine was infused at 5 micrograms kg-1 min-1 in 25 anaesthetized dogs in which nicotinic blockade of the ganglia was achieved with mecamylamine, while total and regional splanchnic intravascular volume changes were determined with a radionuclide imaging technique. Total splanchnic volume decreased by 4.9 +/- 1.0% (P less than 0.0001), splenic volume decreased by 10.3 +/- 2.0% (P less than 0.0001), hepatic volume increased by 5.8 +/- 1.4% (P less than 0.01), extrahepatosplenic volume increased by 6.6 +/- 1.6% (P less than 0.01) and cardiac output increased from 1960 +/- 190 to 2290 +/- 230 ml min-1 (P less than 0.001). After splenectomy (n = 13), the hepatic and extrahepatosplenic volume increments were abolished, and the increase in cardiac output was not attenuated (1600 +/- 260 to 2040 +/- 370 ml min-1). After subsequent evisceration (n = 5), the cardiac output increment associated with acetylcholine was still not attenuated. Acetylcholine-associated splanchnic volume changes were abolished after muscarinic receptor blockade with atropine. Thus, muscarinic receptor stimulation causes a decrease in total splanchnic volume due entirely to a decrease in splenic volume. The splanchnic volume changes do not influence cardiac output.

Full Text

Duke Authors

Cited Authors

  • Morse, MA; Bell, L; Rutlen, DL

Published Date

  • March 1990

Published In

Volume / Issue

  • 138 / 3

Start / End Page

  • 331 - 336

PubMed ID

  • 2327262

International Standard Serial Number (ISSN)

  • 0001-6772

Digital Object Identifier (DOI)

  • 10.1111/j.1748-1716.1990.tb08854.x


  • eng

Conference Location

  • England