To determine the mechanisms responsible for changes in splanchnic organ size during muscarinic receptor stimulation, acetylcholine was infused at 5 μg kg-1 min-1 in 11 anaesthetized pigs which had previously undergone carotid denervation and cervical vagotomy. Blood pressure decreased by 42 ± 4 mm Hg (P < 0.005), portal vein pressure decreased by 1.0 ± 0.3 mm Hg (P < 0.01), IVC pressure increased by 0.2 ± 0.1 mm Hg (P < 0.01), hepatic arterial flow increased by 10 ± 6 ml min-1 (NS), portal vein flow decreased by 89 ± 20 ml min-1 (P < 0.005), splenic segment length (SSL) decreased by 0.52 ± 0.11 mm (P < 0.005) (control 12.49 ± 1.27) (measured with ultrasonic crystals) and hepatic segment length (HSL) increased by 0.29 ± 0.06 mm (P < 0.05) (control 13.94 ± 1.16). Aortic constriction to decrease the splanchnic distending pressure by an amount comparable to that achieved with the acetylcholine-associated decrease in portal flow caused a similar decrease in SSL and increase in HSL. Graded constriction of the portal vein or IVC, to increase SSL or HSL respectively, in the presence and absence of acetylcholine demonstrated no change in splenic or hepatic compliance with acetylcholine. Ligation of the splenic vasculature reduced the acetylcholine-associated HSL increase from 0.41 ± 0.09 to 0.20 ± 0.07 mm (P < 0.05). Acetylcholine infused directly into the portal vein did not alter HSL. Atropine abolished all acetylcholine-associated haemodynamic changes. Thus, muscarinic receptor stimulation does not appear to act directly on splanchnic capacity vessels. Splenic dimension decreases due to a decrease in splanchnic flow and pressure, and hepatic dimension increases due to an increase in IVC pressure and redistribution of volume from the spleen.
|Original language||English (US)|
|Number of pages||8|
|Journal||Acta Physiologica Scandinavica|
|State||Published - 1990|
- Capacitance vasculature
ASJC Scopus subject areas