Effect of acetylcholine on vascular capacity in the dog.

Abstract

A B S T R A C T Acetylcholine produces venoconstriction of isolated vein strip preparations. However, the effect of acetylcholine on overall vascular capacity is not known. To investigate this effect and to elucidate the mechanisms involved, 38 anesthetized dogs were placed on total cardiopulmonary bypass, splenectomized, and given intraarterial infusions of acetylcholine. Almost all of the effect on vascular volume was found to be in the splanchnic circulation, because in four eviscerated animals there was no significant change in capacity. In the animals in which the mesenteric arteries were cannulated to provide constant inflow, and the hepatic vein was cannulated to measure splanchnic venous outflow, acetylcholine infusion for 5 and 21 min increased splanchnic vascular capacity in all animals by 107±28 (SEM) ml (P < 0.01) and 291±132 ml (P < 0.05), respectively. This increase in splanchnic vascular volume was associated with a rapid and sustained increase in transhepatic resistance to portal blood flow for the duration of the infusions (P < 0.01). In the animals in which the portal vein was vented proximal to the liver, no significant volume change occurred in the splanchuiic vasculature with acetylcholine infusion. Increasing hepatic venous pressure to elevate portal venous pressure to the same level as that achieved with acetylcholine resulted in a similar increase in splanchnic vascular volume. Atropine, but not adrenergic blockade, blocked the acetylcholine-induced volume retention, indicating that the effect of acetylcholine was direct. Substantial volume retention was also achieved by stimulation of the distal ends of the sectioned cervical vagi. Thus, acetylcholine administration directly increases transhepatic resistance and is associated with a pooling of volume in the splanchnic vasculature that would, in the intact animal, result in a decrease in venous return to the heart.

Effect of ouabain on total vascular capacity in the dog.

“…Other studies on vascular capacity in the dog in response to beta agonists and to acetylcholine using hepatic vein wedge pressures to localize the site of altered transhepatic resistance have also demonstrated that the change in resistance in these preparations occurred in a postsinusoidal location as in this study (3,4). The elevation of transhepatic resistance is primarily mediated through stimulation of alpha adrenergic receptors, Similarly, stimulation of alpha receptors is the major mechanism whereby intravenous digitalis administration elevates arterial vascular resistance as noted in Figs.…”

“…This small increase could be due to one or more factors. First, digitalis is known to increase vagal activity and recent work suggests that enhanced cholinergic activity may increase transhepatic resistance (4). The presence of a substantial ouabain-associated increase in transhepatic resistance after atropine administration, however, makes it unlikely that increased vagal activity plays a prominent role in elevating transheptic resistance.…”

“…In these experiments 20 mg of atropine was administered into the oxygenator over 5 min. This dose of atropine has been demonstrated to block the effects of infused acetylcholine and of vagal stimulation on transhepatic resistance (4). Both before and after atropine administration, 6 Dogs on total cardiopulmonary bypass slowly accumulate fluid, resulting in a progressive reduction in oxygenator volume.…”

Reflex influence of selective coronary artery occlusion on the total capacitance vasculature in the dog.

“…The attenuation of the response did not appear to be related to the change in resting intravascular-volume associated with atropine administration, since atropine administration was not associated with a directionally consistent change in intravascular volume. While the doses of atropine used in the present study were of the same magnitude as those employed by other investigators to produce muscarinic receptor blockade in a preparation similar to ours (16), it is possible that partial inhibition of autonomic ganglia was also produced with these doses of atropine ( 17). However, since the reflex volume increment was significantly attenuated by section of the vagi at the diaphragm, one may still conclude that the reflex volume increment was mediated, in part, through changes in efferent parasympathetic receptor stimulation.…”

Effet antihypertensif de BpF2, une fraction d\'extrait aqueux de feuilles de <i>Bidens pilosa</i> L. (Asteraceae) chez le lapin

“…En conséquence, cette étude suggère l'existence de substances cholinomimétiques de type muscarinique dans la fraction active de l'extrait de feuilles de Bidens pilosa L. Ces substances pourraient agir selon le même mécanisme que l'acétylcholine. En effet, l'injection intraveineuse d'acétylcholine chez l'homme ou chez l'animal entraîne une chute immédiate et fugace de la pression artérielle provenant du ralentissement cardiaque et de la vasodilatation ( Supple & Powell, 1981;Abo, 1996;N'Guessan et al, 2004). Cette injection provoque une bradycardie par effet sinusal, une diminution de la conduction auriculo-ventriculaire et une diminution de la force de contraction ventriculaire.…”