Action of vasodilator agents in experimental mesenteric circulatory failure
Pawlik, W.W.; Waluś, K.M.; Gustaw, P.; Konturek, S.J.
Folia Medica Cracoviensia 23(2): 155-168
1981
ISSN/ISBN: 0015-5616 PMID: 7344999 Document Number: 177285
This study was designed to evaluate the effectiveness of 3 pharmacologically dissimilar vasodilating agents; adenosine, glucagon and prostacyclin in reversing the hemodynamic and metabolic changes following digoxin-induced vasoconstriction of the canine mesenteric circulation. Experiments were carried out on 27 anesthetized dogs. Blood flow to an intestinal segment was measured with an electromagnetic blood flow meter. The arteriovenous O2 difference across the intestinal circulation was determined photometrically. Intestinal O2 consumption was calculated as the product of arteriovenous O2 difference and mesenteric blood flow. 86Rb clearance was measured to estimate the density of the perfused capillaries. Digoxin 0.5 .mu.g/kg i.v. did not change the systemic arterial pressure but significantly reduced the mesenteric blood flow by 28%; the intestinal O2 consumption by 13% and the density of the perfused capillaries by 18%. In experiments in which adenosine was given during digoxin induced ischemia there were sustained increases in mesenteric blood flow by 25%, in O2 consumption by 12% and capillary density was increased by 14%. Glucagon infused during digoxin induced ischemia produced sustained increases in blood flow by 72%, in O2 consumption by 35% and in intestinal capillary density by 47%. Prostacyclin administered during digoxin-induced ischemia produced increases in mesenteric blood flow by 96%, in intestinal O2 consumption by 35% and in intestinal capillary density by 62%. The observed constrictor action of digoxin on the mesenteric circulation seems to involve arterioles and precapillary sphincters because there is an decrease in mesenteric blood flow, intestinal O2 consumption and intestinal capillary density. Apparently all 3 vasodilatory agents infused intraarterially restored mesenteric blood flow, intestinal O2 consumption and intestinal capillary density to pre-digoxin values. These effects seem to be due to the action of these preparations on mesenteric microcirculatory structures responsible for peripheral vascular resistance and capillary perfusion.