Role of β-adrenergic agonists in the control of vascular capacitance

Abstract

The role of beta-adrenergic agonists, such as isoproterenol, on vascular capacitance is unclear. Some investigators have suggested that isoproterenol causes a net transfer of blood to the chest from the splanchnic bed. We tested this hypothesis in dogs by measuring liver thickness, cardiac output, cardiopulmonary blood volume, mean circulatory filling pressure, portal venous, central venous, pulmonary arterial, and systemic arterial pressures while infusing norepinephrine (2.6 micrograms.min-1.kg-1), or isoproterenol (2.0 micrograms.min-1.kg-1), or histamine (4 micrograms.min-1.kg-1), or a combination of histamine and isoproterenol. Norepinephrine (an alpha- and beta 1-adrenergic agonist) decreased hepatic thickness and increased mean circulatory filling pressure, cardiac output, cardiopulmonary blood volume, total peripheral resistance, and systemic arterial and portal pressures. Isoproterenol increased cardiac output and decreased total peripheral resistance, but it had little effect on liver thickness or mean circulatory filling pressure and did not increase the cardiopulmonary blood volume or central venous pressure. Histamine caused a marked increase in portal pressure and liver thickness and decreased cardiac output, but it had little effect on the estimated mean circulatory filling pressure. Isoproterenol during histamine infusions reduced histamine-induced portal hypertension, reduced liver size, and increased cardiac output. We conclude that the beta-adrenergic agonist, isoproterenol, has little influence on vascular capacitance or liver volume of dogs, unless the hepatic outflow resistance is elevated by agents such as histamine.

Venous tone and cardiac function in the South American rattlesnakeCrotalus durissus: mean circulatory filling pressure during adrenergic stimulation in anaesthetised and fully recovered animals

“…Our results clearly show that activation of ␤-receptors can decrease P CV and MCFP through dilatation of the venous system, and ␤-receptors in the veins may contribute to regulating the venous system in rattlesnakes. Isoproterenol, however, does not significantly affect P CV or MCFP in dogs (Rothe et al, 1989).…”

Hemodynamic Effect of Different Doses of Fluids for a Fluid Challenge: A Quasi-Randomized Controlled Study

“…The Pmsf values reported in this study are similar to previous studies in similar populations 6,7,11 , and the baseline values are very similar in the four groups, which reassure that the haemodynamic effect of the intravascular volume was fairly similar on the four groups. Noradrenaline can increase Pmsf and reduce vascular capacitance 15,16 Pmsf at baseline is a significant predictor, inversely related to the change of Pmsf-arm: for one mmHg of increase of Pmsf-arm at baseline, the ∆Pmsf-arm will decrease by 0.35 mmHg. This may suggest that there is a physiological upper limit for Pmsf regardless the volume given, so that part of the volume is redistributed between stressed and non-stressed compartments or distributed between the intravascular and extravascular space.…”

Blood mobilization from the liver of the anaesthetized dog

“…It has been suggested that there may be a sphincter mechanism regulating hepatic venous outflow (Knisely, Harding & Debacker, 1957;Greenway & Oshiro, 1973). However, the only physiological evidence in support of this has been indirect and has shown hepatic outflow to be influenced by various humoral stimuli (Imai, Satoh & Taira, 1978;Rutlen, Supple & Powell, 1981;Rothe, Flanagan & Maass-Moreno, 1990). No information was provided on where any potential site of obstruction to flow may have been.…”