β2‐adrenergic control of plasma volume in hemorrhage

Abstract

Hemorrhage is associated with absorption of extravascular fluid from skeletal muscle to blood in order to compensate for the loss of intravascular volume. Previous studies have shown that this fluid gain is mainly linked to .beta.-adrenergic microvascular adjustments leading to decrease in capillary hydrostatic pressure and to precapillary sphincter mediated increase in the capillary surface area available for fluid exchange. The importance of .beta.-adrenergic control of plasma volume in bleeding was confirmed by measurement of changes in plasma volume after graded hemorrhage in animals [cats] with intact and blocked vascular .beta.2-adrenoceptors (i.v. administration of the selective .beta.2-blocking agent ICI 118,551 [erythro-DL-1-(f-methylindan-4-yloxy)-3-isopropylamino-butan-2-ol]). With intact .beta.2-adrenoceptors plasma volume was gradually restored after bleeding so that .apprx. 50% of the shed plasma volume (.apprx. 35% of the shed blood volume) was compensated for at 2 h after exsanguination of 20% as well as 40% of the blood volume. The corresponding figures in animals with blocked .beta.2-adrenoceptors were only 14% of the shed plasma volume and 8% of the shed blood volume at both degrees of hemorrhage.