CARDIOVASCULAR ADRENORECEPTOR FUNCTION DURING COMPENSATORY AND DECOMPENSATORY HEMORRHAGIC-SHOCK

  • 1 January 1984
    • journal article
    • research article
    • Vol. 12  (1) , 9-24
Abstract
Prior reports have described the occurrence of an initial compensatory vasoconstriction followed by a decompensatory vasodilation response in animals that progress to irreversible shock induced by blood loss. Further analysis suggests that the secondary vascular decompensation is the result of sympathetic inhibition of adrenergic neurotransmission. The roles of the .alpha. 1 and .alpha. 2 adrenoceptors during initial compensatory and secondary decompensatory phases of hemorrhagic shock were examined. This was accomplished by subjecting rat pairs to a modified Wiggers hemorrhagic shock protocol. One of these rats served as an untreated control (Rc) while the other (Re) received either an adrenergic antagonist or was bilaterally adrenal medullectomized 1-2 days prior to induction of shock. The adrenergic antagonists were: propranolol, a nonspecific .beta. blocker; phenoxybenzamine, a nonspecific .alpha. blocker; tiodazosin, a specific .alpha. 1 blocker; and yohimbine, a specific .alpha. 2 blocker. The .beta. receptors apparently do not play a major role in either the compensatory or decompensatory response. Specific blockade of the .alpha. 2 adrenoceptors accentuates decompensation by .apprx. 35%, while blockade of the .alpha. 1 adrenoreceptors may offer some degree of protection against the vascular decompensatory processes. Evidently, the extrasynaptic .alpha. 2 adrenoreceptors are better able to maintain the vascular compensatory effort than the .alpha. 1 adrenoreceptors.