Cardiovascular adrenoreceptor function during compensatory and decompensatory hemorrhagic shock

Prior reports by Dr. Bond [1] 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 primary purpose of the present studies was to elucidate the roles of the alpha 1 and alpha 2 adrenoreceptors during initial compensatory and secondary decompensatory phases of hemorrhagic shock. 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: (1) propranolol, a nonspecific beta blocker; (2) phenoxybenzamine, a nonspecific alpha blocker; (3) tiodazosin, a specific alpha 1 blocker; and (4) yohimbine, a specific alpha 2 blocker. The results of these studies suggest that the beta receptors do not play a major role in either the compensatory or decompensatory response. Specific blockade of the alpha 2 adrenoreceptors accentuates decompensation by approximately 35%, while blockade of the alpha 1 adrenoreceptors may offer some degree of protection against the vascular decompensatory processes. These data support the conclusion that the extrasynaptic alpha 2 adrenoreceptors are better able to maintain the vascular compensatory effort than the alpha 1 adrenoreceptors.