Supporting role of the adrenal cortex in the induction of hyperfibrinogenemia

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Abstract
In male albino rats plasma fibrinogen levels increased within 24 hr. after single injections of epinephrine, norepinephrine, or histamine. Eight hr. of intermittent electroshock induced hyperfibrinogenemia within 16 hr. after the last shock; each shock produced generalized skeletal muscle contractions of short duration, but no gross signs of tissue damage were noted. Hyperfibrinogenemia did not occur within 24 hr. after injection of large doses of corticosterone, dexamethasone or ACTH; nor did dexamethasone modify the response to epinephrine when the 2 drugs were given concurrently. Rats pretreated with sufficient ACTH to induce a 17% increase in adrenal weight were not different from control animals in their hyperfibrinogenemic response to electroshock stress, histamine, or epinephrine. In another experiment rats were adrenalectomized and maintained on 0.9% NaCl as drinking water for 14 days. Plasma fibrinogen concentrations in these rats were essentially the same as in sham-operated animals, but the hyperfibrinogenemic response to epinephrine was significantly lower following adrenalectomy. In adrenalectomized rats given replacement injections of corticosterone the response was no different from that of sham-operated rats. Hyperfibrinogenemia induced by stress is not directly caused by hyper-secretion of the adrenal cortex, but by another mechanism which depends upon "supporting" or "permissive" levels of circulating adrenal corticoids.