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Hepatic and intestinal adenyl cyclase activity were measured after a single pulse injection of epinephrine or glucagon into normal dogs and into dogs subjected to hemorrhagic shock. The results indicated that hemorrhagic shock abolishes the increase in adenyl cyclase activity seen in normal animals following epinephrine and significantly reduces that induced by glucagon. These changes are reflected in the glucose production from the liver induced by these hormones. The response of adenyl cyclase to the in vitro addition of epinephrine or glucagon, as well as the nonspecific stimulator of adenyl cyclase, sodium fluoride, showed that it is the receptor site of the enzyme which is affected primarily by shock. The treatment of dogs with 30 mg/kg of methylprednisolone following the reinfusion of shed blood significantly improved the response of adenyl cyclase to epinephrine in both liver and intestine, and this improvement was reflected in the glucose production by the liver in response to the hormone.
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☆Supported by the John A. Hartford Foundation.
☆☆Presented at the Thirty-fourth Annual Meeting of the Central Surgical Association, Buffalo, N. Y., March 3–5, 1977.
© 1977 Published by Elsevier Inc.