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Abstract
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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References
- General presence of glucocorticoid receptors in mammalian tissues.Endocrinology. 1974; 94: 998
- Glucocorticoid regulation of ACTH sensitivity of adenyl cyclase in rat fat cell membranes.in: Proc Natl Acad Sci USA. 66. 1970: 995
- Study of conditions and mechanism of the diphenylamine reaction for the colorimetric estimation of DNA.Biochem J. 1956; 62: 315
- Corticosteroids as effective vasodilators in the treatment of low output syndrome.Chest. 1970; 57: 440
- Interraction of glucocorticoids with glucagon and epinephrine in the control of gluconeogenesis and glycogenolysis in liver and lipolysis in adipose tissue.J Biol Chem. 1972; 247: 3579
- Role of lysosomes in the pathogenesis of splanchnic ischemic shock in cats.Circ Res. 1972; 27: 783
- Formation and release of a hormone agonist by rat adipocyctes.J Biol Chem. 1971; 246: 6822
- Adenyl cyclase response in bowel obstruction.J Surg Res. 1976; 25: 335
- Stimulation of leucocyte adenyl cyclase by hydrocortisone and isoprotorenol in asthmatic and non-asthmatic subjects.J Allergy Clin Immunol. 1972; 50: 45
- Cyclic AMP response to epinephrine and shock.Arch Surg. 1975; 110: 316
- Cyclic AMP.Academic Press, Inc, New York1971
- Adenosine-3′, 5′-monophosphate metabolism in the liver in experimental hemorrhagic shock.Surgery. 1973; 74: 660
- Permissive role of glucocorticoids in hepatic carbohydrate metabolism.Biochem Biophys Acta. 1969; 192: 292
- Steroids in the treatment of clinical septic shock.Ann Surg. 1976; 184: 333
- Mechanism of action of glucocorticoids.Metabolism. 1974; 23: 159
Article info
Footnotes
☆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.
Identification
Copyright
© 1977 Published by Elsevier Inc.
