ADRENAL-MEDULLARY COUNTERREGULATORY RESPONSE TO HYPOGLYCEMIA IN DOGS WITH HEPATIC CROSS PERFUSION

The present study was conducted to investigate adrenal medullary respo nses to cross perfusion of the liver in postabsorptive anesthetized do gs. The liver of the first dog (recipient) was perfused with vena cava l and aortic blood of the second dog (donor) through the portal vein a nd hepatic artery, respectively. Hepatic venous blood was returned to the donor through an intracaval double-lumen hepatic catheter placed i n the vena cava of the recipient. A portacaval shunt was made through the right femoral vein in the recipient. Upon the cross perfusion, nor moglycemic clamp in the recipient was started to compensate the loss o f hepatic glucose input into the systemic circulation. When the glucos e infusion was discontinued, aortic glucose level rapidly declined, wi thin 45 min, from 125.2 +/- 10.2 to 30.3 +/- 4.6 mg% (p < 0.05, n = 6) along with a similarly rapid decline of aortic insulin level. Inverse ly, both adrenal venous epinephrine and norepinephrine increased signi ficantly (163.2 +/- 88.0 vs. 794.9 +/- 55.7 ng/mL (p < 0.05) and 36.6 +/- 22.4 vs. 119.7 +/- 15.3 ng/mL (p < 0.05), respectively; n = 6) dur ing this hypoglycemic period. However, in the donor, glucose level did not change either in aortic or vena caval blood, indicating that the recipient's liver was perfused with normal blood glucose levels. In th e control group in which the normoglycemic clamp in the recipient was continued during the cross perfusion, both aortic glucose and adrenal venous catecholamines remained unchanged. The results indicate that th e hepatic cross perfusion caused a rapid and severe hypoglycemia, resu lting in a significant increase in adrenal medullary secretion, due mo st probably to the activation of central glucoreceptor-mediated mechan isms. This model may be useful for studying interactions between hepat ic and central glucoreceptors implicated in regulatory mechanisms of g lucose homeostasis.