Abstract
The effect of epinephrine was studied in the rabbit liver perfused in situ under normothermic and hypothermic conditions. After 2 µg of epinephrine, perfusion flow rate increased within the first 20 seconds in normothermia; this flow response was delayed in hypothermia. The K concentration of the perfusate leaving the liver and the net rate of hepatic K output increased in response to epinephrine. These maxima were reached 30 seconds after 2 µg of epinephrine administration in both normothermia and hypothermia; with 20 µg of epinephrine the K response was more prolonged. The return of K to control levels was delayed in hypothermic experiments. Chloride concentration of the perfusate increased after epinephrine in the hypothermic liver. Administration of epinephrine in 20-µg doses produced an increase in perfusate pH, HCO3 and total CO2, concentrations; this may indicate either increased HCO3- output or increased CO2 output together with uptake of H ion (or its equivalent), or both. The rate of hepatic glucose output reached maximal values in an average of 3 minutes after epinephrine in normothermia, but was somewhat delayed in hypothermia.
Footnotes
- Accepted May 3, 1965.
- The Williams & Wilkins Comapny
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