Effect of glucagon on hepatic lymph (tissue) PO2 after ligation of the hepatic artery: An experimental study

Charles L. Witte, Marlys H. Witte, Kathleen Kintner

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

In 17 greyhound dogs, hepatic oxygenation was examined after hepatic artery ligation (HAL) and subsequent administration of pharmacologic dosages of glucagon during various hemodynamic maneuvers at different per cents of oxygen in the inspired air. Measurements included arterial and portal pressure, PO2 and O2 content of arterial, portal and hepatic venous blood, and hepatic lymph (tissue) PO2. The following were observed: 1) an increase in FIO2 progressively raised hepatic lymph (tissue) PO2; 2) distal HAL decreased hepatic oxygenation; 3) a decrease in portal oxygen delivery by cross-clamping the superior mesenteric artery (X-SMA) aggravated hepatic deoxygenation induced by HAL; 4) with normovolemia and HAL, glucagon increased portal O2 delivery and hepatic venous blood O2 content, but either failed to raise hepatic lymph PO2 (FIO2 of 21% or 40%) or did so transiently (FIO2 — 100%); 5) with an FIO2 of 100%, induced hemorrhage or X-SMA in conjunction with HAL blocked a rise in hepatic lymph PO2 after glucagon. It is concluded that administration of glucagon after HAL increases hepatic O2 delivery via the portal system, but nonetheless has minimal overall effect on hepatic tissue PO2. Accordingly, use of this agent after HAL in patients is probably of limited practical value in raising hepatic tissue PO2.

Original languageEnglish (US)
Pages (from-to)27-33
Number of pages7
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume18
Issue number1
DOIs
StatePublished - Jan 1978

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine

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