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

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.