Displacement of endogenous enterokinase into portal venous blood and bile following luminal perfusion of proximal small intestine in guinea pigs.

The displacement of endogenous enterokinase into portal venous blood or bile was studied in conscious guinea pigs both with the small intestine undisturbed and during gentle, intermittent luminal perfusion of a 25-cm segment of duodenum and proximal jejunum. Perfusates tested included water, 150 mM saline, 5% (v/v) ethanol, 0.2% (w/v) lysolecithin, and mixtures of ethanol and lysolecithin. Enterokinase activity was absent from portal venous blood of control guinea pigs with the intestine undisturbed but perfusion with luminal saline or water was consistently associated with substantial levels of active enterokinase in portal venous blood. Similar concentrations of enterokinase in portal blood were also detected in response to luminal ethanol and lysolecithin. The capacity of the normal liver rapidly to clear the enzyme from portal blood was demonstrated. Of the estimated total endogenous enterokinase displaced, 0.2-0.4% was recovered in catalytically active form from the pooled bile of luminally perfused but not control animals. The readiness with which enterokinase was displaced into the circulation in the absence of mucosal damage raises the unexpected possibility that the event may be physiological. Induced penetration of the mucosa and absorption of luminal components is clearly different from the release into portal venous blood of endogenous mucosal macromolecules.