Activation and release of proteolytic kinin-forming enzymes from rat jejunal loops perfused with hyperosmolar glucose solutions.
Loops of rat jejunum were perfused in vivo for one hour with de Jalon solutions of increasing glucose concentration. The esterolytic activity of the perfusate and of the extracted loop was measured using benzoyl arginine ethyl ester (BAEe) as substrate. The enzymes lactate dehydrogenase, isocitrate dehydrogenase, and acid phosphatase were measured in the perfusate to estimate the degree of cellular damage. There was a significant depletion of kallikrein from the intestine and a raised level in the perfusate during the hyperosmolar perfusions. No significant difference in the kallikrein levels was observed between the normal jejunum and the iso-osmolar perfused jejunum. Prolonged contact with hyperosmolar solutions caused some cellular damage but this effect appeared to be distinct from the release of kallikrein, which occurred very rapidly during the first 20 minutes. These results confirm that hyperosmolar intestinal contents result in the release of kinin-forming proteolytic enzymes into the circulation and suggest that this mechanism is involved in the syndrome of vasomotor dumping after gastric surgery.
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives; D002470:Cell Survival; D004789:Enzyme Activation; D005947:Glucose / Q000494:pharmacology*; D007413:Intestinal Mucosa / Q000201:enzymology / Q000378:metabolism*; D007583:Jejunum / Q000201:enzymology / Q000378:metabolism*; D007610:Kallikreins / Q000378:metabolism*; D009994:Osmolar Concentration; D010447:Peptide Hydrolases / Q000378:metabolism; D010477:Perfusion; D051381:Rats
D001120:Arginine; C009727:benzoylarginine ethyl ester; D010447:Peptide Hydrolases; D007610:Kallikreins; D005947:Glucose