Abstract

Triglycyl-lysine vasopressin (tGLVPP) is activated in the circulation when the N-triglycyl residue of the molecule is cleaved by endothelial peptidases, releasing lysine vasopressin. We compared the effect of an intravenous bolus dose of tGLV (20 micrograms/kg) with a constant infusion (2.75 mU/kg/min) of arginine and lysine vasopressin (Pitressin) in normal mongrel dogs. Portal pressure was artifactually increased by a constricting flow probe. Baseline values were similar in both groups; at the time of near-maximal reduction in portal pressure, both drugs equally reduced portal venous pressure (38 +/- 4 vs 39 +/- 4%), superior mesenteric arterial blood flow (40 +/- 8 vs 39 +/- 9%), portal venous flow (35 +/- 4 vs 40 +/- 5%), and heart rate (9 +/- 2 vs 11 +/- 7%. Cardiac output obtained 10-30 min after tGLVP administration was similar that of VP, and each drug reduced cardiac output significantly when compared with its own baseline (18 +/- 4 vs 21 +/- 7%). Mean arterial pressure increased similarly with both drugs (11 +/- 3 vs 11 +/- 3%). The only difference observed was the hepatic arterial flow response. While tGLVP increased HAF 34 +/- 11%, the physiologic autoregulatory response to a decrease in portal venous flow and pressure; vasopressin was associated with no such compensatory response (1 +/- 6%). Whether this advantage of tGLVP and its more prolonged reduction of portal venous pressure (mean 103 min) are beneficial in the clinical setting requires additional studies.

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