Comparison of vasopressin and triglycyl-lysine vasopressin on splanchnic and systemic hemodynamics in dogs

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Abstract
Triglycyl-lysine vasopressin (tGLVP) is activated in the circulation when theN-triglycyl residue of the molecule is cleaved by endothelial peptidases, releasing lysine vasopressin. We compared the effect of an intravenous bolus dose of tGLVP (20 μg/kg) with a constant infusion (2.75 mU/kg/min) of arginine and lysine vasopressin (PitressinR) 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 to 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.