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1 Departments of Physiology and Biophysias, Pharmacology and Surgery, University of Oklahoma Medical Center, Oklahoma City, Oklahoma
Previous investigations have suggested that admin-istration of cardiac glycosides to the normal dog results in sequestration of blood in the splanchnic bed, which diminishes the venous return and cardiac output. The aim of this study was to evaluate and quantify splanchnic hemodynamic changes caused by administration of ouabain. The dogs were anesthetized with chioralose (50 mg kg-1) and urethane (550 mg kg-1). Direct measurements of mesenteric artery and splenic artery blood flow were obtained with electromagnetic blood flow transducers, systemic arterial and portal venous pressures with strain-gauge transducers, intestinal and splenic weight changes with a strain-gauge weighing device, and liver blood volume with I181-albumin injection and punch biopsies. These parameters were monitored before and after injection of ouabain (50 µg kg-1). We found the following responses to ouabain: 1) significant increases in systemic arterial pressure and calculated splenic and mesenteric vascular resistances and 2) no significant changes in portal venous pressure, splenic or mesenteric blood flow, organ weights or liver blood volume. From these findings, we conclude that there is no evidence for splanchnic congestion with therapeutic doses of ouabain and that the major splanchnic vascular event induced by ouabain is arteriolar vasoconstriction.
Submitted on March 19, 1969