Effects of S-Dobutamine on Venous Blood Return and Organ Nutrient Blood Flow

The selective contractile effects of s-dobutamine were studied in vitro in selected canine arteries and vein preparations; propranolol was included to block potential β-mediated vasodilation. These in vitro data were expanded by quantifying the in vivo effects of s-dobutamine on venous blood return and redistribution of regional nutrient blood flow (NBF) and nonnutrient blood flow (non-NBF) in anesthetized dogs. In in vitro studies with isolated canine arteries and veins, s-dobutamine exhibited vein-selective constriction. At maximally efficacious concentrations of agonist, contractions of carotid, coronary, and femoral arteries in response to s-dobutamine were only 7, 25 and 45% as great as those elicited by norepinephrine (NE). Similarly, in jugular vein, s-dobutamine-mediated contractions were 55% as great as those obtained in response to NE. Coronary and femoral arteries precontracted with NE were relaxed in a doserelated manner by increasing concentrations of s-dobutamine. Effects of NE and s-dobutamine on venous blood return (VR) were compared in dogs. s-Dobutamine increased VR by 49 ± 10 ml, whereas NE increased VR by 14 ± 6 ml during 5-min infusion. s-Dobutamine significantly increased coronary NBF in left ventricular (LV) endocardium from 115 ± 10 to 194 ± 13 and 263 ± 9 ml/min/100 g at doses of 10 and 20 µg/kg/min, respectively. In addition, LV epicardium flow was increased from 87 ± 8 to 189 ± 15 and 262 ± 11 ml/min/100 g at 10 and 20 µg/kg/min, respectively. Infusion of s-dobutamine increased NBF to heart and stomach, whereas flows to brain, kidney, liver, spleen, skeletal muscles, and skin were not affected. Arteriovenous (AV) shunting was decreased during s-dobutamine infusion. Maintenance of NBF suggests that precapillary sphincters were not affected by s-dobutamine