• C Appleton, M Olajos, E Morkin, and S Goldman.
• J. Pharmacol. Exp. Ther. 1985 Jun 1;233(3):729-34.

AbstractTo study alpha adrenergic control of the venous circulation, 17 dogs were lightly sedated and instrumented with thermodilution pulmonary flow and aortic catheters. Hemodynamics, cardiac output and central blood volume were measured at rest. Mean circulatory filling pressure, pressure gradient for venous return and resistance to venous return were calculated from pressures obtained during transient acetylcholine-induced circulatory arrest. Phenylephrine was then infused at two steady-state levels to increase mean aortic pressure by 50 and 100% above control values. Heart rate was controlled with atropine. Phenylephrine increased (P less than .025) mean aortic pressure from 80.7 +/- 2.9 to 121.3 +/- 7.6 to 164.7 +/- 6.1 mm Hg and systemic vascular resistance from 23.3 +/- 2.0 to 32.2 +/- 3.5 to 43.5 +/- 4.1 mm Hg/min/ml and did not change cardiac output (161.9 +/- 12.6-175.6 +/- 13.8-169.6 +/- 11.9 ml/min/kg). Mean circulatory filling pressure increased from 7.1 +/- 0.5 to 9.7 +/- 0.6 to 13.2 +/- 1.3 mm Hg (P less than .025). Pressure gradient for venous return increased from 6.4 +/- 0.4 to 7.7 +/- 0.4 to 8.9 +/- 0.4 mm Hg (P less than .025). Central blood volume increased from 16.2 +/- 0.9 to 19.4 +/- 1.4 to 22.0 +/- 1.9 ml/kg (P less than .025). To eliminate reflex changes in vascular tone, eight dogs received ganglionic blockade with trimethaphan. After ganglionic blockade phenylephrine increased cardiac output, systemic vascular resistance, mean circulatory filling pressure, pressure gradient for venous return and central blood volume (P less than .025). Thus, in conscious dogs, phenylephrine reduces peripheral vascular capacitance and shifts blood from the venous circulation to the central and arterial vascular compartments.

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