Adenosine increases total venous capacitance in awake instrumented rats

To determine the effect of adenosine on the venous system, mean circulatory filling pressure (MCFP) was determined during infusion of intravenous (i.v.) adenosine (66.5 to a maximum of 532 μg · kg^-1 · min^{- 1}) in 9 awake instrumented rats before and during ganglionic blockade with i.v. hexamethonium, 0.6 mg · kg^-1 · min^-1. MCFP, the equilibrated pressure (mm Hg) occurring when the circulation is arrested by transient inflation of a balloon in the right atrium, is inversely related to total venous capacitance. Both adenosine and hexamethonium caused a reduction in mean arterial pressure (MAP); heart rate (HR) decreased during adenosine infusion in the blocked, but not the unblocked, state. In the unblocked state, baseline MCFP was 6.5 ± 0.3 mm Hg; hexamethonium caused baseline MCFP to decrease to 5.3 ± 0.3 mm Hg. In both the unblocked and the blocked state, adenosine caused a dose-related decrease in MCFP [6.5 ± 0.3 to 5.5 ± 0.6 mm Hg (532 μg · kg^-1 · min^-1 adenosine dose) unblocked state; and 5.3 ± 0.3 to 4.3 ± 0.3 mm Hg (400 μg · kg^-1 · min^-1 adenosine dose) blocked state]. This decrease in MCFP induced by adenosine was highly significant. Intravenous adenosine, in an awake instrumented rat model, increases venous capacitance, with and without ganglionic blockade.