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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 microgram.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 mmHg; 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 microgram.kg-1.min-1 adenosine dose) unblocked state; and 5.3 +/- 0.3 to 4.3 +/- 0.3 mm Hg (400 microgram.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.
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