Chest
Volume 107, Issue 1, January 1995, Pages 54-57
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Clinical Investigations: Cardiology: Articles
Comparative Acute Effects of Adenosine and Prostacyclin in Primary Pulmonary Hypertension

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Vasodilators have been a main focus of therapy for primary pulmonary hypertension. Adenosine and prostacyclin have been shown to reduce pulmonary vascular resistance acutely in these patients. In order to compare the acute hemodynamic effects of adenosine and prostacyclin, ten patients with severe primary pulmonary hypertension, unresponsive to medical therapy, were studied. After baseline hemodynamics were obtained, an adenosine infusion, 50 to 100 ng/kg/min, was begun and titrated to the maximum tolerated dose. Hemodynamics were allowed to return to baseline, and thereafter, a prostacyclin infusion was begun at 2 ng/kg/min, and titrated to the maximum tolerated dose. Overall, adenosine (200±53 ng/kg/min) produced a 33±18% (p<0.001) fall in pulmonary vascular resistance and a 52±25% (p<0.001) increase in cardiac output with no effect on pulmonary or systemic arterial pressures. Prostacyclin (8±4 ng/kg/min) caused a 22±18% (p<0.01) fall in pulmonary vascular resistance and a 25±26% (p<0.05) increase in cardiac output with a 14±6% (p<0.001) decrease in systemic arterial pressure, but no change in pulmonary arterial pressure. The effects of adenosine and prostacyclin on pulmonary vascular resistance were similar (r=0.70, r2=0.49, p=0.02). Adenosine and prostacyclin have similar hemodynamic effects acutely in primary pulmonary hypertension. Adenosine may be useful as a test of the potential for long-term prostacyclin therapy in patients with primary pulmonary hypertension.

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Study Patients

Ten patients with primary pulmonary hypertension referred to the University of Illinois were entered into this study (nine female, one male; mean age 43±15 years). All patients were evaluated by clinical history, physical examination, chest radiography, lung scan, pulmonary function testing, echocardiography, and cardiac catheterization. Their conditions were diagnosed based on the criteria used in the National Institute of Health Registry on primary pulmonary hypertension.6 Patients were also

Responses to Adenosine

Overall there was a 33±18% (p<0.001) fall in pulmonary vascular resistance (from 13 U to 9 U) and a 52±25% (p<0.001) increase in cardiac output (from 3.5 L/min to 5.4 L/min) in response to adenosine, with no significant change in mean pulmonary, systemic arterial, or pulmonary capillary wedge pressures (Fig 1). There was, however, a 35±23% (p<0.01) fall in systemic vascular resistance (from 23 to 14 U) with slight but significant increases in right atrial pressure (from 10 mm Hg to 14 mm Hg,

Mechanism of Adenosine

Adenosine is a purine nucleoside with potent coronary and systemic vasodilatory effects.7 These effects are mediated by specific cell membrane receptors (A1 and A2) that are coupled to the adenylate cyclase system via G-proteins.8, 9 Vasodilatory effects are thought to be mediated by activation of subtype A2, which results in increased intracellular cAMP. Several effects of adenosine have also been found to be independent of cAMP, including activation of K+ channels following activation of

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Supported in part by the Department of Veterans Affairs (Office of Research ana Development, Medical Research Service) and by Burrough Wellcome Co.

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