Chest
Clinical Investigations: Cardiology: ArticlesComparative Acute Effects of Adenosine and Prostacyclin in Primary Pulmonary Hypertension
Section snippets
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.