Author + information
- Received September 22, 1993
- Revision received December 13, 1993
- Accepted December 17, 1993
- Published online May 1, 1994.
- James D. Rossen, MD, FACC∗,a,b,
- Helgi Oskarsson, MDa,b,
- Robert L. Minor Jr., MDa,b,
- Charlotte L. Talman, RN, MSNa,b and
- Michael D. Winniford, MD, FACCa,b
- ↵∗Address for correspondence: Dr. James D. Rossen, Department of Internal Medicine, 4212 RCP, The University of Iowa, Iowa City, Iowa 52242.
Objectives. This study was performed io assess the importance of adenosine in mediating metabolic coronary vasodilation during atrial pacing stress in humans.
Background. Numerous animal studies have examined the role of adenosine in the regulation of coronary blood flow, with inconsistent results.
Methods. The effect of the adenosine antagonist aminophylline (6 mg/kg body weight intravenously) on coronary functional hyperemia during rapid atrial pacing was determined in 12 patients. The extent of inhibition of adenosine vasodilation was assessed using graded intracoronary adenosine infusions before and after aminophylline administration in seven patients. Coronary blood flow changes were measured with a 3F intracoronary Doppler catheter.
Results. After aminophylline administration, the increase in coronary flow velocity during adenosine infusions was reduced from 84 ± 48% (mean ± SD) to 21 ± 31% above control values (p < 0.001) at 10 μg/min and from 130 ± 39% to 59 ± 51% above control values (p < 0.001) at 40 μg/min. During rapid atrial pacing under control conditions, coronary blood flow velocity increased by 26 ± 16%. The flow increment during paced tachycardia after aminophylline (23 ± 10%) was unchanged from the control value, despite substantial antagonism of adenosine coronary dilation by aminophylline.
Conclusions. These data suggest that adenosine does not play an important role in the regulation of coronary blood flow in response to rapid atrial pacing in humans.
☆ This study was supported in part by the National Heart, Lung, and Blood Institute Specialized Center of Research in Coronary and Vascular Diseases (HL 32295). National Institutes of Health, Bethesda, Maryland.
- Received September 22, 1993.
- Revision received December 13, 1993.
- Accepted December 17, 1993.