Author + information
- Received December 3, 1985
- Revision received April 30, 1986
- Accepted May 14, 1986
- Published online November 1, 1986.
- Eric R. Powers, MD, FACC*,1,
- Kenneth S. Bannerman, MD, FACC1,
- Ingrid Fitz-James, MD1 and
- Paul J. Cannon, MD, FACC1
- ↵*Address for reprints: Eric R. Powers, MD, Columbia University, College of Physicians and Surgeons, 630 West 168 Street, New York, New York 10032.
This study was designed to examine the effect of increases in the partial pressure of carbon dioxide (Pco2) in coronary artery blood on coronary blood flow, coronary reactive hyperemia and the coronary response to intra-coronary adenosine administration. The left anterior descending coronary artery was cannulated and perfused over a wide range of perfusion pressure (P) and flow (F) with blood equilibrated with 0 to 40% carbon dioxide in 16 open chest dogs. Increases in coronary artery Pco2from 20 ± 2 to 93 ± 8 to 211 ± 22 mm Hg (mean ± SEM) increased the coronary flow from 28 ± 3 to 68 ± 16 to 87 ± 22 ml/min, respectively, at a perfusion pressure of 60 mm Hg and from 49 ± 6 to 139 ± 30 to 206 ± 48 ml/min, respectively, at a perfusion pressure of 100 mm Hg.
Coronary reactive hyperemia following a 30 second coronary perfusion line occlusion and the response to an intracoronary bolus of adenosine (60 μg) were prominent at a low Pco2but absent at a high Pco2. Beta-adrenergic blockade did not abolish the increase in coronary flow that occurred at increased Pco2. Thus, progressive elevations of regional coronary Pco2produced substantial increases in coronary blood flow and maximal or near maximal coronary vasodilation.
- Received December 3, 1985.
- Revision received April 30, 1986.
- Accepted May 14, 1986.
- American College of Cardiology Foundation