ALTERED RESISTIVE VESSEL FUNCTION AFTER CORONARY ANGIOPLASTY IS NOT DUE TO REDUCED PRODUCTION OF NITRIC-OXIDE

Background: The coronary vasodilator reserve with dipyridamole may be impaired immediately after successful angioplasty due to reduced endot helial production or release of nitric oxide. As the vasodilator respo nse to exogenous nitrates is enhanced by endothelium removal or inhibi tion of nitric oxide synthesis, an increased vasodilator response to n itrovasodilators, such as nitroprusside, should occur. Methods: The co ronary vasodilator reserve (maximal/basal coronary blood flow) with in travenous dipyridamole (0.56 mg/min for 4 min) was measured by Doppler catheterization before and after angioplasty in 10 patients with sing le-vessel coronary disease. At peak dipyridamole effect, incremental d oses of nitroprusside (4-50 mu g/min) were given intracoronary until s ystolic blood pressure fell by greater than or equal to 5 mmHg. Result s: Before angioplasty, the coronary blood flow increased from 19.7+/-6 .1 (mean+/-s.d.) at basal to 30.1+/-11.9 ml/min at the peak dipyridamo le effect (P <0.01), giving a coronary vasodilator reserve of 1.62+/-0 .39 (range 1.20-1.96). After angioplasty, the coronary blood flow incr eased from 32.4+/-13.2 at basal to 53.4+/-23.3 ml/min at the peak dipy ridamole effect (P <0.01), giving a coronary vasodilator reserve of 1. 77+/-0.64 (range 1.17-2.42). Sodium nitroprusside had no additional ef fect on coronary flow (49.5+/-20.4 and 52.2+/-18.0 ml/min) before and after a fall in systolic blood pressure, respectively. Conclusions: Th e vasodilator response to dipyridamole was markedly impaired immediate ly after successful angioplasty, and was not augmented by intracoronar y nitroprusside. Thus, a reduced production or release of nitric oxide in the coronary circulation does not seem to be responsible for the i mpaired vasodilator response after angioplasty.