Effects of Distension of Urinary Bladder on Coronary Conduit and Resistance Vessels in Hyperlipidemic Patients

BACKGROUND: Distension of the urinary bladder reflexly causes a change of coronary vasomotor response. The effect of such distension on the coronary circulation in hyperlipidemic patients, a condition with impaired endothelial function, remains unknown. HYPOTHESIS: We tested the hypothesis whether urinary bladder distension caused an exaggerated vasomotor response of epicardial and resistance vasoconstriction in hyperlipidemic patients. METHODS: Thirty patients with early atherosclerosis (< 50% diameter stenosis) were divided into three groups: Group 1 (n = 10): hyperlipidemia without doxazosin administration; Group 2 (n= 10): hyperlipidemia with pretreatment of alpha1-adrenergic receptor blocker (oral doxazosin 2 mg); and Group 3 (n = 10) : normolipidemia. A prospective analysis of the results of quantitative angiograms, intracoronary Doppler flow, and lactate concentrations from aortic root and coronary sinus was performed during distension of urinary bladder. RESULTS: Bladder distension significantly decre= 10): hyperlipidemia with pretreatment of alpha1- adrenergicreceptor blocker ( oral doxazosin 2 mg); and Group 3 (n = 10): normolipidemia. A prospective analysis of the results of quantitative angiograms, intracoronary Doppler flow, and lactate concentrations from aortic root and coronary sinus was performed during distension of urinary bladder. RESULTS: Bladder distension significantly decreased coronary diameter at the stenotic segments (p = 0. 004), coronary blood flow ( p = 0.05), and increased coronary resistance ( p = 0.006) compared with baseline values, in Group 1 patients. In Group 2 patients during bladder distension, coronary diameter, coronary blood flow , and coronary resistance showed no significant changes compared with baseline values. There were significant differences of stenotic coronary diameter ( p = 0.01) between Groups 1 and 3 during bladder distension despite similar changes in rate- pressure product. No significant differences were noted among the groups in the responses of coronary diametercoronary blood flow, and coronary resistance after nitroglycerin administration. CONCLUSIONS: The present study showed that urinary bladder distension caused an abnormal vasomotor response of epicardial vasoconstriction and that a concomitant increased coronary resistance involved mechanisms related to alpha1- adrenoceptors. Hyperlipidemia may further impair the response. Pretreated administration of doxazosin had reversed the changes toward baseline. Vasoconstriction during bladder distension can be relieved after nitroglycerin administration, suggesting an unchanged responsiveness of vascular smooth muscle cells to such distension.