Failure of chronic transmyocardial laser revascularization to alter cardiac nociceptive reflexes: implications for the treatment of angina pectoris.
The aim of this study was to assess the delayed effects of transmyocardial laser revascularization (TMLR) on cardiac nociceptors. Experiments were performed in anesthetized dogs 1 month after thoracotomy with either TMLR (n = 17) or sham laser procedure (n = 17). All dogs underwent sinoaortic denervation and vagotomy to isolate the sympathetic afferent system. Left ventricular sympathetic afferents were stimulated by intracoronary bradykinin and transmural myocardial ischemia. Efferent responses were measured by direct recording of renal sympathetic nerve activity. Renal nerve responses to intracoronary bradykinin administered to the laser-treated anterior ventricular wall were not significantly different from those observed from the unlased posterior wall. Anterior transmural ischemia elicited similar renal nerve responses in laser-treated and sham groups. Pathologic analysis showed intact neural structures in the subepicardial regions both near and remote from the lased channels. We conclude that reflexes mediated by left ventricular sympathetic afferents are preserved after chronic TMLR. These findings do not support the neural hypothesis for angina relief.
Banerjee
Deepak D
DD
Department of Internal Medicine (Cardiology), Medical College of Virginia Campus of Virginia Commonwealth University, Richmond, VA 23249, USA.
Quinn
M Susan
MS
Mohanty
Laxmi B
LB
Minisi
Anthony J
AJ
D000787:Angina Pectoris / Q000628:therapy*; D000818:Animals; D002908:Chronic Disease; D004285:Dogs; D006321:Heart / Q000294:innervation* / Q000502:physiology; D006352:Heart Ventricles / Q000294:innervation*; D053685:Laser Therapy / Q000295:instrumentation / Q000379:methods*; D023421:Models, Animal; D017202:Myocardial Ischemia / Q000628:therapy; D009206:Myocardium; D009619:Nociceptors / Q000528:radiation effects*; D013564:Sympathetic Nervous System; D013908:Thoracotomy; D013997:Time Factors; D017211:Treatment Failure; D016276:Ventricular Function