Cardiac nociceptive reflexes after transmyocardial laser revascularization: Implications for the neural hypothesis of angina relief

Objective: The mechanism by which transmyocardial laser revascularization r elieves angina is not understood. One theory is that laser-induced thermal damage to cardiac nerves results in cardiac denervation. This study examine d the acute effects of transmyocardial laser revascularization on reflex re sponses mediated by cardiac nociceptors, the left ventricular receptors wit h sympathetic afferent Fibers that are thought to mediate anginal chest pai n. Methods: Experiments were performed in 13 chloralose-anesthetized dogs with sinoaortic denervation and vagotomy. Left ventricular receptors with sympa thetic afferent fibers were activated by epicardial and intracoronary brady kinin before and 45 minutes after transmyocardial laser revascularization. Reflex responses elicited by bradykinin were quantitated by direct recordin g of efferent renal sympathetic nerve activity. Transmyocardial laser revas cularization was performed in the open-chest model with a hand-held holmium : YAG laser (2.1-mum wavelength). Results: An average of 44.5 +/- 1.0 channels were created. Before transmyoc ardial laser revascularization, reflex increases in renal sympathetic nerve activity were elicited by both epicardial and intracoronary bradykinin, Af ter transmyocardial laser revascularization, there was no significant atten uation in the reflex responses to either epicardial (before, 66% +/- 8%; af ter, 100% +/- 24%; P =.19) or intracoronary (before, 124% +/- 37%; after, 1 08% +/- 25%; P =.44) bradykinin. Conclusions: Transmyocardial laser revascularization has no significant sho rt-term effect on reflexes mediated by left ventricular receptors with symp athetic afferent fibers in anesthetized dogs. These results indicate that t ransmyocardial laser revascularization does not acutely interrupt the affer ent nerves, which are believed to transmit the perception of anginal pain.