Abstract

We previously demonstrated that transmural laser channels made after coronary occlusion did not acutely enhance blood flow or reduce infarct size. In contrast, other studies (which did not measure blood flow) reported increased survival and/or reduction of necrosis when laser channels were made prior to coronary occlusion. To reconcile this apparent paradox, we speculated that laser channels made prior to occlusion might protect the heart via a mechanism independent of blood flow. To test this hypothesis, we randomized 12 rats to either; (1) control: 1 hour of coronary artery occlusion followed by 5 hours of reperiusion. or (2) laser: 6 non-transmural channels were made in the anterior wall of the left ventricle using a holmium:YAG laser coupled to a 400 micron diameter optic fiber. Two minutes after the last channel was made, the left coronary artery was occluded for 1 hour and then reperiused for 5 hours. We monitored lead I of the ECG and noted the incidence of ventricular tachycardia (VT) and fibrillation (VF). At the end of the protocol. the artery was briefly reoccluded and we determined the area at risk (AR) by injection of pigment into the circulation. Heart slices were incubated in triphenyltetrazolium chloride solution to delineate the area of necrosis (AN), which was expressed as a percent of area at risk (AN/AR). [data given as mean ± SEM]Empty CellARAN/ARVT/vFControl49 ± 361 ± 95Laser45 ± 535 ± 4*0**p < 0.03 versus control p < 0.03 versus control Although laser channels were associated with thermally-induced necrosis, total infarct size was smaller in laser-treated hearts. Protection of muscle was most prominent in heart slices containing laser channels. but also occurred in slices without channels. Laser treatment also significantly reduced the incidence of VT and VF. In conclusion, non-transmural laser channels “preconditioned” the heart against subsequent ischemia. Although the mechanism of protection is unknown, it cannot be attributed to increased blood flow to the tissue because the channels did not connect to the ventricular cavity.

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