Transmyocardial laser treatment destroys cardiac nerve fibers, which may contribute to the reduced angina pectoris seen clinically.

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Spinal cord ischemia in rabbits induces morphological and biochemical changes suggestive of apoptosis. These data raise the possibility that apoptosis contributes to neuronal cell death after spinal cord ischemia.

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The results suggest that both N-methyl-D-aspartate receptor-mediated excitotoxicity and apoptosis contribute to spinal cord neuronal death after ischemia and that pharmacologic treatments directed at blocking both of these processes may have therapeutic utility in reducing spinal cord ischemic injury.

Background and Purpose-Spinal cord ischemia is a serious complication of surgery of the aorta. NMDA receptor activation secondary to ischemia-induced release of glutamate is a major mechanism of neuronal death in gray matter. White matter injury after ischemia results in long-tract dysfunction and disability. The AMPA/kainate receptor mechanism has recently been implicated in white matter injury. Methods-We studied the effects of AMPA/kainate receptor blockade on ischemic white matter injury in a rat model of spinal cord ischemia. Results-Intrathecal administration of an AMPA/kainate antagonist, 6-nitro-7-sulfamoyl-(f)-quinoxaline-2,3-dione (NBQX), 1 hour before ischemia reduced locomotor deficit, based on the Basso-Beattie-Bresnahan scale (0ϭtotal paralysis; 21ϭnormal) (sham: 21Ϯ0, nϭ3; saline: 3.7Ϯ4.5, nϭ7; NBQX: 12.7Ϯ7.0, nϭ7, PϽ0.05) 6 weeks after ischemia. Gray matter damage and neuronal loss in the ventral horn were evident after ischemia, but no difference was noted between the saline and NBQX groups. The extent of white matter injury was quantitatively assessed, based on axonal counts, and was significantly less in the NBQX as compared with the saline group in the ventral (sham: 1063Ϯ44/200ϫ200 m, nϭ3; saline: 556Ϯ104, nϭ7; NBQX: 883Ϯ103, nϭ7), ventrolateral (sham: 1060Ϯ135, nϭ3; saline: 411Ϯ66, nϭ7; NBQX: 676Ϯ122, nϭ7), and corticospinal tract (sham: 3391Ϯ219, nϭ3; saline: 318Ϯ23, nϭ7; NBQX: 588Ϯ103, nϭ7) in the white matter on day 42. Conclusions-Results indicate severe white matter injury in the spinal cord after transient ischemia. NBQX, an AMPA/kainate receptor antagonist, reduced ischemia-induced white matter injury and improved locomotor function.

The combination of aortic arch occlusion with induced hypovolemia resulted in a reproducible model of SCII in rats.

Transventricular laser treatment of hypoperfused myocardium decreased left ventricular contractility in the acute phase, possibly due to development of perichannel hematomas and disruption of the wall architecture. In addition, TvL did not alter the regional myocardial oxygen supply/demand balance. These results call for caution in the treatment of patients with coronary artery disease by transventricular Ho-YAG laser when there is significant impairment of the left ventricular contractile function.