These observations demonstrate that remote in vivo administration of GLN before cardiac I/R injury can improve post-I/R cardiac function. This effect may be mediated via improved myocardial metabolism and enhanced reduced glutathione content.
Three-dimensional imaging of mitral regurgitant jets is feasible in the majority of patients. This improved technique provides additional information to that obtained from the 2D examination. Particularly, in patients with paravalvular leaks 3D color flow Doppler provides information on the origin and the extent of the dehiscence, as well as insight into the jet direction. In addition, in patients with eccentric mitral regurgitation, this new modality overcomes the inherent limitations of 2D echo Doppler by depicting the full extent of the jet trajectory.
The left atrial appendage is one source of thromboemobolus. Complete occlusion of this appendage is required to sever communication with the left atrium; however, current ligation techniques can potentially leave residual communication. A novel technique of occluding the appendage has been developed using a bipolar device and radiofrequency energy. Twelve patients underwent an off-pump, epicardial Maze procedure using radiofrequency ablation. As an adjunct to the procedure, ligation of the left atrial appendage was completed using the LigaSure Xtd (Valleylab, Tyco Healthcare, Boulder, CO) with a modified application technique. Patients were followed to ensure sinus or paced rhythm. All twelve patients are in sinus or paced rhythm upon follow-up. Four patients required pacemakers for sick sinus syndrome. To date there have been no incidents of strokes, thromboembolic events, postoperative bleeding or deaths in all patients. Complete occlusion of the left atrial appendage is necessary to eliminate communication, which is accomplished by this radiofrequency, bipolar device. Extensive studies are necessary to verify the efficacy of this novel occluding technique.
We wanted to determine whether oxygen radicals open the mitochondrial ATP-dependent potassium channels (KATP) during an ischemic period to reduce cell death and oxidant stress. Chick embryonic cardiomyocytes were used. Cell viability was quantified with propidium iodide (5 µM), and free radicals was measured using 2′,7′-dichlorofluorescin diacetate. Preconditioning was produced by 10 min of simulated ischemia followed by 10 min of reoxygenation. Acetylcholine (1 mM), infused for 10 min instead of preconditioning, reduced cell death similarly (24 ± 5%, n = 7 and 18 ± 2%, n = 7, respectively, vs. controls, 49 ± 6%, n = 8). In control series, 60 min of simulated ischemia and 3 h of reoxygenation generated free radicals more than 300% above the baseline (ischemia: 3.63 ± 0.58, reoxygenation: 3.66 ± 0.47, n = 8). Preconditioning and acetylcholine markedly attenuated the oxidant stress during simulated ischemia (1.18 ± 0.41, n = 6 and 1.34 ± 0.60, n = 7 vs. controls 3.63 ± 0.58, n = 8) and re-oxygenation (1.23 ± 0.36, n = 6 and 1.50 ± 0.59, n = 7 vs. controls 3.66 ± 0.47, n = 8). The protection of acetylcholine was abolished with pretreatment with the antioxidant thiol reductant 2-mercaptopropionyl glycine and posttreatment with 5-hydroxydecanoate, a selective mitochondrial KATP channel antagonist (37 ± 7%, n = 7). These results demonstrate that oxygen radicals open mitochondrial KATP channels, which mediates the acetylcholine-induced preconditioning effect, and that stimulation of this signaling pathway attenuates oxidant stress.
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