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Articles by O. Ritter
Total Records ( 2 ) for O. Ritter
  N Burkard , T Williams , M Czolbe , N Blomer , F Panther , M Link , D Fraccarollo , J. D Widder , K Hu , H Han , U Hofmann , S Frantz , P Nordbeck , J Bulla , K Schuh and O. Ritter

We previously demonstrated that conditional overexpression of neuronal nitric oxide synthase (nNOS) inhibited L-type Ca2+ channels and decreased myocardial contractility. However, nNOS has multiple targets within the cardiac myocyte. We now hypothesize that nNOS overexpression is cardioprotective after ischemia/reperfusion because of inhibition of mitochondrial function and a reduction in reactive oxygen species generation.

Methods and Results—

Ischemia/reperfusion injury in wild-type mice resulted in nNOS accumulation in the mitochondria. Similarly, transgenic nNOS overexpression caused nNOS abundance in mitochondria. nNOS translocation into the mitochondria was dependent on heat shock protein 90. Ischemia/reperfusion experiments in isolated hearts showed a cardioprotective effect of nNOS overexpression. Infarct size in vivo was also significantly reduced. nNOS overexpression also caused a significant increase in mitochondrial nitrite levels accompanied by a decrease of cytochrome c oxidase activity. Accordingly, O2 consumption in isolated heart muscle strips was decreased in nNOS-overexpressing nNOS+/MHC-tTA+ mice already under resting conditions. Additionally, we found that the reactive oxygen species concentration was significantly decreased in hearts of nNOS-overexpressing nNOS+/MHC-tTA+ mice compared with noninduced nNOS+/MHC-tTA+ animals.


We demonstrated that conditional transgenic overexpression of nNOS resulted in myocardial protection after ischemia/reperfusion injury. Besides a reduction in reactive oxygen species generation, this might be caused by nitrite-mediated inhibition of mitochondrial function, which reduced myocardial oxygen consumption already under baseline conditions.

  P Nordbeck , W. R Bauer , F Fidler , M Warmuth , K. H Hiller , M Nahrendorf , M Maxfield , S Wurtz , W Geistert , J Broscheit , P. M Jakob and O. Ritter

Background— Cardiac MRI offers 3D real-time imaging with unsurpassed soft tissue contrast without x-ray exposure. To minimize safety concerns and imaging artifacts in MR-guided interventional electrophysiology (EP), we aimed at developing a setup including catheters for ablation therapy based on carbon technology.

Methods and Results— The setup, including a steerable carbon catheter, was tested for safety, image distortion, and feasibility of diagnostic EP studies and radiofrequency ablation at 1.5 T. MRI was performed in 3 different 1.5-T whole-body scanners using various receive coils and pulse sequences. To assess unintentional heating of the catheters by radiofrequency pulses of the MR scanner in vitro, a fluoroptic thermometry system was used to record heating at the catheter tip. Programmed stimulation and ablation therapy was performed in 8 pigs. There was no significant heating of the carbon catheters while using short, repetitive radiofrequency pulses from the MR system. Because there was no image distortion when using the carbon catheters, exact targeting of the lesion sites was possible. Both atrial and ventricular radiofrequency ablation procedures including atrioventricular node modulation were performed successfully in the scanner. Potential complications such as pericardial effusion after intentional perforation of the right ventricular free wall during ablation could be monitored in real time as well.

Conclusion— We describe a newly developed EP technology for interventional electrophysiology based on carbon catheters. The feasibility of this approach was demonstrated by safety testing and performing EP studies and ablation therapy with carbon catheters in the MRI environment.

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