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Several photosensitisers are known to accumulate selectively in atheromas, regardless of the size of the involved artery. The new photosensitizer, mono-L-aspartyl chlorin e6 (NPe6), specifically accumulates in the atheroma. In the presence of NPe6, the atheroma could be recognized by detecting the specific fluorescence spectrum of NPe6 using a spectrophotometer. We developed a spectrum analysis system and reported that the fluorescence spectra of NPe6 emitted from atherosclerotic plaques on the descending thoracic aorta were recognized by this analysis system with an angioscopic approach in the animal model of atherosclerosis. We also detected the fluorescence spectrum peak at 675 nm of NPe6 laparoscopically only in parts of the abdominal aorta with an atheroma. This spectrum analysis system is useful to recognize the atheroma, but not to recognize the atherosclerotic lesions of the artery as a whole. So, we developed a fluorescence endoscope. Using the endoscopic analysis system, atheromas on the carotid artery were visualized as reddish spots from inside and outside the artery. Then we developed an epifluorescence stereoscope system, and using this device we visualized small coronary atherosclerosis specifically at the beating heart surface. We extensively examined the effects of photodynamic therapy with NPe6 on the atheroma. We studied the change in the lipid components of the atheroma using Fourier transform infrared (FTIR) microspectroscopy. FTIR microspectroscopic analysis showed a dissociation of ester bonds of cholesterol esters in the atheroma after photodynamic therapy. The framework of the atheroma and the lipids accumulated in the atheroma were destroyed. We also evaluated the change in the elastic framework in the atheroma using scanning electron microscopy. The destruction of the architecture of the elastic fiber network in the atheroma was revealed.
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