永井 良三

三尖弁狭窄症(TS)を合併し,焼灼に難渋した房室結節回帰性頻拍の1例を経験した.解剖学的アプローチでコッホ三角部と考えられる部位の電位はすべていわゆるon the valve型であり,small A largeV型の電位はヒス東電位記録部位(HBE)から2mm以内でしか記録されず,スローポテンシャルは記録されなかった.3次元エレクトロアナトミカルマッピングシステム(CARTOTM)を用いて,HBEをマッピングし,解剖学的アプローチで冠静脈洞側から焼灼を開始したが,成功通電部位はHBEから3mmの点であり,この局所電位もon the valve型であった.右房右室間に拡張期に10mmHgの圧格差を認め,右房造影と経食道心エコーでTSを認めた.形態的に三尖弁輪の異常を伴い,ヒス束近傍での通電を要する症例ではCARTOTMは有用と考えられ報告した.

A novel murine model of aging (kl/kl mice) has been developed by in vivo mutagenesis. We analyzed endothelial function in this strain. Ring preparations of the thoracic aorta were obtained from 6- to 9-week old wild-type (+/+) and heterozygous (kl/+) klotho mice. The aortas of kl/+ mice showed an exaggerated contractile response to norepinephrine and attenuated vasodilator responses to acetylcholine and lecithinized superoxide dismutase (SOD) compared to +/+ mice. The response to sodium nitroprusside was unaltered in kl/+ mice. The contraction in response to norepinephrine was augmented by treatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-5) M) to a greater extent in +/+ mice than in kl/+ mice. Treatment with L-NAME abolished the vasodilator responses to both acetylcholine and lecithinized SOD. NO metabolites (NO2- and NO3-) and cGMP concentrations in the urine were significantly reduced in kl/+ mice compared to +/+ mice. However, the urinary excretion of 6-keto-prostaglandin F1alpha was unaltered. There was little immunostaining for NO synthase and vascular endothelial growth factor (VEGF) in the aorta of kl/+ mice. No immunostaining for NO synthase was noted in the aorta of kl/kl mice. The expression of the klotho gene product may have a role in the regulation of VEGF expression and is tightly linked to endothelial release of NO.