CAJ | 학술논문

四氢生物蝶呤缺乏可导致一氧化氮合酶脱偶联、氧自由基生成增多。在氧化应激过程中，氧自由基产生增强并且其防御机制发生改变，通过促进心肌细胞凋亡、心肌肥厚和纤维化，使心肌重构、内皮功能障碍、炎症及血管重构，最终导致心脏舒张功能发生损害。氧化应激可降低四氢生物蝶呤的生物利用度，给予外源性的四氢生物蝶呤对心室舒张功能障碍有明显的治疗作用。该文就四氢生物蝶呤在左心室舒张功能障碍中的作用予以综述。
사경생물접령결핍가도치일양화담합매탈우련、양자유기생성증다。재양화응격과정중，양자유기산생증강병차기방어궤제발생개변，통과촉진심기세포조망、심기비후화섬유화，사심기중구、내피공능장애、염증급혈관중구，최종도치심장서장공능발생손해。양화응격가강저사경생물접령적생물이용도，급여외원성적사경생물접령대심실서장공능장애유명현적치료작용。해문취사경생물접령재좌심실서장공능장애중적작용여이종술。
Tetrahydrobiopterin depletion leads to nitric oxide synthase uncoupling ,and increased forma-tion of reactive oxygen species.During the oxidative stress, oxygen free radicals production is increased and its defense mechanism is changed, and through the promotion of myocardial cell apoptosis,myocardial hyper-trophy and fibrosis, myocardial remodeling, endothelial dysfunction, inflammation and vascular remodeling, eventually leads to cardiac diastolic function damage .The oxidative stress impaires the bioavailability of tetra-hydrobiopterin, therefore exogenous tetrahydrobiopterin treatment has obvious effect on the ventricular dias-tolic dysfunction.Here is to make a review of the progress of tetrahydrobiopterin in the treatment of left ven-tricular diastolic dysfunction .