中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2009年
4期
276-279
,共4页
马逸%陈斌%胡剑麟%王鸿祥%韩银发%王益鑫%黄翼然
馬逸%陳斌%鬍劍麟%王鴻祥%韓銀髮%王益鑫%黃翼然
마일%진빈%호검린%왕홍상%한은발%왕익흠%황익연
阳萎%磷酸二酯酶抑制剂%白膜%弹力纤维
暘萎%燐痠二酯酶抑製劑%白膜%彈力纖維
양위%린산이지매억제제%백막%탄력섬유
Impotence%Phosphodiesterase inhibitors%Tunica albuginea%Elastic fibers
目的 观察高脂、高胆固醇饮食诱导勃起功能障碍(ED)大鼠阴茎白膜的变化,明确长期小剂量给予5型磷酸二酯酶抑制剂(PDE-5Ⅰ)他达拉非后的治疗作用,研究白膜组织在阴茎正常勃起过程中的作用及其意义.方法 30只2月龄雄性SD大鼠随机分成3组,每组10只.对照组:喂以正常饮食16周;高脂组:喂以高脂、高胆固醇饮食(正常饮食中加入2%胆固醇+10%猪油)16周;治疗组:在喂以高脂、高胆固醇饮食16周的基础上,从第13周起给予他达拉非2 mg·kg-1·d-1灌胃1个月.各组大鼠经血脂测定后,测定海绵体内压及平均动脉压比值(ICP/MAP)以评估阴茎勃起功能,运用维多利亚蓝-丽春红对阴茎白膜弹力纤维染色,最后对标本进行显微镜图像分析.结果 高脂组勃起功能(ICP/MAP:0.49±0.05)明显低于对照组(0.82±0.06,P<0.01);治疗组大鼠勃起能力(ICP/MAP:0.60±0.02)高于高脂组(P<0.05).高脂组白膜弹力纤维(468±152)明显低于对照组(3292±1123,P<0.01),治疗组白膜弹力纤维(2062±560)高于高脂组(P<0.05).结论 高脂、高胆固醇饮食可诱导大鼠发生ED,大鼠阴茎白膜弹力纤维减少是导致ED的机制之一,PDE-51可以在一定程度上逆转这种变化.
目的 觀察高脂、高膽固醇飲食誘導勃起功能障礙(ED)大鼠陰莖白膜的變化,明確長期小劑量給予5型燐痠二酯酶抑製劑(PDE-5Ⅰ)他達拉非後的治療作用,研究白膜組織在陰莖正常勃起過程中的作用及其意義.方法 30隻2月齡雄性SD大鼠隨機分成3組,每組10隻.對照組:餵以正常飲食16週;高脂組:餵以高脂、高膽固醇飲食(正常飲食中加入2%膽固醇+10%豬油)16週;治療組:在餵以高脂、高膽固醇飲食16週的基礎上,從第13週起給予他達拉非2 mg·kg-1·d-1灌胃1箇月.各組大鼠經血脂測定後,測定海綿體內壓及平均動脈壓比值(ICP/MAP)以評估陰莖勃起功能,運用維多利亞藍-麗春紅對陰莖白膜彈力纖維染色,最後對標本進行顯微鏡圖像分析.結果 高脂組勃起功能(ICP/MAP:0.49±0.05)明顯低于對照組(0.82±0.06,P<0.01);治療組大鼠勃起能力(ICP/MAP:0.60±0.02)高于高脂組(P<0.05).高脂組白膜彈力纖維(468±152)明顯低于對照組(3292±1123,P<0.01),治療組白膜彈力纖維(2062±560)高于高脂組(P<0.05).結論 高脂、高膽固醇飲食可誘導大鼠髮生ED,大鼠陰莖白膜彈力纖維減少是導緻ED的機製之一,PDE-51可以在一定程度上逆轉這種變化.
목적 관찰고지、고담고순음식유도발기공능장애(ED)대서음경백막적변화,명학장기소제량급여5형린산이지매억제제(PDE-5Ⅰ)타체랍비후적치료작용,연구백막조직재음경정상발기과정중적작용급기의의.방법 30지2월령웅성SD대서수궤분성3조,매조10지.대조조:위이정상음식16주;고지조:위이고지、고담고순음식(정상음식중가입2%담고순+10%저유)16주;치료조:재위이고지、고담고순음식16주적기출상,종제13주기급여타체랍비2 mg·kg-1·d-1관위1개월.각조대서경혈지측정후,측정해면체내압급평균동맥압비치(ICP/MAP)이평고음경발기공능,운용유다리아람-려춘홍대음경백막탄력섬유염색,최후대표본진행현미경도상분석.결과 고지조발기공능(ICP/MAP:0.49±0.05)명현저우대조조(0.82±0.06,P<0.01);치료조대서발기능력(ICP/MAP:0.60±0.02)고우고지조(P<0.05).고지조백막탄력섬유(468±152)명현저우대조조(3292±1123,P<0.01),치료조백막탄력섬유(2062±560)고우고지조(P<0.05).결론 고지、고담고순음식가유도대서발생ED,대서음경백막탄력섬유감소시도치ED적궤제지일,PDE-51가이재일정정도상역전저충변화.
Objective To investigate the pathological changes of tunica albuginea in erectile dysfunction (ED), the role of tunics albuginea in penis erection, and the therapeutic effect of phosphodiesterase-5 inhibitor (PDESI) on ED. Methods Thirty 8-week-old male Sprague-Dawley rats were randomly divided into 3 equal groups:(1) control group fed with normal diet for 16 weeks, (2) high-fat group fed with the diet containing 2% cholesterol and 10% pork fat, and(3) Tadalafil group fed with high-fat diet for 16 weeks and undergoing gastric perfusion of Tadalafil 2 mg/kg daily since the 13th week for 4 weeks. Sixteen weeks later, intracavernous pressure and mean arterial pressure were measured, and the ratio of maximal intracavernous pressure to mean arterial pressure (ICP/MAP) was calculated blood samples were collected. Blood samples were collected from the abdominal aorta to undergo lipid profile test. Then penis was cut. Victoria blue/ponceau red staining and color image analysis were used to observe the content of elastic fibers in the tunics albuginea. Results The ICP/MAP of the high-fat group was 0. 49 ± 0. 05, significantly lower than that of the control group (0. 82±0. 06, P <0. 01 ). The ICP/MAP of the Tadalafil group was 0. 60 ± 0. 02, significantly higher than that of the high-fat group ( P < 0. 05 ). The content of elastic fibers in tunica albuginea of the high-fat group was 468 ± 152, significantly lower than that of the the control group (3292 ± 1123, P < 0. 01 ). The content of elastic fibers in tunica albuginea of the Tedalafil group was 2062 ± 560, significantly higher than that of the high-fat group (P < 0.05 ). Conclusion High fat diet may lead to ED and reduction of elastic fibers in tunica albuginea, and PDE-5Ⅰ reverses such pathological changes.