糖尿病性阴茎勃起功能障碍大鼠阴茎海绵体一氧化氮合酶 …

目的 探讨糖尿病（ＤＭ）性阴茎勃起功能障碍（ＥＤ）的发病机理。方法 ＳＤ大鼠注射链脲佐菌素建立ＤＭ动物模型后,注射阿朴吗啡观察６周,８周及１２周大鼠阴茎勃起情况,筛选ＤＭ性ＥＤ大鼠模型,测定其阴茎海绵体组织一氧化氮合酶（ＮＯＳ）的活性。结果ＤＭ性ＥＤ大鼠阴茎海绵体组织ＮＯＳ活性与对照组相比显著降低,随ＤＭ病程延长,ＮＯＳ活性明显下降。     

糖尿病性阴茎勃起功能障碍大鼠模型球海绵体肌和坐骨耻骨肌重量及显微结构的研究

ＳＤ大鼠注射链脲佐菌素制造糖尿病（ＤＭ）动物模型后,注射阿朴吗啡观察６周、８周及１２周大鼠队茎勃起情况,筛选ＭＤ性阴茎勃起功能障碍（ＥＤ）大鼠模型,研究其海绵体肌及坐骨耻骨肌重量及显微结构的改变,并测定其血清睾酮浓度,以探讨ＤＭ性ＥＤ的发病机理。结果：ＤＭ性ＥＤ大鼠模型球海绵体肌和坐骨耻骨肌重量及血清睾酮浓度显著降低;显策结构发生明显病理性改变,且上述变化与ＤＭ病程密切相关。揭示ＤＭ严重影响阴茎勃     

高血压大鼠海绵体平滑肌细胞间连接的变化

目的:比较自发性高血压大鼠(SHR)和正常血压大鼠阴茎海绵体平滑肌细胞间连接改变及与阴茎勃起功能的关系。方法:注射阿朴吗啡(APO)观察14周龄SHR(SHR组,n=5)、W istar-Kyoto大鼠(WKY组,n=5)阴茎勃起情况,用透射电镜观察其阴茎海绵体平滑肌细胞间连接超微结构,RT-PCR测定海绵体平滑肌细胞Connexin 43的mRNA表达,免疫组化观察Connexin 43蛋白表达。结果:SHR组大鼠阴茎勃起次数明显低于WKY组(P<0.05),电镜发现SHR组大鼠阴茎海绵体平滑肌细胞间大量胶原纤维增生,Connexin 43蛋白及其mRNA表达较WKY组显著降低(P<0.05)。结论:高血压影响阴茎勃起功能,阴茎海绵体平滑肌细胞间连接的病理改变可能是高血压性勃起功能障碍的发病机制之一。     

糖尿病性阴茎勃起功能障碍动物模型血清雄激素测定

ＳＤ大鼠注射链脲佐菌素制造溏尿病（ＤＭ）动物模型后,注射阿朴吗啡观察不同时期大鼠阴茎勃起情况,筛选ＤＭ性阴茎勃起功能障碍（ＥＤ）大鼠模型,测定其血清ＬＨ、ＦＳＨ及睾酮的浓度,并观察睾丸组织的显微结构,研究ＤＭ性ＥＤ的发病机理。结果ＤＭ性ＥＤ大鼠血清睾酮浓度显著降低,睾丸组织显微结构发生明显病理性改变,且上述变化与ＤＭ病程密切相关;ＬＨ在ＤＭ早期无改变、晚期明显降低;ＦＳＨ无明显改变。提示ＤＭ严重影阴茎勃起功能及雄激素的合成分泌,雄激素降低可能是其主要发病机理之一。     

阳萎患者阴茎海绵体平滑肌细胞超微结构的研究

阴茎海绵体平滑肌细胞超微结构的改变对阴茎勃起功能具有重要的意义。以阳萎患者与对照组对比研究的方法，观察了阳萎患者阴茎海绵体组织细胞超微结构改变。结果表明，阳萎阴茎海绵体平滑肌细胞超微结构有明显的病理改变，以线粒体退变、微丝减少或消失、内质网损害扩张、糖原缺乏等为主，也可见到微血管腔闭塞的现象，提示局部有微循环障碍的问题。引起这种病理损害的原因可能与局部组织缺血缺氧有关。认为海绵体组织的这种病理改变可能是引起阳萎的直接因素之一。     

糖尿病性阴茎勃起功能障碍大鼠阴茎海绵体一氧化氮合酶活性的测定

目的　探讨糖尿病 (DM )性阴茎勃起功能障碍 (ED)的发病机理。　方法　SD大鼠注射链脲佐菌素建立DM动物模型后 ,注射阿朴吗啡观察 6周、8周及 12周大鼠阻茎勃起情况 ,筛选DM性ED大鼠模型 ,测定其阴茎海绵体组织一氧化氮合酶 (NOS)的活性。　结果　DM性ED大鼠阴茎海绵体组织NOS活性与对照组相比显著降低 (P <0 0 0 1或P <0 0 1) ,随DM病程延长 ,NOS活性明显下降 (P <0 0 1)。　结论　DM严重影响阴茎勃起功能 ,海绵体组织NOS活性降低可能是其发病机理之一。     

吸烟对大鼠阴茎血管内皮细胞P-选择素表达的影响

目的:观察不同吸烟量大鼠阴茎血管内皮细胞P-选择素的表达和海绵体超微结构的改变,初步探讨吸烟导致阴茎勃起功能障碍的发病机制。方法:健康Wistar大鼠50只,随机均分为正常对照组、长期大量吸烟组、长期小量吸烟组、短期大量吸烟组和戒烟组。皮下注射阿朴吗啡(APO)检测阴茎勃起功能。采用ELISA法测定大鼠阴茎血管内皮细胞P-选择素的水平,透射电镜观察大鼠阴茎海绵体超微结构的变化。结果:正常对照组P-选择素为(10.78±1.71)ng/L;长期大量吸烟组为(62.62±5.95)ng/L;长期小量吸烟组为(40.06±3.97)ng/L;短期大量吸烟组为(41.37±4.06)ng/L;戒烟组为(22.80±3.15)ng/L。4组与对照组比较均有显著性差异(P<0.05)。电镜观察吸烟各组内皮细胞、血窦、平滑肌细胞分布杂乱,血管内皮细胞连续性破坏;内皮细胞和平滑肌细胞超微结构被破坏。大量间质组织增生、纤维化。结论:吸烟可致阴茎血管内皮细胞P-选择素表达增加,破坏海绵体组织超微结构,可能是吸烟致阴茎勃起功能障碍的主要途径之一。     

慢性肾功能衰竭性勃起功能障碍大鼠阴茎海绵体有效成分的测定

目的:探讨慢性肾功能衰竭(CRF)性勃起功能障碍(ED)的发病机制。方法:应用SD雄性大鼠分两期行5/6肾脏切除术,建立CRF动物模型。将假手术组(NCRF组,n=30)、CRF模型大鼠(CRF组,n=45)分别随机均分为Ⅰ(2周)、Ⅱ(4周)、Ⅲ(6周)3组,并分别于2、4、6周注射阿朴吗啡(APO,80μg/kg)后观察大鼠阴茎勃起情况,筛选CRF性ED模型大鼠;测定阴茎海绵体组织一氧化氮合酶(NOS)的活性,及其组织的M asson染色图像分析。结果:CRF性ED大鼠阴茎海绵体组织NOS活性及平滑肌面积显著降低(P<0.01或P<0.05),胶原纤维略有增加,且上述变化与CRF病程密切相关。海绵窦血管腔无明显变化。结论:CRF严重影响阴茎勃起功能,阴茎海绵体组织NOS活性降低及阴茎海绵体平滑肌面积的减少可能是其重要的发病机制。     

褪黑素抗氧化治疗糖尿病大鼠阴茎勃起功能障碍的研究

目的 观察褪黑素对糖尿病大鼠阴茎勃起功能的影响,探讨氧化应激在糖尿病性勃起功能障碍发病机制中的作用.方法 一次性腹腔注射STZ建立糖尿病大鼠模型,随机分为糖尿病组、褪黑素(MT)治疗组以及对照组.8周后通过电刺激各组大鼠勃起神经来检测海绵体内压,评价勃起功能;采用硫代芭比妥酸法检测阴茎海绵体组织中丙二醛(MDA)含量,黄嘌呤氧化酶法测超氧化物氧化酶(SOD)活性;免疫组化染色半定量分析各组大鼠阴茎海绵体中平滑肌及内皮的含量.结果 与正常对照组相比,阴茎海绵体组织中MDA含量显著增加(P＜0.01),SOD活性降低(P＜0.05),最大海绵体内压(ICP)亦显著降低(P＜0.05);与糖尿病组相比,MT组大鼠海绵体MDA含量明显降低(P＜0.05),其SOD活性和ICP显著升高(P＜0.05);且其海绵体平滑肌及海绵窦内皮细胞含量明显提高.结论 MT可通过改善组织中氧化应激水平,促进阴茎海绵体平滑肌和内皮组织修复,提高勃起功能;抗氧化治疗可能为糖尿病性勃起功能障碍的防治提供新的策略.     

阴茎包埋对海绵体形态结构的影响

目的:探讨阴茎包埋对大鼠阴茎海绵体形态结构的影响。方法:通过建立隐匿阴茎大鼠模型获得实验标本,分2月组、4月组进行观测,每组25只大鼠。各阶段又分包埋组(15只)、正常组(10只),光镜和电镜下观察海绵体形态结构的改变。结果:阴茎包埋2月组海绵体形态结构无明显变化,4月组病理改变较为明显,光镜下见大鼠阴茎海绵体平滑肌细胞,内皮细胞分布杂乱,细胞间大量间质组织增生,海绵窦狭窄;电镜下见阴茎海绵体平滑肌细胞及内皮细胞萎缩、线粒体退变、内质网扩张,致密体及收缩纤维减少,脂滴增加,空泡形成。包埋组与正常组阴茎海绵体在外观和重量上无明显差异(P>0.05)。结论:阴茎包埋对海绵体外观和重量无明显影响,但随着包埋时间的延长,海绵体组织发生超微结构上的病理改变。     

Antifibrogenic role of valproic acid in streptozotocin induced diabetic rat penis

We investigated the therapeutic effects of valproic acid (VPA) on erectile dysfunction and reducing penile fibrosis in streptozocin (STZ)‐induced diabetic rats. Eighteen male rats were divided into three experimental groups (Control, STZ‐DM, STZ‐DM plus VPA) and diabetes was induced by transperitoneal single dose STZ. Eight weeks after, VPA and placebo treatments were given according to groups for 15 days. All rats were anesthetised for the measurement of in vivo erectile response to cavernous nerve stimulation. Afterward penes were evaluated histologically in terms of immune labelling scores of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and transforming growth factor‐β1 (TGF‐β1). Slides were also evaluated in terms of collagen/smooth muscle ratio and penile apoptosis. After the treatment with VPA, erectile responses were found as improved when compared with STZ‐DM rats but not statistically meaningful. eNOS and VEGF immune expressions diminished in penile corpora of STZ‐DM rats and improved with VPA treatment. VPA led to decrease in TGF‐β1 expression and collagen content of diabetic rats’ penes. Penile apoptosis was not diminished with VPA. In conclusion, VPA treatment seems to be effective for reducing penile fibrosis in diabetic rats and more prolonged treatment period may enhance erectile functions.     

Ultrastructural comparison of penile cavernous tissue between hypertensive and normotensive rats

Our aim was to compare the ultrastructure of penile cavernous tissue in the spontaneous hypertensive rat (SHR) and normotensive rat, and study the relation of blood pressure with erectile function. After injection of apomorphine (APO), penile erectile frequency in 16-week-old SHR (group A) and Wistar-Kyoto rat (WKY) (group B) was observed and noted. The ultrastructure of the penile cavernous tissue was studied by scanning electron microscope and transmission electron microscope. The mean blood pressures were significantly higher in group A than in group B (P=0; 171.20+/-10.94 and 117.60+/-12.38, n=5, for group A and group B, respectively). After treatment of the two groups with APO, the erectile frequency in group A was significantly less than in group B (P=0.007; 0.40+/-0.55 and 2.40+/-1.14, n=5, for group A and group B, respectively). Significant ultrastructural pathological changes were observed in the tunica albuginea and penile cavernous tissue of SHR. The elastic fibers were decreased and the collagen fibers of the sinusoid were increased in group A. The tunica albuginea thickness (mean+/-s.d.) was 100.20+/-7.22 microm and 126.00+/-7.65 microm in group A and group B, respectively. The tunica albuginea of group A was significantly thinner than that in B (P=0.001). Some endothelial cells and smooth muscle cells exhibited damaged mitochondria, and endoplasmic reticulums and Schwann cells were degenerated in group A. Although the function of penile erection might be affected by a secondary effect related to endothelial dysfunction of hypertension, these ultrastructural pathological changes of the penile cavernous tissue might also be one of the important mechanisms of erectile dysfunction caused by hypertension.     

Effect of basic fibroblast growth factor incorporating gelatin microspheres on erectile function in the diabetic rat

PURPOSE: We report the potential of basic fibroblast growth factor (bFGF) incorporating gelatin microspheres to preserve erectile function in a diabetic rat model. MATERIALS AND METHODS: A total of 48 adult male rats were divided into 3 groups, namely control (nondiabetic rats), diabetes mellitus (DM) (diabetic rats that received gelatin microspheres with saline) and bFGF (diabetic rats that received gelatin microspheres with bFGF). After 4 and 8 weeks we examined intracavernous pressure responses with electrical stimulation to the cavernous nerve. For histological examination of the penis we performed Azan-Mallory staining for smooth muscle and collagen, and immunohistochemistry for endothelial nitric oxide synthase (NOS) in endothelium and neuronal NOS in cavernous nerve fiber. RESULTS: Although the intracavernous pressure response was significantly lower in the DM group than in the control group, pressure in the bFGF group was maintained at the normal level found in controls. Azan-Mallory staining showed a mass decrease in smooth muscle in cavernous tissue in the DM group. However, that in the bFGF group was maintained. There was no significant difference in endothelial NOS positive areas and the distribution of the diameter of neuronal NOS positive nerve fibers in cavernous tissue among the 3 groups. CONCLUSIONS: We report the maintenance of erectile function with bFGF incorporating gelatin microspheres in diabetic rats. The rationale of this maneuver is smooth muscle preservation by the long-term release of bFGF. This is a novel therapeutic option that is clinically applicable for diabetes induced erectile dysfunction.     

Vascular impotence: focal or diffuse penile disease.

Using computerized image analysis the percentage of smooth muscle fibers was measured in several biopsies of the penis from 10 cadavers and 5 patients with vascular impotence. No significant difference was observed between the proximal and distal areas, and/or between the peripheral and central areas in 1 corpus cavernosum, and between the 2 corpora cavernosa for each patient or cadaver. The percentage of smooth muscle fibers was less in impotent patients in comparison with the cadavers, in which the erectile status was not known, and this reduction occurred throughout both cavernous bodies. Vascular impotence is a diffuse penile disease. Therefore, a cavernous body biopsy can be used to study the penile structure in the assessment of vascular impotence.     

糖尿病性勃起功能障碍大鼠阴茎组织内Cx43和eNOS表达的研究

目的:探讨糖尿病(DM)性勃起功能障碍(DMED)与阴茎组织中连接蛋白(Cx43)和eNOS水平变化的相关性。方法:25只SD大鼠腹腔内注射四氧嘧啶建立DM模型,8周后注射阿朴吗啡观察大鼠阴茎勃起情况,筛选出DMED大鼠,应用RT-PCR和免疫组化法分别检测阴茎组织中Cx43和eNOSmRNA表达水平。结果:DMED大鼠阴茎海绵体组织eNOSmRNA表达(0.155±0.157)与DM组(0.508±0.242)比较,显著降低(P<0.01),而Cx43mRNA则显著升高(0.993±0.157vs0.545±0.138,P<0.01),二者存在负相关性(r=-0.987)。免疫组化检测也显示DMED组大鼠阴茎组织平滑肌细胞中eNOS蛋白表达减少,而Cx43蛋白水平增多。结论:阴茎组织内eNOS水平下降可能是DM患者发生ED的主要机制之一;同时,Cx43的表达呈代偿性增加,其功能有待进一步探讨。