当归对大鼠海绵体神经损伤后阴茎NOS活性的影响

目的 :探讨海绵体神经 (CN)钳夹损伤后阴茎组织一氧化氮合酶 (NOS)活性的变化及局部使用当归注射液对其活性的影响。　方法 :30只SD大鼠随机平均分成当归组、对照组和正常组 ,对前两组大鼠通过手术建立双侧CN钳夹损伤模型 ,经耻骨上在CN周围每天分别注射 2 5 %当归注射液或相当剂量生理盐水 (10ml/kg) ,正常组只注射生理盐水而不行手术 ;两周后用分光光度法检测阴茎组织NOS活性。　结果 :NOS活性均值当归组为 (1.36 0±0 .139)U/mg·prot,达正常组的 77.4% ,而对照组为 (0 .945± 0 .0 98)U/mg·prot,只有正常组的 5 3.8% ,二者比较有极显著性差异 (P <0 .0 1)。　结论 :CN损伤可致阴茎组织NOS活性降低 ,局部使用当归能够一定程度地避免其活性下降。     

肺纤维化对大鼠阴茎勃起功能的影响

目的:研究肺纤维化对大鼠勃起功能的影响及其机制。方法:12周雄性SD大鼠40只,随机分为4组:正常对照4周组(A组)、6周组(B组)和肺纤维化大鼠4周组(C组)、6周组(D组)各10只,分别用生理盐水(A、B组)及博莱霉素(5 mg/kg)气管内注入,饲养4周(A、C组)、6周(B、D组)后,测定大鼠血清睾酮、动脉血气分析、阴茎海绵体内压/平均颈动脉压(ICP/MAP),取阴茎标本测定NOS活性及cGMP含量,实时荧光PCR检测eNOS、iNOS和nNOS的mRNA在阴茎海绵体的表达,W estern印迹检测阴茎海绵体eNOS蛋白的表达。结果:电刺激的3 V,5 V C组ICP/MAP×100(16.37±2.19,27.19±3.18)较A组(30.78±2.66,50.09±6.97)显著降低(P<0.05),D组ICP/MAP×100,3 V,5 V(10.17±1.31,17.40±1.74)较B组(31.45±3.07,51.23±7.23)显著降低(P<0.05),D组ICP/MAP×100值较C组显著降低(P<0.05)。C组PaO2(75.50±13.87)mmHg较A组(103.80±6.88)mmHg显著降低(P<0.05),D组PaO2(83.60±5.50)mmHg较B组(102.70±5.77)mHg显著降低(P<0.05)。C组血清睾酮水平(391.1±264.7)ng/d l较A组(175.9±53.0)ng/d l显著升高(P<0.05),D组血清睾酮水平(745.4±408.8)ng/d l较B组(177.8±52.3)ng/d l显著升高(P<0.05),同时D组血清睾酮水平较C组显著升高(P<0.05)。C组NOS活性及cGMP含量[(1.50±0.14)U/mg prot,(35.69±3.64)pmol/mg]较A组[(2.66±0.39)U/mg prot,(51.10±7.22)pmol/mg]显著降低(P<0.05),D组NOS活性及cGMP含量[(1.40±0.20)U/mg prot,(34.55±4.30 pmol/mg)]较B组[(2.75±0.36)U/mg prot,(52.15±6.86)pmol/mg]显著降低(P<0.05),C组与D组比较NOS活性及cGMP含量无显著性差异(P>0.05)。C组eNOS蛋白表达量(0.79±0.01)较A组(0.87±0.01)显著降低(P<0.01),D组eNOS蛋白表达量(0.71±0.02)较B组(0.88±0.01)显著降低(P<0.05),D组较C组eNOS蛋白表达量显著降低(P<0.05)。C组eNOS mRNA表达量(4.46±0.92)较A组(2.61±0.68)显著升高(P<0.05),D组eNOS mRNA(2.79±0.60)表达量与B组(2.69±0.65)无显著性差异(P>0.05),nNOS及iNOS的mRNA表达量在A、B组与C、D组间均无显著性差异(P>0.05)。结论:肺纤维化可通过抑制阴茎海绵体eNOS蛋白的表达、降低总NOS活性及cGMP含量等机制抑制阴茎勃起功能。     

尼古丁对大鼠阴茎海绵体内源性CO浓度及NOS活性的影响

目的:观察尼古丁对成年雄性大鼠阴茎海绵体内源性一氧化碳(CO)浓度及一氧化氮合酶(NOS)活性的影响,探讨吸烟对勃起功能损害的可能机制。方法:40只成年雄性Wistar大鼠分为4组,尼古丁注射1个月组、2个月组、3个月组和对照组,尼古丁注射组尼古丁0.5 mg/(kg.d)皮下分别注射1、2、3个月,对照组注射生理盐水。处理后,取阴茎海绵体,用改良双波长分光光度法检测CO浓度,改良Griess法检测NOS活性。结果:对照组CO浓度为(13.66±0.40)μmol/mg prot,NOS活性为(9.72±0.47)U/mg prot。尼古丁注射1个月,CO浓度和NOS活性分别下降为(12.43±0.56)μmol/mg prot和(8.44±0.69)U/mg prot,显著低于对照组(P均<0.01);尼古丁注射2个月,CO浓度和NOS活性分别下降为(11.41±0.52)μmol/mg prot和(7.53±0.24)U/mg prot,显著低于对照组和尼古丁注射1个月组(P<0.01);尼古丁注射3个月,海绵体CO浓度和NOS活性分别下降为(10.52±0.59)μmol/mg prot和(6.64±0.31)U/mg prot,均显著低于对照组和尼古丁注射1个月、2个月组(P均<0.01)。结论:尼古丁可导致成年雄性大鼠阴茎海绵体内源性CO浓度及NOS活性下降,提示内源性CO及NOS参与吸烟引起勃起功能障碍的病理生理过程。     

衰老对大鼠阴茎海绵体内皮细胞功能的影响

目的 :探讨衰老对大鼠阴茎海绵体内皮细胞功能的影响。　方法 :利用YH 4压力传感器分别检测了青龄(5个月 )和老龄 (2 0个月 )两组大鼠阴茎海绵体内压 (ICP)在乙酰胆碱 (Ach)、硝普钠 (SNP)和A2 3187作用下的变化 ;并测定了两组大鼠阴茎海绵体一氧化氮合酶 (NOS)的活性。　结果 :青龄组基础ICP为 (9.4± 2 .3)mmHg(1mmHg=0 .133kPa) ,老龄组为 (7.2± 1.7)mmHg,二者间差异无显著性 (P >0 .0 5 )。在浓度分别为 10 -6、10 -5、10 -4mol/L的Ach作用下 ,两组大鼠ICP值间差异均有显著性 (P <0 .0 1)。当Ach浓度为 10 -4mol/L时 ,两组大鼠ICP值达到最高 ,青龄组为 (5 4 .8± 4 .2 )mmHg ,老龄组为 (40 .3± 2 .8)mmHg。A2 3187(10 μmol/L)可以进一步提高老龄组ICP值 ,由(40 .3± 2 .8)mmHg上升到 (5 6 .2± 4 .1)mmHg ,两者间差异有显著性 (P <0 .0 1) ;青龄组提高不明显 ,由 (5 4 .8± 4 .2 )mmHg上升到 (5 5 .8± 4 .7)mmHg ,两者间差异无显著性 (P >0 .0 5 )。在SNP(10 -4mol/L)作用下青龄组ICP值为(5 8.9± 4 .7)mmHg ,老龄组为 (5 1.7± 5 .3)mmHg ,两者间差异无统计学意义 (P >0 .0 5 )。两组大鼠阴茎海绵体内NOS的活性差异无统计学意义 (P >0 .0 5 )。　结论 :大鼠阴茎海绵体内皮细胞对内皮细胞激动剂     

雄激素对大鼠视前内侧区一氧化氮合酶阳性神经元的影响

目的 探讨雄激素对大鼠下丘脑一氧化氮合酶(NOS)阳性神经元的影响。方法 2个月龄雄性大鼠分成A组(去势组)、B组(假手术组)、C组(去势 睾酮替代组)以及D组(保列治喂饲组)，分别于处理前、处理后2周和2个月观察大鼠30min非接触性阴茎勃起(NCE)的次数，对视前内侧区(MPOA)、视上核(SON)、室旁核(PVN)以及终纹床核行尼克酰胺腺嘌呤二核苷酸黄递酶(NADPH—d)组织化学染色。结果 A组和D组大鼠30min NCE次数明显少于B组和C组。在NADPH组织化学染色中，术后2周各组大鼠脑组织阳性着色差异无显著性，术后2个月，A组与D组MPOA阳性着色明显少于B组和C组，而其他脑区阳性着色在各组间差异仍无显著性。结论 大鼠阴茎勃起功能对雄激素具有依赖性，而雄激素对性反应调节中枢的影响可能与调节MPOA NOS阳性神经元有关；其中5α—双氢睾酮可能是主要的雄激素活性成分。     

血红素氧合酶在去势大鼠阴茎海绵体的表达

目的:研究血红素氧合酶(HO)在去势大鼠阴茎海绵体的表达,探讨其在雄激素缺乏的勃起功能障碍发生中的机制。方法:40只10周龄雄性SD大鼠随机分成:假手术2周组(A组),假手术4周组(B组),去势2周组(C组),去势4周组(D组)。术后2、4周检测血清睾酮水平,免疫组化及RT-PCR技术检测HO及nNOS在大鼠阴茎海绵体的表达。结果:去势组大鼠较假手术组血清睾酮水平显著下降,[AvsC:(283.222±117.171)ng/dlvs(7.117±3.700)ng/dl;BvsD:(289.280±87.413)ng/dlvs(48.826±19.477)ng/dl](P<0.01)、HO-1、HO-2蛋白表达明显降低(P<0.01),去势组HO-1、HO-2及nNOSmRNA表达较假手术组显著降低(P<0.01)。结论:雄激素可能通过HO-CO系统部分调控阴茎勃起功能。     

雌激素对大鼠阴道组织NOS活性的影响

目的　研究雌激素对阴道组织一氧化氮合酶 (NOS)活性的影响 ,探讨雌激素在维持女性性反应中的分子学机制。方法　 40只雌性成年SD大鼠随机分为 3组 :卵巢切除去势组 (10只 )、雌激素替代组 (10只 )及假手术对照组 (2 0只 ) ,通过阴道涂片筛选出待取材的动物。于术后第 14天取出阴道组织、用分光光度计测定其一氧化氮合酶(NOS)活性。结果　卵巢切除去势组NOS活性显著低于对照组 (P <0 .0 1) ,雌激素替代能使NOS活性显著上升 (P <0 .0 1) ,并接近对照组正常水平 (P >0 .0 5 )。结论　雌激素可能通过调节阴道NOS活性而维持女性性反应。     

雄激素诱导大鼠阴茎细胞增殖的研究

本研究试图探讨雄激素补充治疗能否诱导去势大鼠阴茎勃起组织细胞增殖。 30只成年SD雄性大白鼠随机分为对照组、去势组及补充组。补充组术后 2周肌注十一酸睾酮 (13.7mg/kg) ,并分别于补充治疗后 2 4、48、72及 96h处死 ,最后处死对照组及去势组动物 ,取中段阴茎海绵体 ,用免疫组化技术 (SP法 )检测其细胞增殖情况。发现正常情况下阴茎组织中存在中等强度的细胞增殖 (39.8± 3.47) ,去势 2周后几乎无细胞新生 (P <0 .0 1) ,睾酮补充 48h后即诱导DNA合成 (2 1± 2 .2 9) ,96h后增殖细胞显著增多 (95 .2± 9.6 5 ,P <0 .0 1)。增殖细胞包括平滑肌细胞、成纤维细胞及内皮细胞等。结果表明雄激素能诱导去势大鼠阴茎勃起组织多种类型细胞增殖     

血红素氧合酶2在去势大鼠阴茎海绵体内的表达

目的:研究去势大鼠阴茎海绵体血红素氧合酶2(HO-2)和内皮型一氧化氮合酶(eNOS)的表达,探讨雄激素与HO-2、eNOS在ED中的作用及相关性。方法:10周龄雄性SD大鼠40只,分为4、8、12周组和正常对照组各10只,实验组采取手术切除双侧睾丸,对照组采取假手术。分别于术后4、8、12周测定大鼠血清睾酮(T)、阴茎海绵体内压(ICP)、平均颈动脉压(MAP),取阴茎标本,采用Western印迹分析阴茎海绵体HO-2含量,免疫组化分析HO-2和eNOS的表达。结果:去势各组血清T水平较正常对照组显著下降(P<0.05)。经3V、5V电压刺激后去势各组ICP/MAP值明显下降(P<0.05)。HO-2在正常和去势大鼠阴茎海绵体组织均有表达,去势4周组HO-2光密度分布曲线下面积(341.50±99.70)较正常组(876±443.36)和去势8周组(705.00±152.74)明显下降(P<0.05),去势8周与正常组之间无显著变化(P>0.05),去势12周没有检测到HO-2的表达。eNOS主要表达于阴茎海绵体血管内皮细胞,去势组eNOS(123.94±30.23)较正常组(421.21±125.12)差异有显著性(P<0.05)。T与eNOS和HO-2表达呈高度正相关(r=0.976、0.946,P均<0.05)。结论:雄激素可能通过影响大鼠阴茎海绵体HO-2、eNOS的表达参与阴茎勃起功能调控。     

去势对大鼠阴茎海绵体功能和结构的影响

目的 :探讨雄激素对阴茎海绵体功能和结构的影响。　方法 :30只成年雄性大白鼠随机分为 3组 :阉割组、替代组及假手术对照组。于 1周后取阴茎海绵体 ,用紫外分光光度计测定其一氧化氮合酶 (NOS)活性 ,同时用ISEL法检测其细胞凋亡情况。　结果 :阉割组海绵体NOS活性下降 70 %并出现细胞凋亡 (P <0 .0 1) ,睾酮替代能阻止NOS活性降低及凋亡的发生 (P >0 .0 5 )。　结论 :雄激素可通过调节NOS活性及细胞的增殖与凋亡而维持阴茎海绵体的结构与功能。     

Involvement of L-arginine/nitric oxide pathway at the paraventricular nucleus of hypothalamus in central neural regulation of penile erection in the rat

The objective of this study is to investigate whether the L-arginine/nitric oxide pathway is involved in the neurotransmission of paraventricular nucleus of hypothalamus (PVN) activation-induced penile erection in the rat. Male adult Sprague-Dawley rats anesthetized with pentobarbital were used. The femoral artery was cannulated to measure systemic and mean arterial pressure (SAP and MAP), and heart rate (HR). A 26-gauge needle was inserted into corpus cavernosum to measure the intracavernous pressure (ICP) simultaneously with SAP, MAP and HR on a polygraph. Four groups of study were arranged: (1) stereotaxically delivery of L-arginine (500 nmol/500 nl) into PVN; (2) administration of a mixture (1 microl) containing N(G)-Nitro-L-arginine methyl ester (L-NAME) 500 nmol and L-arginine 500 nmol into PVN; (3) microinjection of saline 500 nl into PVN as a vehicle control; and (4) intracavernous injection of L-arginine (100 nmol/50 microl). The ICP, SAP, MAP and HR were monitored for at least 2 h after each administration of the experimental agents. Upon administration of L-arginine into PVN, there was a significant increase of ICP from resting 9.6+/-2.5 mmHg to peaked at 64.4+/-9.8 mmHg after a latency of 3016.0+/-1749.7 s and with a duration of 27.6+/-15.8 min. There was no change of resting ICP after administration of the mixture of L-NAME and L-arginine into PVN. Application of saline to PVN and intracavernous injection of L-arginine failed to increase ICP. Based on elicitation of penile erection upon administration of L-arginine into PVN, and elimination of this L-arginine induced penile erection by co-administration of L-NAME with L-arginine, the results of this study suggest that L-arginine/nitric oxide pathway may be involved in the neurotransmission of PVN activation-induced penile erection in the rat.     

Selegiline enhances erectile activity induced by dopamine injection in the paraventricular nucleus of the hypothalamus in anesthetized rats

Apomorphine delivered in the paraventricular nucleus of the hypothalamus (PVN) induces penile erection in rats, suggesting a role of dopaminergic projection to the PVN in the control of penile erection. We assessed whether the selective inhibitor of monoamine oxidase B, selegiline, could enhance the erectile activity induced by dopamine delivery in the PVN. Intracavernous and blood pressure (ICP and BP) were monitored in anesthetized rats to quantify ICP rises (number and percentage of ICP maximum/mean BP (ICPmax/BP x 100)) elicited by 10 micro g dopamine injection in the PVN after saline or 3 mg/kg i.v. selegiline (8 rats per group). The number of ICP rises (mean+/-s.d.: 4.5+/-2.9 vs 1.4+/-1.9; P=0.017) and their ICPmax/BP x 100 (49+/-8% vs 34+/-9%; P=0.015) were significantly greater upon dopamine injection in the PVN than upon vehicle. Compared to saline i.v., 3 mg/kg selegiline pretreatment significantly increased the number of ICP rises induced by dopamine injection in the PVN (9.4+/-2.6 vs 4.5+/-2.9; P<0.001), without affecting their amplitude. This suggests that drugs potentiating dopaminergic responses in the central nervous system might enhance proerectile commands of supraspinal origin.     

大鼠阴茎组织NOS活性对雄激素的依赖性

目的探讨ＮＯＳ活性与雄激素在阴茎勃起中的关系。方法将３０只成年雄性大白鼠随机分为去势组,替代组及对照组,去势组与替代组分别切除双侧睾丸,其中替代组在切除睾丸后给予睾酮替代。于术后１周取阴茎组织,用紫外分光光度法检测其ＮＯＳ活性。结果去势组ＮＯＳ活性较对照下降７０％（Ｐ＜０．０１）,睾酮替代组和对照组ＮＯＳ活性差异无显著性（Ｐ＞０．０５）。结论雄激素可能通过调节ＮＯＳ活性而在阴茎勃起中发挥重要作用。     

DOPAMINERGIC NEUROTRANSMISSION AT THE PARAVENTRICULAR NUCLEUS OF HYPOTHALAMUS IN CENTRAL REGULATION OF PENILE ERECTION IN THE RAT

PURPOSE: To investigate whether the paraventricular nucleus of hypothalamus (PVN) is involved in the central regulation of apomorphine-induced penile erection in the rat, and to decipher dopamine receptor subtypes in the PVN that are involved in apomorphine-induced penile erection. MATERIALS AND METHODS: Male adult Sprague-Dawley rats (200 to 300 gm.) anesthetized with pentobarbital sodium were used. The intracavernous pressure (ICP), recorded along with systemic and mean arterial pressure (SAP, MAP) as well as heart rate (HR), was measured via a 26-gauge needle inserted into one corpus cavernosum. The PVN was activated by stereotaxically delivered apomorphine hydrochloride (0.1 nmol./100 nl.). Injection of saline into PVN served as a vehicle control. To investigate the participation of dopamine receptor subtypes in the PVN on apomorphine-induced penile erection, D1 or D2 receptor antagonist, SCH-23390 (100 pmol./100 nl.) or sulpiride (100 pmol./100 nl.) respectively, was administered into the PVN prior to subcutaneous application of apomorphine (80 microg./kg.). The effects on ICP of microinjection of D1, D2 or D3 receptor agonist, SKF-38393 (200 pmol./100 nl.), lisuride (200 pmol./100 nl.) or 7-hydroxy-DPAT (200 pmol./100 nl.) respectively, into the PVN were also evaluated. RESULTS: The mean resting ICP was 5.2+/-0.4 mm. Hg. Upon administration of apomorphine into the PVN, there was a significant increase in ICP that peaked at 50.7+/-5.3 mm. Hg and persisted for 45.2+/-18.0 minutes after an onset latency of 677.7+/-311.6 seconds. Yawning and teeth gnashing were also observed in most of animals during the period of ICP increase. There was no significant change in SAP, MAP or HR. In addition, there was no elevation in ICP after administration of saline to the PVN or direct injection of apomorphine into the cavernous tissue. Microinjection of D1 or D2 receptor antagonist into the PVN blocked the increase in ICP after subcutaneous administration ofapomorphine. Direct application of D2, but not D1 or D3 receptor agonist into the PVN, on the other hand, increased the ICP. CONCLUSIONS: Our results demonstrate that application of apomorphine to the paraventricular nucleus of hypothalamus elicited penile erection in the rat. Such an increase in ICP to apomorphine was due mainly to activation of the D2 receptor subtype in the PVN. These observations indicate that PVN may be involved in the central regulation of apomorphine-induced penile erection in the rat.     

The effects of androgen on penile reflex, erectile response to electrical stimulation and penile NOS activity in the rat

Aim: To investigate the effects of androgen on penile erection through the reflex arc and penile corpus cavernosum,and study the respective roles of testosterone (T) and dihydrotestosterone (DHT) in penile erection ira rats. Methods:Male Sprague-Dawley rats were castrated and implanted with silastic brand silicone tube containing T or DHT, with orwithout daily injections of a 5a-reductase inhibitor, MKM-434. The penile reflex, erectile response to electrical stimula-tion (ES) of the cavernous nerves and penile nitric-oxide synthase (NOS) activity were observed under varying andro-genic status. Results: Penile reflex erection in the rat was, on the whole, related to serum T levels though the numberof glans engorgernents was not. The number of cups and flips was significantly decreased by castration, and restoredto the control level by T supplementation. Erectile response to ES and NOS activity in penile tissue was also related toserum T level. T administered together with a ,5a-reductase inhibitor no longer restored the number of reflex erection,erectile responses to ES and NOS activity in the corpus cavemosum. Conclusion: Androgen influenced the penile re-flex arc, corpus cavemosum, and the perinea] striated muscles, ha reflex erection, erectile response to ES and penileNOS activity in the rat, T seeras to be first conyerted to DHT, the more active androgen modality. (Asian JAndrol1999Dec; 1: 169-174)     

Metachlorophenylpiperazine (m-CPP) induced intracavernous pressure responses in anaesthetized rats

Here we have recorded the effects of metachlorophenylpiperazine (m-CPP) on intracavernous pressure (ICP) in anesthetized rats pretreated with various pharmacological agents in an attempt to determine the mechanism and relevance of the m-CPP induced ICP response to other models of erection. m-CPP elicited consistent and significantly greater increases in ICP (71.5+/-6.6 mmHg) compared with the mixed 5-HT(2a/2c) agonists trifluoromethylphenylpiperazine (3.4+/-1.3 mmHg) and quipazine (10.9+/-1.8 mmHg). Blockade of 5-HT(2a) receptors with ketanserin failed to unmask any stimulatory effect of quipazine (7.2+/-1.0 mmHg). m-CPP induced ICP responses (71+/-7.0 mmHg) were unaffected in the presence of mianserin (63+/-5 mmHg) and ketanserin (51+/-12 mmHg). Spiperone significantly reduced the m-CPP induced increase in ICP (8.0+/-1.0 mmHg). Naloxone, yohimbine and 8-hydroxy-2-(di-n-propylamino)tetralin (8-OHDPAT) failed to elicit increases in ICP on their own. All three drugs significantly reduced the latency to the first m-CPP induced ICP response compared to saline. Yohimbine increased the duration of m-CPP induced ICP responses whereas 8-OHDPAT increased the mean number of m-CPP induced ICP responses compared to saline. The effects of m-CPP on ICP in anesthetized rats may not be mediated by 5-HT(2c) receptors and appears to be similar to erection in copula, but not erection elicited by other drugs or penile sheath retraction.     

电刺激阴茎背神经和海绵体内注射药物诱导大鼠阴茎海绵体内压反应

目的:评价阴茎海绵体内压(ICP)监测在电刺激阴茎背神经和海绵体内注射罂粟碱诱导大鼠阴茎勃起反应中的应用。方法:选取性成熟雄性SD大鼠8只,20%氨基甲酸己酯(1000mg/kg)腹腔注射麻醉下,暴露阴茎并解剖阴茎背神经(DN),将充满肝素盐水并连接于压力传感器的25G针头插入一侧海绵体,取另一30G头皮针插入对侧海绵体,分别用于测定ICP和注射血管活性药物。分别以电刺激海绵体神经(刺激参数:电压4V,波幅0.5ms,频率16Hz,持续20s)和海绵体内注射罂粟碱(0.4mg)诱发阴茎勃起,采用SMUPPC型生物信号处理系统记录ICP变化。结果:麻醉大鼠的ICP基线水平为(12.3±3.1)mmHg(1mmHg=0.133kPa),DN电刺激后约30～60sICP明显升高[(36.4±2.3)mmHg,P<0.05],电刺激结束后缓慢下降至基线水平。海绵体内注射罂粟碱后5～8min可诱发ICP明显升高[(28.4±6.1)mmHg,P<0.05]。结论:监测电刺激大鼠DN及海绵体内药物注射诱发的ICP,为阴茎勃起这一复杂神经血管活动的动物模型在体实验研究提供了一种客观准确的科学工具,对于进一步研究阴茎勃起生理和勃起功能障碍的发病机制,评价治疗勃起功能障碍新疗法的疗效等具有重要意义。     

Participation of Paraventricular Nucleus of Hypothalamus in Central Regulation of Penile Erection in the Rat

Purpose

To investigate the possible participation of the paraventricular nucleus of hypothalamus in central regulation of penile erection.

Materials and Methods

Male adult Sprague-Dawley rats were anesthetized and maintained with pentobarbital sodium. The intracavernous pressure (ICP) was used as an experimental index for penile erection, and was recorded alongside systemic arterial pressure and heart rate. The effect on ICP of electrical (30-s train of 30-120 micro A, 40-160 Hz, 1-ms rectangular pulses) or chemical (L-glutamate, 0.5 nmol/50 nl.) activation of the paraventricular nucleus of hypothalamus (PVN) or hippocampal formation was evaluated.

Results

Electrical activation of the PVN elicited both multiple and single episodes of elevation in ICP, along with visible erection and ejaculation. The former pattern exhibited an increase in ICP that was more sustained, with higher peak amplitude and longer latency. Chemical stimulation of neuronal perikarya in the PVN also resulted in similar patterns of rise in ICP and visible erection. These effects were, nonetheless, not accompanied by significant alterations in systemic arterial pressure and heart rate. Activation of the hippocampal formation, as we reported previously, similarly elicited multiple and single episodes of increase in ICP. These erectile responses, however, were substantially reduced or eliminated upon electrolytic lesion of the ipsilateral PVN.

Conclusion

These observations suggest that the PVN may be an important nucleus that participates in central neural regulation of penile erection in the rat. Furthermore, an efferent pathway(s) from the hippocampal formation to PVN may constitute part of the neural circuitry in the forebrain in the regulation of erectile functions.     

Intracavernosal pressure monitoring in mice: responses to electrical stimulation of the cavernous nerve and to intracavernosal drug administration

With the development of transgenic mice to evaluate mechanisms of erectile function, it appears particularly advantageous to develop a standardized mouse model of penile erection. The purpose of the study reported here was to evaluate the novel application of intracavernosal pressure (ICP) monitoring in the mouse during electrophysiologic and pharmacologic induction of penile erection. In anesthetized adult male mice, the cavernous nerves (CN) were isolated unilaterally, and the corpora cavernosa were exposed. A 24-gauge angiocath (intravenous catheter) was inserted into the right corpus cavernosum to monitor the ICP, and a 30.5-gauge needle was inserted into the left corpus cavernosum for intracavernosal drug administration. ICP was recorded during CN-stimulated or pharmacostimulated erections. Electrical stimulation of the CN significantly increased the ICP (from 10.09 +/- 2.01 to 34.62 +/- 2.71 mm Hg, P < .05), which then returned to baseline pressure after termination of the electrical stimulation. Pretreatment with intracavernosal administration of the nitric oxide synthase inhibitor, nitro-L-arginine methyl ester (0.1 mg), inhibited the electrical stimulation-induced changes in ICP (7.17 +/- 1.46 vs 10.38 +/- 2.17 mm Hg, not significant [NS]). Also, intracavernosal administration of papaverine (0.4 mg) produced a significant increase in ICP (from 8.51 +/- 0.69 to 26.37 +/- 5.7 mm Hg, P < .05). We concluded that this technique might be applied to perform quantitative erection physiologic experiments with the mouse as an economical and experimentally advantageous animal model, particularly with the development of transgenic mice to evaluate mechanisms of erectile function.