补骨脂抑制人工关节假体周围骨溶解的研究

目的：探讨中药补骨脂对人工关节置换术后假体周围骨溶解,假体无菌性松动的核因子KB受体活化因子配体-核因子KB受体活化因子受体-骨保护素（RANKL-RANK-OPG）信号通路的作用。方法：取24只200＋5g雌性SD大鼠。随机分为A、B、C组,均注射钛颗粒溶液建立骨溶解模型,术后A组采用中药补骨脂水溶液腹腔注射,B组采用外源性OPG腹腔注射作为阳性对照,C组采用生理盐水腹腔注射作为阴性对照。给药4周后,通过免疫组化及反转录聚合酶链反应（RT-PCR）检测各组动物体内RANKL／RANK的表达水平变化。结果：用药4周后,3组12只大鼠背部气囊均为厚壁囊腔,骨溶解模型成功建立,免疫组化及RT-PCR检测RANKIJRANK均呈阳性表达。免疫组化RANKL平均光密度（AOD）值A组（0．168±0．017）、B组（0．147±0．009）明显低于C组（0．314±0．011）,差异有统计学意义（P〈0．05）;A组、B组之间比较无明显差异。RANKAOD值测定A组（0．172±0．015）、B组（0．193±0．045）明显低于C组（0．342±0．007）,差异有统计学意义（P〈0．05）;A组、B组之间比较无明显差异。RT-PCR检测RANKL相对量A组（0．575±0．143）、B组（0．543±0．174）明显低于C组（0．951±0．362）,差异有统计学意义（P〈0．05）;A组、B组之间比较无明显差异。RANK相对量A组（0．433±0．025）、B组（0．611±0．209）明显低于C组（0．871±0．211）,差异有统计学意义（P〈0．05）;A组、B组之间比较无明显差异。结论：中药补骨脂对人工关节置换术后假体周围骨溶解,假体无菌性松动具有抑制作用。     

脾虚证IBS模型WHBE兔血浆环核苷酸水平的变化

目的观察脾虚型肠易激综合征（IBS）模型WHBE兔环核苷酸水平的变化。方法取WHBE兔和日本大耳白兔各18只,分别随机分成两组,即正常对照组6只,模型对照组12只,采用湿热应激加灌服番泻叶煎剂的方法造成脾虚证肠易激综合征（tBs）免模型,其中模型对照组造模后处理6只,剩余兔自然恢复10d,观察实验兔的血浆环核苷酸水平的变化。结果与正常对照组比较,WHBE兔模型对照组血浆cAMP和cGMP水平均显著升高（P〈0．05,P〈0．01）,且自然恢复10d后血浆cAMP和cGMP水平仍高于正常对照组（P〈O．05,P〈O．01）;日本大耳白兔模型对照组造模后及自然恢复10d后血浆cAMP和cGMP水平略有所升高,但差异均不显著（P〉O．05）;且模型对照组和自然恢复组cAMP／cGMP比值均略低于正常对照组,但差异不显著（P〉O．05）。结论本实验脾虚证IBS模型兔的血浆环核苷酸水平随阴阳盛衰而变化,具有双重特点：既有阴虚特点,又有阳虚特点,且WHBE兔更适合于脾虚证IBS模型研究理想的实验动物。     

肝脏CT值与动脉粥样硬化关系

目的探讨肝脏CT值与动脉粥样硬化（AS）程度的关系,寻找AS活体量化观测指标,提高AS干预实验的质量。方法40只日本大耳白兔随机分为A（绞股蓝）组、B（辛伐他汀）组、C（高脂模型）组、E（对照组）组,分别喂饲高脂饲料＋绞股蓝5g,kg、高脂饲料＋辛伐他汀5mg／kg、高脂饲料、标准饲料。实验前和实验后3周、6周、9周检测三酰甘油（TG）、胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）。第7周和第9周进行CT检查。进行动脉和肝脏病理学检测。结果①TG、TC、LDL-C、HDL-C：A组、B组、C组饲养后TG、TC、LDL-C明显升高（P〈0．05）,A组和B组TG、TC、LDL-C低于C组（P〈0．05）,A组TG、HDL-C、LDL-C优于B组（P〈0．05）。②CT检查：饲养后7周、9周,A、B、C组CT值明显下降,比较有显著性差异（P〈0．05）,A组高于B组、C组（P〈0．01）,B组高于C组（P〈0．01）。③主动脉病理学：C组严重的大面积AS,A组和B组AS面积和程度显著低于C组（P〈0．01）。④肝脏病理学：A组、B组、C组肝脏弥漫性肿大,边缘钝而厚,灰黄色,A组较B组、C组肝脏色泽红润、肿大程度轻。A组2／3以上肝细胞发生脂肪样变。B、C组肝脏脂肪样变几乎为100％。结论肝脏CT值与AS的程度有一定的关系,可作为AS程度的量化指标,对指导实验过程有一定的价值。     

高位硬膜外阻滞用于乳腺癌改良根治术的临床观察

目的探讨1．33％利多卡因用于高位硬膜外阻滞乳腺癌改良根治术麻醉中对呼吸、循环功能的影响。方法选择ASAⅠ～Ⅱ级拟行乳癌根治术患者60例,随机分为1．33％利多卡因组（A组）和0．25％布比卡因组（B组）,每组各30例。于T2～3间隙行硬膜外穿刺,向头端置管,分别注入1．33％利多卡因或0．25％布比卡因。结果两组硬膜外阻滞效果均满意．注入局麻药后两组RR增加（P〈0．05）,BP降低（P〈0．05或〈0．01）,A组RR增加和BP下降幅度小于B组（P〈0．05或〈0．01）。硬膜外阻滞后A组SpO2维持在96％～97％,无呼吸困雌发生,8组出现轻度呼吸困难4例。结论1.33％利多卡因用于高位硬膜外阻滞施行乳腺癌改良根治术的麻醉效果满意,对通气功能的抑制比0．25％布比卡因轻。     

缬沙坦胶囊联合肾炎康复片治疗糖尿病微量蛋白尿的研究

目的：研究缬沙坦联合肾炎康复片治疗糖尿病微量蛋白尿的疗效及安全性。方法：采用随机、对照原则将60例有微量蛋白尿期糖尿病患者分为缬沙坦对照组（A组）和缬沙坦联合肾炎康复片治疗组（B组）,每组各30例。A组给予缬沙坦160mg,每日1次口服;B组给予肾炎康复片（薄膜衣片）每次5粒,每日3次口服和缬沙坦160mg,每日1次口服。疗程均为12w。比较2组治疗前、治疗第4、8和12w尿白蛋白排泄率（UAER）及治疗前、后肾功能、24h尿蛋白定量等生化指标的变化及肌酐50％倍增率。结果：2组治疗后血压、Scr、CRP指标均低于治疗前（P〈0．05）,而血FBG、PBG、HbAlc、Alb、BUN、24h尿蛋白定量指标变化无差异（P〉0．05）;B组治疗后与对照组比较,B组有较低Scr、CRP值（P〈0．05）,而余生化指标及血压变化无差异（P〉0．05）,B组第8、12w时尿蛋白排泄率下降幅度低于A组（P〈0．05）,B组治疗中12w的肌酐50％倍增率低于A组（P〈0．05）。结论：缬沙坦胶囊联合肾炎康复片治疗糖尿病微量蛋白尿是有效安全的。     

脂负荷性饵食对家兔脂代谢的影响

目的探讨建立兔饵食性高脂血症模型的方法,观察高脂饮食对兔体重、死亡率及血脂变化情况。方法取普通级雄性新西兰大耳白兔,其中随机抽取10只作为普通饮食组,喂以普通饮食;其他动物给予高脂饮食,4周后,根据血清TC水平分为高脂饮食敏感组和高脂饮食非敏感组,继续喂养9周,观察三组间兔血清总胆固醇（TC）、甘油三脂（TG）、高密度脂蛋白胆固醇（HDL-C）和低密度脂蛋白胆固醇（LDL-C）的变化。结果与普通饮食组相比,高脂饮食敏感组在第4～13周时血清TC、TG、HDL-C、LDL-C水平显著升高（P〈0.01）,高脂饮食非敏感组在第7～13周时,动物血清TC、HDL-C、LDL-C水平显著升高（P〈0.01）,而高脂饮食非敏感组血清TG水平的改变无统计学意义（P〉0.05）。与高脂饮食敏感组相比,高脂饮食非敏感组家兔血清TC、TG、HDL-C和LDL-C水平的上升程度均显著低于高脂饮食敏感组动物（P〈0.01）。结论首次发现兔对高脂饮食敏感性存在差异,高脂饮食非敏感组家兔抗病能力、对环境的适应能力和耐受性均高于高脂饮食敏感组兔。与高脂饮食敏感组家兔相比,高脂饮食非敏感组家兔对高脂饮食耐受性强。     

呼吸道合胞病毒感染促进豚鼠产生气道高反应性及其机制研究

目的：通过检测气道反应性和M2受体功能,研究呼吸道合胞病毒（RSV）感染与哮喘发病的关系及机制。方法：34只豚鼠随机分为4组：Hep-2滴鼻＋生理盐水雾化（Hep-2／NS,A）组,RSV滴鼻＋生理盐水雾化（RSV／NS,B）组,Hep-2滴鼻＋鸡卵蛋白（OVA）雾化（Hep-2／OVA,C）组和RSV滴鼻＋OVA雾化（RSV／OVA,D）组,其中A和B纽各9只,C和D组各8只,以A组为对照组。21d通过电刺激迷走神经检测各组气道反应性和M2受体功能,行嗜酸性粒细胞计数以及病理学观察。结果：B组气道内压力（mmH2O）与A组无明显差异（P〉0．05）,给予匹罗卡品,IP下降幅度高于A组,但差别无显著性（P〉0．05）。C组IP明显高于A且（P〈0．05）,且给予匹罗卡品,IP下降幅度明显低于A组,差别有显著性（P〈0．05）。D组IP明显高于C组（P〈0．05）,给予匹罗卡品后IP下降幅度明显低于C组（P〈0．05）。结论：RSV感染可促进过敏原引起的M2R功能障碍,从而促进AHR发生。     

新型酮康唑喷膜对豚鼠体癣模型疗效的观察

目的 观察新型酮康唑喷膜对豚鼠体癣模型的疗效。方法 选择健康豚鼠20只,用穿刺法制备豚鼠体癣模型。将体癣模型随机分A组（新型酮康唑喷膜治疗组）,B组（喷膜基质治疗组）,C组（复方酮康唑霜治疗组）和D组（对照组）。根据豚鼠皮疹和真菌学检查进行疗效评估。结果 A组和C组的豚鼠治疗后局部红斑和水肿明显减轻,与治疗前比较有显著意义（P〈0．05）;停药2周时,A组和C组真菌镜检、培养阴性率均为100％,明显高于B和D组（P〈0．05）。结论 新型酮康唑喷膜对豚鼠体癣模型有良好的抗真菌活性。     

胰岛素对糖尿病兔牙槽骨缺损修复的影响

目的：探讨胰岛素对糖尿病兔牙槽骨缺损修复治疗的效果,为糖尿病所致的牙周炎提供临床治疗的依据,方法：40只大耳白兔随机分为4组：A组制备健康兔的牙槽骨缺损;B组为胰岛素组,制备健康兔牙槽骨缺损后,用胰岛素治疗;C组为糖尿病组,制备糖尿病兔牙槽骨缺损;D组为糖尿病胰岛素治疗组,制备糖尿病兔牙槽骨缺损后,用胰岛素治疗。每组10只,缺损制备后4、8周各处死5只,对各组成骨情况进行组织学观察及测定。结果：组织学观察A、B、D组修复区可见大量新骨形成,以B组为显著;C组仅见少许成骨,多为纤维组织。新生骨面积比和成骨细胞数在4、8周时均为D组大于c组,B组大于A组,组间差异有统计学意义（P〈0．05）。证明应用胰岛素促进糖尿病兔缺损牙槽骨形成新骨的效果明显。结论：胰岛素能够促进糖尿病兔牙槽骨缺损的戍骨,为,临床上治疗糖尿病并发牙周炎提供一种新的手段。     

急性兔脑栓塞模型的建立

目的建立稳定的兔脑栓塞模型,以期为进一步开展脑栓塞的病理生理变化及影像学研究提供可靠实用的工具。方法30只健康新西兰兔,随机分成3组,其中A组3只,为空白对照组;B组5只,为假手术对照组;C组22只,为栓塞组。分离右侧颈部血管,经颈外动脉向颈内动脉注入直径约0.5~1.0 mm的SiO2颗粒10枚左右,栓塞后30 min行CT灌注检查,利用多层螺旋CT灌注成像对各组动物的脑缺血情况进行观察。24 h处死动物取脑组织进行病理研究。结果A、B组CT灌注及病理均未见异常。C组栓塞过程中3只兔死亡。16只兔CT灌注异常,表现为右侧局部CBF降低、MTT延长、CBV无明显变化或轻度上升、下降。3只兔灌注未见异常。HE染色可见8只兔脑梗塞,7只兔脑缺血,4只兔未见明显异常。结论采用该方法和技术能够建立稳定的兔脑栓塞模型,结果可靠,具有可操作性和重复性。     

Onset of pulsatile pressure causes transiently increased filtration through artery wall

Convective fluid motion through artery walls aids in the transvascular transport of macromolecules. Although many measurements of convective filtration have been reported, they were all obtained under constant transmural pressure. However, arterial pressure in vivo is pulsatile. Therefore, experiments were designed to compare filtration under steady and pulsatile pressure conditions. Rabbit carotid arteries were cannulated and excised from male New Zealand White rabbits anesthetized with pentobarbitol sodium (30 mg/kg i.v. administered). Hydraulic conductance was measured in cannulated excised rabbit carotid arteries at steady pressure. Next, pulsatile pressure trains were applied within the same vessels, and, simultaneously, arterial distension was monitored using Optical coherence tomography (OCT). For each pulse train, the volume of fluid lost through filtration was measured (subtracting volume change due to residual distension) and compared with that predicted from steady pressure measurements. At 60- and 80-mmHg baseline pressures, the experimental filtration volumes were significantly increased compared with those predicted for steady pressure (P < 0.05). OCT demonstrated that the excess fluid volume loss was significantly greater than the volume that would be lost through residual distension (P < 0.05). After 30 s, the magnitude of the excess of fluid loss was reduced. These results suggest that sudden onset of pulsatile pressure may cause changes in arterial interstitial hydration.     

阿托伐他汀联合普罗布考对动脉硬化家兔血流及斑块影响

目的:探讨阿托伐他汀钙片联合普罗布考治疗对兔颈动脉斑块稳定性的影响及血液流场改变。方法:选取清洁级日本大耳白兔40只,随机分为正常组、模型组、实验组、对照组,每组10只,复制颈动脉粥样硬化模型。对照组按照阿托伐他汀钙10 mg/(kg·d)的剂量,给兔按照不同体重予以不同药量治疗,将药物以生理盐水稀释至5 mL灌胃,实验组在对照组基础上加用普罗布考片0.25 g/(kg·d),与阿托伐他汀钙一同以生理盐水稀释至5 mL灌胃,模型组及正常组予以5 mL生理盐水灌胃。干预持续4周。用动物超声影像系统对兔进行颈动脉超声检查,彩色多普勒血流显像及血管成像检测颈动脉狭窄程度,血流速度,血流动力学改变。结果:1治疗后实验组阿托伐他汀钙片联合普罗布考治疗对兔颈动脉内-中膜厚度、斑块面积与模型组相比均明显改善,稳定斑块数明显增加,与对照组比较,实验组改善明显,差异有统计学意义(P0.05);2正常组颈动脉正常,治疗后,实验组狭窄明显减轻,血流速度接近正常,对照组有所改善,模型组颈动脉狭窄程度最重,血流速度快,血流动力学发生改变,斑块不稳定性增加,差异有统计学意义(P0.05)。结论:阿托伐他汀钙片联合普罗布考治疗能够有效提高兔颈动脉粥样硬化斑块的稳定性,改善颈动脉狭窄,使血液流速接近正常水平,值得做进一步药理研究及深入探讨。     

胶原/纤维蛋白止血效果观察

目的研究胶原/纤维蛋白对新西兰兔的止血作用,并与胶原蛋白海绵止血效果作比较。方法选用胶原/纤维蛋白止血贴,对新西兰兔耳部动、静脉出血、耳表创面、股动脉割伤、肝损伤、体表创面进行止血试验,同时与胶原蛋白海绵止血效果作比较,观察其止血时间、失血量、敷料与创面的粘合等情况,并定期观察创面愈合、体内吸收和抗炎情况。结果胶原/纤维蛋白复合止血贴组、胶原蛋白海绵组新西兰兔耳动、静脉、耳表创面、股动脉割伤、标准肝创伤的止血时间与对照组比较,差异显著（P〈0.05）。胶原/纤维蛋白复合止血贴组新西兰兔耳动、静脉、耳表创面的止血时间与胶原蛋白海绵组,差异显著（P〈0.05）。胶原/纤维蛋白复合止血贴组、胶原蛋白海绵组动物的耳表创面、标准肝创伤失血量与对照组比较,差异显著（P〈0.05）。体内标准肝创伤、体表创伤后期观察,胶原/纤维蛋白复合止血贴与胶原蛋白海绵均能在21d内完全吸收,未见炎症反应。结论胶原/纤维蛋白复合止血贴对新西兰兔耳动脉割伤、耳静脉割伤、耳标创伤、股动脉割伤和标准肝损伤模型都具有明显的止血作用,体表创面伤口恢复良好,体内吸收速度快,具有一定的抗炎作用,而且在新西兰兔耳动脉、耳静脉割伤和耳表创伤的止血效果明显优于胶原蛋白海绵。胶原/纤维蛋白复合止血贴是一种较安全有效的局部止血生物材料。     

Correlation between quantitative analysis of wall shear stress and intima-media thickness in atherosclerosis development in carotid arteries

Background

This paper presents quantitative analysis of blood flow shear stress by measuring the carotid arterial wall shear stress (WSS) and the intima-media thickness (IMT) of experimental rabbits fed with high-fat feedstuff on a weekly basis in order to cause atherosclerosis.

Methods

This study is based on establishing an atherosclerosis model of high-fat rabbits, and measuring the rabbits’ common carotid arterial WSS of the experimental group and control group on a weekly basis. Detailed analysis was performed by using WSS quantification.

Results

We have demonstrated small significant difference of rabbit carotid artery WSS between the experimental group and the control group (P<0.01) from the 1st week onwards, while the IMT of experimental group had larger differences from 5th week compared with the control group (P<0.05). Next, we have shown that with increasing blood lipids, the rabbit carotid artery shear stress decreases and the rabbit carotid artery IMT goes up. The decrease of shear stress appears before the start of IMT growth. Furthermore, our receiver operator characteristic (ROC) curve analysis showed that when the mean value of shear stress is 1.198 dyne/cm², the rabbit common carotid atherosclerosis fatty streaks sensitivity is 89.8%, and the specificity is 81.3%. The area under the ROC curve is 0.9283.

Conclusions

All these data goes to show that WSS decreasing to 1.198 dyne/cm² can be used as an indicator that rabbit common carotid artery comes into the period of fibrous plaques. In conclusion, our study is able to find and confirm that the decrease of the arterial WSS can predict the occurrence of atherosclerosis earlier, and offer help for positive clinical intervention.

     

CAS和CEA治疗颈内动脉重度狭窄疗效及对脑血流量、血清miR-145、IGF1R的影响

目的:探讨颈动脉支架植入术(CAS)和颈动脉内膜剥脱术(CEA)治疗颈内动脉重度狭窄疗效及对脑血流量、血清miR-145、胰岛素样生长因子1受体(IGF1R)的影响。方法:回顾性分析2018年1月至2019年12月我院收治的100例颈动脉重度狭窄患者的临床资料,按照手术方式不同分为A组和B组,每组50例,A组给予CAS治疗,B组给予CEA治疗。比较两组围术期情况、脑血流量、血清miR-145、IGF1R、简易精神状态检查表(MMSE)量表、蒙特利尔认知评估量表(MoCA)的变化,并比较术后并发症、再狭窄率及死亡率。结果:两组患者手术时间、术中失血量、术后机械通气时间、ICU停留时间、住院时间比较,差异无统计学意义(P>0.05);术后3个月时,两组脑血流量指标相对达峰时间(rTTP)、相对平均通过时间(rMTT)、相对脑血容量(rCBV)、相对脑血流量(rCBE)、血清miR-145、IGF1R、MMSE量表、MoCA量表评分比较差异均无统计学意义(P>0.05);术后30 d内,两组心动过缓、心肌酶谱升高、高灌注综合征、局部血肿、颈动脉急性闭塞比较差异无统计学意义(P>0.05),A组脑卒中、低血压发生率明显高于B组,B组高血压发生率明显高于A组(P<0.05);术后1年时,两组患者死亡率、再狭窄率比较差异无统计学意义(P>0.05)。结论:CAS和CEA治疗颈内动脉重度狭窄患者的疗效相似,均可有效改善脑血流量,调节血清miR-145、IGF1R水平的表达,促进认知功能恢复,但CAS术后脑卒中、低血压发生率更高,CEA术后高血压发生率更高。     

肾动脉射频消融对兔压力负荷性高血压的作用研究

目的：建立新西兰兔的高血压模型和观察肾动脉射频消融（Renal Sympathetic Denervation,RSD）对高血压的影响。方法：通 过腹主动脉内径缩窄50%~60%建立兔高血压模型,建模后分为假手术对照组、对照组+ 射频组、高血压组、高血压+ 射频组4 组,建模2个月后使用临床常用的射频消融导管经腹进行双侧肾动脉外膜消融去除肾交感神经,术后继续饲养2 个月,通过颈动 脉插管测定血压数值变化。结果：通过腹主动脉缩窄术成功建立新西兰兔压力负荷高血压模型。RSD 术后2月,新西兰兔的心率 无明显区别（P>0.05）,高血压组的血压仍然明显高于对照组（P<0.05）,然而,高血压+射频组的血压低于高血压组（P<0.05）;同时 对照+射频组与对照组的血压无明显差异(P>0.05)。结论：通过腹主动脉缩窄术可以稳定地建立新西兰兔压力负荷高血压模型, 经RSD 后血压明显下降,且这种降压作用只对高血压有作用。我们首次从动物水平验证RSD可以降低压力负荷导致的血压升 高。     

The neurohypophyseal capillary bed. I. Anatomy and arterial supply.

Vascular casts of the pituitary-median eminence complex of mice,rats, dogs, sheep and monkeys were examined with the scanning electron microscope. Microfil-injected specimens of the rabbit and monkey pituitary-median eminence complex were examined by light microscopy after intracranial internal carotid artery occlusion. In each species a common neuropophyseal capillary network was found uniting infundibulum (median eminence), infundibular stem and infundibular process. This capillary bed is supplied from above by superior hypophyseal arteries and from below by inferior hypophyseal arteries. An artery to the infundibular stem was found in some species. With occlusion of the intracranial internal carotid arteries, flow through superior hypophyseal arteries did not occur. Yet the entire neurohypophyseal capillary bed filled upon injection with Microfil. These observations suggest the concept of a restricted arterial supply to the median eminence with drainage to the underlying adenohypophsis on one hand and to the infundibular process with drainage to the systemic circulation on the other must be modifed and that blood flow within the neurohypophyseal capillary bed (between infundibular process and median eminence) occurs.     

Myocardial ischaemia following electrical stimulation of the left circumflex coronary artery in sheep: a role for thromboxane A2?

The electrical stimulation model of thrombus formation was tested on rabbit carotid artery and adapted to sheep left circumflex coronary artery (LCCA). LCCA blood flow, mean arterial pressure (MAP), heart rate (HR) and ECG were monitored continuously and arterial and coronary venous blood samples were taken for radioimmunoassay of thromboxane B2. Stimulation of the LCCA mimicked acute myocardial infarction; reduction in LCCA blood flow preceded a fall in MAP and appearance of ECG abnormalities. Thromboxane B2 levels rose by 126% 35 min after stimulation. These findings support the proposal by other authors that thromboxane plays an important role in the pathogenesis of acute myocardial infarction.     

Freeze-dried microarterial allografts

Rehydrated freeze-dried microarterial allografts were implanted to bridge arterial defects using New Zealand White rabbits as the experimental model. Segments of artery from the rabbit ear and thigh were harvested and preserved for a minimum of 2 weeks after freeze-drying. These allografts, approximately 1 mm in diameter and ranging from 1.5 to 2.5 cm in length, were rehydrated and then implanted in low-pressure and high-pressure arterial systems. Poor patency was noted in low-pressure systems in both allografts and autografts, tested in 12 rabbits. In the high-pressure arterial systems, allografts that were freeze-dried and reconstituted failed in a group of 10 rabbits with an 8-week patency rate of 30 percent. Gamma irradiation in an effort to reduce infection and antigenicity of grafts after freeze-drying was associated with a patency rate of 10 percent at 8 weeks in this system in another group of 10 rabbits. Postoperative cyclosporin A therapy was associated with a patency rate of 22.2 percent in the high-pressure arterial system in a 9-rabbit group. Control autografts in this system in a group of 10 rabbits showed a 100 percent patency at 8 weeks. Microarterial grafts depend on perfusion pressure of the vascular bed for long-term patency. Rehydrated freeze-dried microarterial allografts do not seem to function well in lengths of 1 to 2.5 cm when implanted in a high-pressure arterial system. Freeze-dried arterial allografts are probably not antigenic.     

Influence of experimental diabetes on regulatory mechanisms of vascular response of rabbit carotid artery to acetylcholine

The purpose of this study was to analyse the influence of experimental diabetes on vascular response of rabbit carotid artery to acetylcholine (Ach). We compared the Ach-induced relaxant response of isolated arterial segments obtained from both control and diabetic animals. To assess the influence of the endothelium, this cell layer was mechanically removed in some of the arterial segments ("rubbed arteries") from each experimental group. Ach induced a concentration-related endothelium-mediated relaxation of carotid artery from control rabbits that was significantly higher with respect to that obtained in diabetic animals. Pre-treatment with N(G)-nitro-L-arginine (L-NA) induced a concentration-dependent inhibition of relaxant response to Ach, which was significantly higher in carotid arteries isolated from diabetic rabbits. Incubation of rubbed arteries with L-NA almost abolished the relaxant response to Ach in arterial segments from both control and diabetic animals. Indomethacin potentiated Ach-induced response of carotid arteries from control rabbits, without modifying that obtained in those from diabetic animals. Aminoguanidine did not significantly inhibit the relaxant action of Ach in arterial segments from either control or diabetic rabbits. These results suggest that diabetes impairs endothelial modulatory mechanisms of vascular response of rabbit carotid artery to Ach. This endothelial dysfunction is neither related with a lower release of nitric oxide (NO) or prostacyclin. Diabetes impairs the production of some arachidonic acid vasoconstrictor derivative. There has been observed an increased modulatory activity of NO, but this is not related with the expression of an inducible isoform of NO synthase.