丁苯酞软胶囊治疗脑小血管病的临床研究

目的探讨丁苯酞软胶囊治疗脑小血管病的临床疗效。方法选取2016年3月—2018年2月在天津中医药大学第一附属医院就诊的脑小血管病患者100例,随机分为对照组(50例)和治疗组(50例)。对照组给予常规治疗,治疗组在此基础上口服丁苯酞软胶囊,2粒/次,3次/d,持续治疗2个月。观察两组患者临床疗效,同时比较治疗前后两组患者NIHSS、Fugl-Meyer量表、MBI评分,反应性充血指数(RHI)和内皮祖细胞(EPCs)数以及细胞因子水平。结果治疗后,对照组临床有效率为60.0%,显著低于治疗组的76.0%,两组比较差异具有统计学意义(P0.01)。治疗后,两组NIHSS评分显著降低,FMA-UE、FMA-LE、MBI评分显著升高,同组治疗前后比较差异具有统计学意义(P0.05、0.01);且治疗后治疗组上述评分均显著优于对照组,两组比较差异具有统计学意义(P0.05、0.01)。两组RHI、EPCs均较治疗前明显升高,同组治疗前后比较差异具有统计学意义(P0.05);且治疗后治疗组RHI、EPCs明显高于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者血清ET-1、v WF水平均显著降低,NO水平显著升高,同组治疗前后比较差异具有统计学意义(P0.05、0.01);且治疗后治疗组上述血清细胞因子水平显著优于对照组,两组比较差异具有统计学意义(P0.05、0.01)。结论丁苯酞软胶囊能显著改善脑小血管病患者的运动功能和生活自理能力,增加外周血EPCs数目、有效调节ET-1/NO平衡,具有一定的临床应用价值。     

丁苯酞软胶囊治疗急性脑梗死的疗效观察

目的探讨丁苯酞软胶囊治疗急性脑梗死的临床疗效。方法选取2013年6月—2016年6月博罗县人民医院收治的急性脑梗死患者104例,所有患者采用随机数字表法分为对照组和治疗组,每组各52例。对照组给予常规治疗,包括脱水降颅内压、服用阿司匹林抗凝、阿替普酶或尿激酶静脉溶栓、依达拉奉改善脑循环、服用脑保护剂等,并根据患者情况进行原发病对症治疗。治疗组在对照组基础上口服丁苯酞软胶囊,0.2 g/次,2次/d。两组患者均连续治疗2周。观察两组的临床疗效,比较美国国立卫生研究院卒中量表(NHISS)评分、Barthel指数、血液流变学、颈总动脉后壁内中膜厚度(IMT)和颈总动脉血流阻力指数(RI)。结果治疗后,对照组和治疗组的总有效率分别为69.23%、90.38%,两组比较差异具有统计学意义(P0.05)。治疗后,两组全血黏度、血浆黏度、纤维蛋白原水平均显著降低,而血细胞比容显著升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组NIHSS评分显著下降,而Barthel指数显著上升,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组IMT和RI均显著降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标明显低于对照组,两组比较差异具有统计学意义(P0.05)。结论丁苯酞软胶囊治疗急性脑梗死具有较好的临床疗效,可显著改善神经功能缺损情况,提升生活质量,降低血液黏稠度,改善颈动脉粥样硬化,具有一定的临床推广应用价值。     

丁苯酞联合尼莫地平治疗血管性认知障碍的临床观察

目的探讨丁苯酞联合尼莫地平治疗血管性认知障碍的临床效果。方法选取2011年6月—2015年5月陕西省第二人民医院收治的血管性认知障碍患者72例,随机分为对照组和治疗组,每组各36例。对照组口服尼莫地平片,30 mg/次,3次/d。治疗组在对照组基础上口服丁苯酞软胶囊,0.2 g/次,4次/d。两组均治疗8周。观察两组的临床疗效,比较治疗前后双侧大脑前动脉(ACA)、双侧大脑中动脉(MCA)、双侧大脑后动脉(PCA)、双侧椎动脉(VA)和基底动脉(BA)平均血流速度、蒙特利尔认知评估量表(MOCA)评分、简易智力状态检查量表(MMSE)评分、神经元特异性烯醇化酶(NSE)、血栓素B2(TXB2)的变化。结果治疗后,对照组和治疗组的总有效率分别为72.22%、91.67%,两组比较差异有统计学意义(P0.05)。治疗后,两组双侧ACA、双侧MCA、双侧PCA、双侧VA和BA平均血流速度均上升,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的上升程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组MMSE和MOCA评分均上升,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的上升程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组TXB2和NSE水平均降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的下降程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。结论丁苯酞联合尼莫地平治疗血管性认知障碍具有较好的临床疗效,可改善认知功能和脑血液循环,降低炎症因子水平,安全性较好,具有一定的临床推广应用价值。     

丁苯酞联合阿替普酶治疗急性缺血性脑梗死的临床研究

目的观察丁苯酞氯化钠注射液、丁苯酞软胶囊联合注射用阿替普酶治疗急性缺血性脑梗死的临床疗效。方法选取2013年10月—2016年3月在潍坊市中医院的缺血性脑梗死患者60例作为研究对象,所有患者随机分为对照组和治疗组,每组各30例。对照组给予注射用阿替普酶0.9 mg/kg,首先1 min内静脉推注总量的10%,然后60 min静脉泵入剩余90%,最大剂量90 mg。治疗组在对照组基础上静脉滴注丁苯酞氯化钠注射液100 m L/次,2次/d,连续治疗14 d,然后改为口服丁苯酞软胶囊0.2 g/次,3次/d,连续治疗90 d。观察两组的临床疗效,比较两组的美国国立卫生研究院卒中量表(NIHSS)评分和血清基质金属蛋白酶-9(MMP-9)水平情况。结果治疗后,对照组和治疗组的总有效率分别为83.3%、93.3%,两组比较差异有统计学意义(P0.05)。治疗7、14、90 d后,两组NIHSS评分均显著下降,同组治疗前后比较差异有统计学意义(P0.05);且同期治疗组这些观察指标的下降程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗7、14 d后,两组MMP-9水平均显著下降,同组治疗前后比较差异有统计学意义(P0.05);且同期治疗组这些观察指标的下降程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。结论丁苯酞氯化钠注射液、丁苯酞软胶囊联合注射用阿替普酶治疗急性缺血性脑梗死具有较好的临床疗效,可改善神经功能损伤,降低血清MMP-9水平,具有一定的临床推广应用价值。     

丁苯酞软胶囊联合依达拉奉治疗脑梗死的临床研究

目的研究丁苯酞软胶囊联合依达拉奉注射液治疗脑梗死的临床疗效。方法选取2015年8月—2016年7月常德市第一人民医院收治的脑梗死患者86例,按照治疗方案不同分为对照组和治疗组,每组各43例。对照组静脉滴注依达拉奉注射液,30 mg加入到生理盐水150 mL中,2次/d。治疗组在对照组基础上口服丁苯酞软胶囊,0.2 g/次,3次/d。两组患者均连续治疗14 d。观察两组的临床疗效,比较两组的血清神经营养因子、炎症反应、神经功能评分和日常生活能力(ADL)评分情况。结果治疗后,对照组和治疗组的总有效率分别为74.42%、93.02%,两组比较差异有统计学意义(P0.05)。治疗后,两组神经元特异性烯醇化酶(NSE)水平显著降低,神经生长因子(NGF)和脑源性神经营养因子(BDNF)水平显著升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组白细胞介素-8(IL-8)、白细胞介素-10(IL-10)和C反应蛋白(CRP)水平明显降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的下降程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组神经功能评分明显降低,ADL评分明显升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度明显优于对照组,两组比较差异有统计学意义(P0.05)。结论丁苯酞软胶囊联合依达拉奉注射液治疗脑梗死具有较好的临床疗效,能改善神经功能和日常生活能力,调节血清神经营养因子和炎症反应,安全性较好,具有一定的临床推广应用价值。     

丁苯酞软胶囊联合多奈哌齐治疗阿尔茨海默病的临床研究

目的探讨丁苯酞软胶囊联合多奈哌齐片治疗阿尔茨海默病的临床疗效。方法选取2014年3月—2018年3月于武汉市第三医院光谷院区治疗的150例阿尔茨海默病患者为研究对象,将患者按随机数表法分为对照组和治疗组,每组各75例。对照组于睡前口服多奈哌齐片,2次/d,起始剂量为1片/次,2周后调整剂量为2片/次。治疗组在对照组基础上口服丁苯酞软胶囊,3次/d,起始剂量为1粒/次,逐渐增加剂量,4周后调整剂量为2粒/次。两组均连续治疗6个月。观察两组的临床疗效,比较两组的简易精神状态量表(MMSE)评分、认知功能评定量表(ADAS-cog)评分、日常生活能力量表(ADL)评分、大脑后动脉血流速度、血清因子水平。结果治疗后,对照组和治疗组的总有效率分别为77.33%、90.67%,两组比较差异有统计学意义(P0.05)。治疗后,两组MMSE评分均显著提高,ADAS-cog评分和ADL评分均显著降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组的MMSE评分、ADAS-cog评分和ADL评分明显优于对照组,差异有统计学意义(P0.05)。治疗后,治疗组患者左右侧大脑后动脉刺激期血流速度、静息期血流速度和平均血流速度均显著高于对照组,差异具有比较意义(P0.05)。治疗后,两组患者同型半胱氨酸(Hcy)、尿酸(UA)水平均显著下降,人β淀粉样蛋白1-42(Aβ1-42蛋白)水平显著升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组血清因子水平显著优于对照组,差异具有比较意义(P0.05)。结论丁苯酞软胶囊联合多奈哌齐片治疗阿尔茨海默病具有较好的临床疗效,能改善患者认知功能,促进大脑后动脉血流速度,调节血清因子水平,安全性较好,具有一定的临床推广应用价值。     

丁苯酞软胶囊联合神经节苷脂治疗急性分水岭脑梗死的临床研究

目的探讨丁苯酞软胶囊联合注射用单唾液酸四己糖神经节苷脂钠治疗急性分水岭脑梗死的临床疗效。方法选取2016年1月—2017年10月郑州市第九人民医院收治的急性分水岭脑梗死患者76例作为研究对象,根据随机数字表法将所有患者分为对照组和治疗组,每组各38例。对照组静脉滴注注射用单唾液酸四己糖神经节苷脂钠,100 mg加入到0.9%氯化钠注射液250 m L中,1次/d。治疗组在对照组治疗的基础上口服丁苯酞软胶囊,0.2 g/次,3次/d。两组患者均连续治疗2周。观察两组的临床疗效,比较两组的美国国立卫生研究院卒中量表(NIHSS)评分、Barthel指数(BI)评分、促血栓形成因子和血液流变学指标。结果治疗后,对照组和治疗组的总有效率分别为71.05%、89.47%,两组比较差异有统计学意义(P0.05)。治疗后,两组NIHSS评分显著降低,BI评分明显升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组NIHSS评分和BI评分明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组抗凝血酶Ⅲ(ATⅢ)水平明显升高,血小板聚集率(PAG)、纤维蛋白原(FIB)、D-二聚体(DD)水平明显降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组促血栓形成因子水平明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组血浆黏度(PV)、全血高切黏度(HBV)、全血低切黏度(LBV)、红细胞聚集指数(Arbc)水平显著降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组血液流变学指标水平明显低于对照组,两组比较差异具有统计学意义(P0.05)。结论丁苯酞软胶囊联合注射用单唾液酸四己糖神经节苷脂钠治疗急性分水岭脑梗死具有较好的临床疗效,可调节促血栓形成因子和血液流变学指标,改善神经功能,提升日常生活能力,具有一定的临床推广应用价值。     

养血清脑颗粒联合丁苯酞软胶囊治疗轻中度脑梗死的临床研究

目的探讨养血清脑颗粒联合丁苯酞软胶囊治疗轻中度脑梗死的临床疗效。方法选取2017年1月—2018年12月在三门峡市中心医院就诊的92例轻中度脑梗死患者为研究对象,按照随机数字表法将全部患者分为对照组和治疗组,每组各46例。对照组口服丁苯酞软胶囊,200 mg/次,3次/d。治疗组在对照组治疗的基础上温水冲服养血清脑颗粒,4 g/次,3次/d。两组患者连续治疗20 d。观察两组的临床疗效,比较两组的血液流变学、血管内皮功能指标、美国国立卫生研究院卒中量表(NIHSS)评分。结果治疗后,对照组和治疗组的总有效率分别为80.43%、93.48%,两组比较差异有统计学意义(P0.05)。治疗后,两组全血黏度、血浆黏度、D-二聚体、纤维蛋白原水平均明显降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗后,治疗组的全血黏度、血浆黏度、D-二聚体、纤维蛋白原水平明显低于对照组,两组差异有统计学意义(P0.05)。治疗后,两组一氧化氮(NO)水平明显升高,内皮素-1(ET-1)、血栓素A2(TXA2)水平均明显降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗后,治疗组的NO水平高于对照组,ET-1、TXA2水平低于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组NIHSS评分显著降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗后,治疗组的NIHSS评分低于对照组,两组差异有统计学意义(P0.05)。结论养血清脑颗粒联合丁苯酞软胶囊治疗轻中度脑梗死具有较好的临床疗效,可改善血液流变学和血管内皮功能,有助于降低神经功能缺损程度,具有一定的临床推广应用价值。     

丁苯酞软胶囊联合尤瑞克林治疗急性脑梗死疗效的研究

目的探讨丁苯酞软胶囊联合尤瑞克林治疗急性脑梗死的疗效。方法选择100例2015年10月~2016年10月住院治疗的急性脑梗死患者进行研究,所有患者随机分组,每组50例。对照组接受常规治疗,研究组在此基础上给予丁苯酞软胶囊联合尤瑞克林治疗。治疗前后进行NIHSS评分,治疗后观察临床疗效。结果 NIHSS评分治疗后两组均显著较治疗前低,差异无统计学意义(P0.05);研究组NIHSS治疗后较对照组低,差异有统计学意义(P0.05)。两组总有效率比较,研究组显著高于对照组,差异有统计学意义(P0.05)。结论丁苯酞软胶囊联合尤瑞克林治疗急性脑梗死具有较好的临床疗效,能显著改善神经功能。     

丁苯酞联合银杏叶提取物注射液治疗大面积脑梗死的临床研究

目的探讨丁苯酞联合银杏叶提取物注射液治疗大面积脑梗死的临床疗效。方法选取2012年6月—2015年6月于威海市中心医院神经内科住院的大面积脑梗死患者130例为研究对象,所有患者按就诊时间先后顺序随机分为对照组和治疗组,每组各65例。对照组静脉滴注银杏叶提取物注射液,70 mg加入到生理盐水250 mL,1次/d,连续使用21 d。治疗组在对照组基础上静脉滴注丁苯酞氯化钠注射液,100 mL/次,2次/d,连续使用14 d,然后改为口服丁苯酞软胶囊,0.2 g/次,3次/d,连续使用7 d。观察两组的临床疗效,比较两组的美国国立卫生研究院卒中量表(NIHSS)评分、日常生活能力量表(ADL)评分和血浆脂蛋白相关性磷脂酶A2(LP-PLA2)水平。结果治疗后,对照组和治疗组的总有效率分别为73.85%、93.85%,两组比较差异有统计学意义(P0.05)。治疗后,两组NIHSS评分均显著降低,ADL评分均显著升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗10、21 d后,两组血浆LP-PLA2水平均显著下降,同组治疗前后比较差异有统计学意义(P0.05);且治疗组LP-PLA2水平明显低于对照组,两组比较差异具有统计学意义(P0.05)。结论丁苯酞联合银杏叶提取物注射液治疗大面积脑梗死具有较好的疗效,可改善神经功能缺损和日常生活活动能力,调节血浆LP-PLA2水平,安全性较好,具有一定的临床推广应用价值。     

非痴呆性血管性认知功能障碍的中、西医研究现况

非痴呆性血管性认知功能障碍是血管性认知功能障碍的早期阶段,具有可逆性,故对该病的防治倍受关注。本文就目前中、西医对非痴呆性血管性认知功能障碍的认识及其治疗方法作一概述,以期为该病的临床治疗和科研活动提供一些新思路。     

Tissue levels of cephradine in ischaemic limbs following a single intravenous injection

Summary

A single dose of 2g cephradine was administered intravenously at the time of anaesthetic induction to 20 patients with occlusive arterial disease. Concentrations of cephradine were measured in serum, subcutaneous fat from the groins of 10 patients undergoing arterial reconstruction and in the subcutaneous fat and skeletal muscle of 10 legs amputated for severe arterial ischaemia. Concentrations of cephradine were adequate for antibacterial prophylaxis at the time of operation in all serum samples, 9 out of 10 samples of subcutaneous fat from reconstruction cases, all muscle and 8 of 10 fat samples from the level of section of amputated limbs, and in 8 of 10 muscle and fat samples from the distal parts of amputated limbs. These results confirm that a single intravenous dose of 2?g cephradine given with anaesthetic induction provides adequate serum and tissue concentrations for antibacterial prophylaxis during vascular surgery.     

Renal and iliac vascular effects of dopamine in the anaesthetized rat

Summary The renal and iliac vascular effects of dopamine were compared in pentobarbital anaesthetized rats. Local vascular resistances were calculated from simultaneous measurement of blood pressure, renal and iliac blood flow. Without pretreatment, dopamine increased renal and iliac vascular resistance. After pretreatment with prazosin, dopamine decreased the renal vascular resistance while the iliac vascular resistance was still increased. After a combination of yohimbine and prazosin pretreatment, dopamine lowered both the renal and iliac vascular resistance by 30%. These responses were not modified by the beta-adrenoceptor antagonist, sotalol, or by pretreating the rats with reserpine. The renal but not the iliac vascular response to dopamine was abolished by (+)-butaclamol, a stereoselective dopamine receptor antagonist, and by SCH 23390, the DA₁-selective dopamine receptor antagonist. The decrease in iliac vascular resistance was not modified by indomethacin or the non-selective 5-HT receptor antagonist, metitepin. These results show that after blockade of alpha₁ and alpha₂-adrenoceptors, dopamine induces iliac vasodilation by a postsynaptic mechanism independent of an interaction with beta-adrenoceptors, dopamine or serotonin receptors. They also confirm in the rat in vivo the existence of renal vasodilation mediated by DA₁ dopamine receptors. Send offprint requests to: M. Schmidt at the above address     

A study on tissue concentrations of cephradine achieved in patiens with peripheral vascular disease

Summary

The levels of cephradine were measured in serum, voluntary muscle and subcutaneous fat samples collected from 30 patients during surgical operations for peripheral vascular disease. Cephradine 2 g was administered in two equal doses by intramuscular and intravenous routes before each operation. The mean levels found in the serum and muscle were well above the minimum inhibitory concentrations required for most important Gram-positive and Gram-negative pathogens, in contrast to the relatively low mean level found in subcutaneous fat.     

皂苷类成分对血管内皮细胞功能的调节作用研究进展

血管内皮细胞在维持血管生理稳态中发挥了重要的作用,其功能障碍是动脉粥样硬化、冠心病、脑卒中、肿瘤等多种重大疾病发生发展的病理基础,调节血管内皮细胞功能是防治上述疾病的主要途径之一。大量研究表明,皂苷类成分可通过改善血管内皮功能达到治疗疾病的目的。综述了近年来报道的皂苷类成分调节血管内皮功能的研究进展,旨在为皂苷类成分作用机制的阐明和相关重大疾病的防治提供一定参考。     

Differential effects of the adenosine A1 receptor agonist adenosine amine congener on renal, femoral and carotid vascular conductance in preterm fetal sheep

1. Adenosine A(1) receptor activation is critical for endogenous neuroprotection from hypoxia-ischaemia, raising the possibility that treatment with A(1) receptor agonists may be an effective physiological protection strategy for vulnerable preterm infants. However, the A(1) receptor can mediate unwanted systemic effects, including vasoconstriction of the afferent glomerular arteriole. There is limited information on whether this occurs at doses that improve cerebral perfusion in the immature brain. 2. Therefore, in the present study, we examined whether infusion of the selective A(1) receptor agonist adenosine amine congener (ADAC) is associated with reduced renal perfusion in chronically instrumented preterm (0.7 gestation) fetal sheep. In the present study, ADAC was given in successive doses of 2.5, 5.0 and 15.0 microg, 45 min apart. 3. Treatment with ADAC was associated with a marked reduction in renal vascular conductance (and blood flow), whereas carotid conductance was increased and there was no significant effect on femoral conductance. In contrast with the stable effects of increasing ADAC dose on vascular conductance, there was a significant dose-related fall in fetal heart rate and blood pressure. 4. In conclusion, these short-term data support the concern that A(1) receptor agonist infusion can selectively impair renal perfusion, even at low doses.     

阿司匹林铜对离体兔主动脉血管条收缩的影响(英文)

目的:观察阿司匹林铜对离体免胸主动脉血管平滑肌的作用。方法:取免胸主动脉条,观察阿司匹林铜对去甲肾上腺素(NE)、KCl、CaCl_2诱导收缩作用的影响。结果:证实阿司匹林铜和对照物硫酸铜拮抗NE诱导的兔胸主动脉条收缩,IC_(50)分别为31nmol/L和0.29μmol/L,而阿司匹林本身没有拮抗作用。阿司匹林铜对KCl、CaCl_2诱导的收缩没有影响。在去内皮细胞兔胸主动脉条上,观察到相同的作用。结论:阿司匹林铜具有较强的拮抗NE诱导离体兔胸主动脉条收缩的作用,但不能拮抗KCl、CaCl_2诱导的收缩,提示阿司匹林铜通过阻断受体调控钙通道,舒张血管平滑肌。     

皮质下缺血性血管性痴呆的MRI相关高危因素研究

目的探索皮质下缺血性脑血管病MRI表现与血管性痴呆之间的关系。方法对比分析40例皮质下多发梗死痴呆患者和45例皮质下多发梗死非痴呆患者的MRI表现,采用Logistic回归分析皮质下缺血性血管性痴呆的影像学相关高危因素。结果经logistic多因素分析后,只有平均脑沟宽度（OR=2．740,P=0．017）、侧脑室指数（OR=1．767,P=0．012）和丘脑梗死的数目（OR=5．807,P=0．036）进入了方程。结论皮质下缺血性血管性痴呆可能与脑萎缩的程度和丘脑梗死的数目密切相关。     

New perspectives on vascular wall signaling: role of perivascular adipocytes and fibroblasts

This communication represents personal perspectives of recent development in the newly evolved areas in vascular signaling mechanisms at the anatomical level of vascular walls from outside in, that is, from perivascular adventitial side to effectuate the control of vascular reactivity. Since half a century ago, the focus of interest in vascular biology has been confined primarily to the study of the excitation-contraction coupling of vascular smooth muscle (VSM) as well as neuroeffector mechanisms. During the past 3 decades, considerable advancement in the understanding of vascular signaling has been made via the discovery of endothelium-derived relaxation factors (EDRF), endothelium-derived hyperpolarizing factors (EDHF) and endothelium-derived contracting factors (EDCF). The discovery of nitric oxide (NO) as a major cellular messenger has also helped open up another huge area of research in oxidative stress and vascular diseases. In the past decade, concepts on vascular wall signaling have been extended from vascular endothelial cells and then translated to the other seemingly inert cellular components, such as perivascular adipocytes and adventitial fibroblasts. Growing body of evidences show that these cellularities contribute to both functional as well as structural integrity in vasculature with significant pathophysiological implications.     

Vascular effects of loop diuretics: an in vivo and in vitro study in the rat

The vascular effects of loop diuretics were studied in two models designed to eliminate hemodynamic repercussions linked to sodium and water depletion: in vivo, in unilaterally nephrectomized rats with a contralateral uretero-venous shunt, and in vitro, in the isolated perfused rat kidney.In anesthetized rats, local vascular resistance was calculated from the simultaneous recording of blood pressure and renal, iliac and carotid blood flows (electromagnetic flowmeter, Skalar). Furosemide and piretanide (10 to 80 mg/kg i. v.) induced a comparable dose-dependent decrease in renal vascular resistance, which was not modified by reserpine and indomethacin pre-treatment. The iliac relaxing response was blunted by vasoconstriction, which disappeared after combined treatment with reserpine and indomethacin. The relaxation induced in the iliac and carotid vasculature persisted after bilateral nephrectomy.In vitro, the vasorelaxing effect of diuretics in isolated rat kidneys perfused in an open circuit was studied after vascular tone had been re-established by a continuous perfusion of PGF₂. Furosemide, piretanide and ozolinone induced a concentration-dependent decrease in renal tone (EC₅₀ = 0.47 × 10-4 mol/l, 1.03 × 10^–4 mol/l and 2.07 × 10^–4 mol/l respectively) in Wistar rats. A similar response to piretanide was found in spontaneously hypertensive stroke-prone rats (EC₅₀ = 0.32 × 10^–4 mol/l) and in their normotensive controls (EC_SO = 0.74 × 10^–4 mol/l).Our results show that loop diuretics induce a direct relaxation in the renal, iliac and carotid vasculature. This vascular effect, which appears at relatively high concentrations of the drugs, is prostaglandin independent and persists after bilateral nephrectomy. Correspondence to: M. Barthelmebs at the above address