不同中医治法对帕金森病大鼠6-酮前列腺素、血栓素B_2和内皮素的影响

目的研究不同中医治法对帕金森病(PD)大鼠内皮素(ET)、6-酮前列腺素F1α(6-keto-PGF1α)和血栓素B2(TXB2)的影响。方法采用经典的6-羟基多巴胺损毁注射法制作PD模型,并应用活血化瘀(代表方桃红四物汤)、涤痰熄风(代表方涤痰汤)、滋阴熄风(代表方天麻钩藤饮)和复合治法(代表方复方地黄方)等不同方剂进行治疗,同时设立正常对照组、假手术组作对照。放射免疫法测定大鼠血液ET、6-keto-PGF1α和TXB2的含量。结果模型组TXB2、ET明显升高、6-keto-PGF1α明显降低,与正常对照组和假手术组相比差异均有统计学意义(P0.01)。与模型组相比,各药物治疗组ET差异均具有统计学意义(P0.01);天麻钩藤饮组、复方地黄方组的三个指标差异均有统计学意义(P0.05或P0.01)。天麻钩藤饮组和复方地黄方组分别与桃红四物汤组比较,TXB2和6-keto-PGF1α差异均有统计学意义(P0.05或P0.01);天麻钩藤饮组和复方地黄方组分别与涤痰汤组比较,各指标差异均无统计学意义(P0.05);天麻钩藤饮组和复方地黄方组比较,各指标差异均无统计学意义(P0.05)。结论各种治法均有明显的使PD大鼠血液血管活性物质TXB2、ET和6-keto-PGF1α的部分或全部指标向正常水平恢复的作用,但以天麻钩藤饮为代表的滋阴熄风治法和以复方地黄方为代表的复合治法为好。     

天麻钩藤饮、温胆汤、血府逐瘀汤对自发性高血压大鼠心肌组织与血浆ALDO和AngⅡ的影响

目的探讨天麻钩藤饮、温胆汤、血府逐瘀汤对自发性高血压大鼠(SHR)心肌组织与血浆醛固酮(AL-DO)和血管紧张素Ⅱ(AngⅡ)的影响。方法将50只16周龄SHR随机分为5组,SHR对照组、卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组各10只;另取10只血压正常大鼠作为正常对照组。卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组给予相应的药物灌胃,SHR对照组、正常对照组给予等量生理盐水灌胃;均连续用药8周。用药后,采用放免法检测各组血浆及心肌组织的AngⅡ、ALDO含量。结果用药8周后,卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组的血浆及心肌组织AngⅡ、ALDO含量均显著降低(P均<0.01);与SHR对照组、正常对照组用药后比较均有统计学差异(P均<0.01)。结论天麻钩藤饮、血府逐瘀汤、温胆汤可明显降低SHR的心肌组织和血浆AngⅡ、ALDO含量,有一定的抗心肌纤维化作用;其机制可能与抑制肾素—血管紧张素—醛固酮系统的激活有关。     

天麻钩藤饮合白术厚朴汤治疗土运不及之年肝阳上亢型高血压病的临床研究

目的 观察天麻钩藤饮联合运气理论指导下的白术厚朴汤治疗土运不及之年肝阳上亢型1级高血压病的临床疗效。方法 选取2019年7月1日—2019年12月31日济宁市中医院门诊及住院治疗的高血压病(1级)病人130例,按照随机数字表法分为对照组和治疗组,每组65例。对照组给予天麻钩藤饮治疗,治疗组给予天麻钩藤饮合白术厚朴汤治疗。观察两组临床疗效、血压及中医证候积分变化情况。结果 治疗组中医证候疗效总有效率为88.33%,对照组为59.32%,两组比较差异有统计学意义(P<0.01)。两组治疗后收缩压、舒张压水平均较治疗前下降(P<0.01),且治疗组下降幅度更明显(P<0.01);与对照组比较,治疗组治疗后中医证候评分明显降低(P<0.01),中医各证候有效率均明显升高(P<0.05)。结论 天麻钩藤饮联合运气理论指导下的白术厚朴汤能够改善肝阳上亢型1级高血压病病人血压水平及中医证候。     

天麻钩藤膏改善自发性高血压大鼠心肌纤维化的作用及其机制研究

目的观察天麻钩藤膏对自发性高血压大鼠(SHR)心肌纤维化的影响及其可能机制。方法将50只SHR随机均分为模型组(给予蒸馏水)、卡托普利组(给予卡托普利0.025 g/kg)及天麻钩藤膏低、中、高剂量组(分别给予天麻钩藤膏5.36 g/kg、11.34 g/kg、24.36 g/kg),另以正常血压(WKY)大鼠10只为空白对照组(给予蒸馏水),共6组。每日灌胃2次,连续4周。对比各组收缩压、左室质量(LVW)、左室质量指数(LVWI)、心肌胶原含量、血管周围胶原面积与管腔面积比例(PVCA)及心肌胶原容积分数(CVF),并采用放射免疫法检测心肌组织及血浆内肿瘤坏死因子-α(TNF-α)、单核细胞趋化蛋白(MCP-1)、粒细胞集落刺激因子(G-CSF)含量。结果卡托普利组及天麻钩藤膏高、中、低剂量组LVWI、LVW及心肌胶原含量均明显低于模型组,差异具有统计学意义(P0.01),天麻钩藤膏高、中、低剂量组及卡托普利组PVCA、CVF与模型组比较均明显降低,差异具有统计学意义(P0.01);天麻钩藤膏高剂量组PVCA、CVF与卡托普利组比较,差异有统计学意义(P0.01);天麻钩藤膏高、中、低剂量组及卡托普利组与模型组比较TNF-α、MCP-1、G-CSF均下降,差异有统计学意义(P0.01),天麻钩藤膏高剂量组与卡托普利组比较TNF-α、MCP-1、G-CSF,差异有统计学意义(P0.01)。结论天麻钩藤膏可明显降低SHR的LVW、LVWI、心肌胶原含量、PVCA、CVF以及血清中TNF-α、MCP-1、G-CSF的含量,促进心肌胶原降解,抑制心肌纤维化,其有效作用机制可能与降低心肌细胞炎症反应有关。     

针刺泻法对高血压中医证候及血清NO、ET-1水平的影响

目的观察针刺泻法对高血压的临床疗效、中医证候及血清一氧化氮(NO)、内皮素-1(ET-1)水平的影响。方法将60例高血压病人随机分为针刺泻法组、针刺留针组及假针刺组,每组20例。所有病人均进行常规西药降压治疗,3组分别用不同的手法针刺太冲穴,均以28 d为1个疗程,治疗1个疗程后判定疗效。观察治疗前后血压、中医证候及血清NO、ET-1水平变化。结果治疗后,针刺泻法组与针刺留针组均较假针刺组降压效果更明显(P<0.05),针刺泻法组较针刺留针组降压效果更明显(P<0.05);治疗后,针刺泻法组及针刺留针组中医证候疗效均优于假针刺组(P<0.05);治疗后,针刺泻法组与针刺留针组血浆ET-1和血清NO水平与假针刺组比较,差异均有统计学意义(P<0.05);与针刺留针组比较,针刺泻法组血清NO水平升高更明显(P<0.05)。结论针刺太冲穴治疗能明显改善高血压病人降压效果、中医证候及血清ET-1、NO水平,其治疗高血压的作用机制可能与其对血管内皮细胞功能的双向调节密切相关。     

精简天麻钩藤饮合ACEI类药对高血压患者血压及生存质量的影响

目的探讨精简天麻钩藤饮合血管紧张素转换酶抑制剂(ACEI)类药对高血压患者血压、生存质量的影响。方法将120例高血压患者随机分为中西药组、中药组和西药组,每组40例。中西药组口服精简天麻钩藤饮配方颗粒和依那普利治疗;中药组口服精简天麻钩藤饮配方颗粒治疗;西药组口服依那普利治疗。3组疗程均为4周。治疗前后观察并记录各组患者血压变化,临床症状积分和生存质量积分,疗程结束后对证候疗效和生存质量改善作出评价。结果治疗4周后,3组患者血压较治疗前显著降低(P<0.01),治疗后中西药组优于中药组(P<0.05);中医证候疗效总有效率中西药组优于西药组(P<0.05);中西药组的生存质量改善程度优于中药组和西药组(P<0.01)。结论精简天麻钩藤饮合ACEI类药有显著的降压效果,能明显改善高血压病患者症状,提高高血压病患者生存质量,疗效优于单纯使用精简天麻钩藤饮或ACEI类药。     

血府逐瘀汤、温胆汤、天麻钩藤饮对SHR大鼠心肌组织TNF-α、IFN-γ、G-CSF、MCP-1表达的影响

目的观察血府逐瘀汤、温胆汤、天麻钩藤饮对自发性高血压(SHR)大鼠心肌组织中TNF-α、IFN-γ、粒细胞集落刺激因子(G-CSF)、单核细胞趋化蛋白-1(MCP-1)等炎性细胞因子表达的影响。方法将50只16周龄SHR大鼠随机分为5组,SHR对照组、卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组各10只;另取10只血压正常的WKY大鼠作为正常对照组。卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组分别给予相应的药物灌胃,SHR对照组、正常对照组给予等量生理盐水灌胃,均2次/d,连续灌胃8周。之后断头处死各组大鼠,取其心脏,采用LiquiChip液相蛋白芯片系统检测大鼠心肌组织TNF-α、IFN-γ、G-CSF、MCP-1等炎性细胞因子。结果用药8周后,天麻钩藤饮组、血府逐瘀汤组、温胆汤组大鼠心肌组织TNF-α、G-CSF、MCP-1等炎性细胞因子的表达水平明显降低,IFN-γ的表达升高,与SHR对照组、正常对照组大鼠用药后相比,P均<0.01;血府逐瘀汤组与天麻钩藤饮和温胆汤组相比,P均<0.05。结论血府逐瘀汤、温胆汤、天麻钩藤饮有一定的抗心肌纤维化作用,其机制可能与抑制大鼠心肌组织中TNF-α、G-CSF、MCP-1的表达和提高IFN-γ的表达有关。     

天麻钩藤饮联合苯磺酸左旋氨氯地平对原发性高血压患者血压、血清炎性因子水平及血管内皮功能的影响研究

目的探讨天麻钩藤饮联合苯磺酸左旋氨氯地平对原发性高血压患者血压、血清炎性因子水平及血管内皮功能的影响。方法选取2014年6月—2015年6月临沂市第三人民医院收治的原发性高血压患者134例,按照随机数字表法分为对照组与观察组,每组67例。对照组患者予以苯磺酸左旋氨氯地平治疗,观察组患者在对照组基础上加用天麻钩藤饮治疗,疗程为8周。观察两组患者临床疗效,治疗前后血压(舒张压、收缩压)、血清炎性因子〔白介素6(IL-6)、白介素8(IL-8)、超敏C反应蛋白(hs-CRP)〕水平、血管内皮功能指标〔一氧化氮(NO)、内皮素1(ET-1)〕及治疗期间不良反应发生情况。结果观察组患者临床疗效优于对照组(u=6.872,P0.05)。治疗前两组患者舒张压、收缩压比较,差异无统计学意义(P0.05);治疗后观察组患者舒张压、收缩压低于对照组(P0.05)。治疗前两组患者血清IL-6、IL-8、hs-CRP、NO、ET-1水平比较,差异无统计学意义(P0.05);治疗后观察组患者血清IL-6、IL-8、hs-CRP、ET-1水平低于对照组,血清NO水平高于对照组(P0.05)。两组患者均未发生严重不良反应。结论天麻钩藤饮联合苯磺酸左旋氨氯地平治疗原发性高血压的临床疗效确切,可有效降低患者血压,减轻炎性反应及改善血管内皮功能,且安全性较高。     

天麻钩藤饮对帕金森病大鼠神经行为学及氧化应激反应的影响

目的 观察天麻钩藤饮对帕金森病(PD)大鼠神经行为学及氧化应激的影响.方法 采用6羟基多巴胺(6-OHDA)注射于脑右侧黑质造成单侧PD损毁模型,并用中药天麻钩藤饮(浓度为5.13 g/ml)进行治疗,共给药14 d.同时设立正常对照组、假手术组,观察各组大鼠神经行为学的变化,同时运用化学比色法测定大鼠中脑黑质、纹状体部位活性氧、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、丙二醛(MDA)的活性.结果 神经行为学方面,模型组大鼠治疗前后旋转圈数无显著差异;天麻钩藤饮组大鼠旋转圈数较模型组显著减少(P＜0.05),且治疗前后比较差异显著(P＜0.05);模型组活性氧、MDA明显升高,GSH、GSH-Px、SOD明显降低,与正常对照组、假手术组比较,差异显著(P＜0.05或P＜0.01);而天麻钩藤饮对其均有明显的改善作用(P＜0.05).结论 天麻钩藤饮可以明显改善PD大鼠的神经行为学变化,并可以提高机体的抗氧化和清除自由基的能力.     

天麻钩藤饮对腹主动脉狭窄-高盐型高血压大鼠血压等因素的影响

目的 观察天麻钩藤饮对腹主动脉狭窄-高盐型高血压大鼠血压等因素的影响.方法 将25只SD大鼠随机分为假手术组、实验性高血压组、实验性高血压天麻钩藤饮灌胃组.用手术和高盐饲养的方法制成腹主动脉狭窄-高盐摄入型高血压大鼠,在制备高血压病理模型的同时,用药组每天用天麻钩藤饮灌胃,观察30 d后对大鼠血压、心率及心指数的影响.结果 30 d后,高血压病理模型未用药组与假手术组比较血压明显升高,心率加快,心指数增加,均有统计学意义(P<0.05);高血压病理模型用药组与未用药组比较血压减低,心率减慢,心指数减少,均有统计学意义(P<0.05).结论 天麻钩藤饮可降低腹主动脉狭窄-高盐型高血压大鼠的血压、心率及心指数.     

Chronic endothelin-1 improves nitric oxide-dependent flow-induced dilation in resistance arteries from normotensive and hypertensive rats.

Endothelin-1 (ET-1) is released on stimulation by shear stress of the vascular wall. In several pathological situations, an involvement of ET-1 is suspected. Nevertheless, the effect of a chronic increase in circulating ET-1 on vascular tone in resistance arteries is not yet fully understood. We investigated the response to tensile stress (pressure-induced myogenic tone) and shear stress (flow-induced dilation, FD) of rat mesenteric resistance arteries cannulated in an arteriograph. Intraluminal diameter was measured continuously. Rats (normotensive Wistar-Kyoto rats [WKYs] and spontaneously hypertensive rats [SHRs]) were treated for 2 weeks with ET-1 (5 pmol. kg(-1). min(-1) SC; n=8 to 16 per group). Systolic arterial blood pressure increased significantly in ET-1-treated rats (171+/-7 versus 196+/-6 mm Hg in WKYs and 216+/-8 versus 245+/-6 mm Hg in SHRs, P<0.05). Passive arterial diameter in isolated resistance arteries ranged from 78+/-9 to 169+/-4 microm in WKYs and from 62+/-6 to 149+/-7 microm in SHRs (pressure from 10 to 150 mm Hg). Myogenic tone was not significantly affected by chronic ET-1. Flow (9 to 150 microL/min) significantly increased the arterial diameter by 2+/-0.5 to 22+/-2 microm in WKYs and by 1.3+/-0. 7 to 8.3+/-0.8 microm in SHRs (P<0.001 versus WKYs). The NO synthesis blocker N(G)-nitro-L-arginine methyl ester (L-NAME; 100 micromol/L) attenuated FD in WKYs (eg, 22+/-2 versus 15+/-3 microm after L-NAME, flow=150 microL/min) and, to a lesser extent, in SHRs (P<0.001 versus WKYs). The cyclooxygenase inhibitor indomethacin (3 micromol/L) attenuated the remaining FD in WKYs (eg, 15+/-3 versus 8+/-3 microm, flow=150 microL/min) and in SHRs (eg, 7.5+/-0.5 versus 5.0+/-0.6 microm). Chronic ET-1 significantly increased FD in SHRs but not in WKYs. In both strains, NO-dependent FD was significantly increased by chronic ET-1. Furthermore, indomethacin-sensitive FD was increased by chronic ET-1 in SHRs only. Thus, chronic ET-1 increased NO-dependent FD in resistance mesenteric arteries from both WKYs and SHRs and increased indomethacin-sensitive FD in SHRs only.     

Endothelin-1-receptor-mediated responses in resistance vessels of young and adult spontaneously hypertensive rats

OBJECTIVE: To assess whether primary changes in endothelin-1 (ET-1) receptor responsiveness or secondary vessel functional modifications could characterize the effects evoked by ET-1 in the mesenteric vascular bed (MVB) of prehypertensive 5-week-old and 12-week-old spontaneously hypertensive rats (SHRs). DESIGN AND METHODS: We used male 5-week-old and 12-week-old SHRs and sex- and age-matched Wistar-Kyoto (WKY) rats as controls. ET-1 receptor responsiveness was evaluated by ET-1 (0.04-2 micromol/l) concentration-response curves and repeated with indomethacin and BQ-123 (0.1-0.5 micromol/l), the latter a selective ETA receptor antagonist. ETB receptor responsiveness was tested by sarafotoxin S6c (1-100 nmol/l) and IRL-1620 (0.1-10 nmol/l) concentration-response curves, obtained in the noradrenaline-precontracted MVB. RESULTS: At 5 weeks of age, ET-1 induced a similar concentration-dependent contraction in SHRs and WKY rats, with an overlapping BQ-123 pA2 value (negative common logarithm of the antagonist that produces an agonist dose ratio of 2) in the two strains. Indomethacin was ineffective in both groups. Sarafotoxin S6c and IRL-1620 both evoked an ETB-mediated, significant relaxation, only in WKY rats. In 12-week-old SHRs, ET-1 evoked a markedly increased maximal effect compared with the response in WKY rats (P< 0.01); this was prevented by treatment with indomethacin. The BQ-123 pA2 value was higher in SHRs than in WKY rats (P< 0.01). Both sarafotoxin S6c and IRL-1620 evoked a significant concentration-dependent relaxation in WKY rats, which was not detected in SHR preparations. CONCLUSIONS: Our results could suggest that the different responses evoked by ET-1 in the MVB of SHRs during the onset of hypertension may be related partially to primary alterations in the ET-1 receptorial pattern and partially to the onset of high blood pressure, leading to an impairment in the haemodynamic balance.     

Constitutive phosphodiesterase activity restricts spontaneous beating rate of cardiac pacemaker cells by suppressing local Ca2+ releases

We hypothesized that activation of angiogenesis by chronic hypoxia may affect vascular resistance and, subsequently, blood pressure levels in spontaneously hypertensive rats (SHRs). Five-week-old prehypertensive SHRs and age-matched normotensive Wistar-Kyoto (WKY) rats (n=8 per group) were maintained under normobaric normoxic or hypoxic (10% O(2)) conditions for 8 weeks. Three weeks later, the systolic blood pressure was lower by 26% in hypoxic SHRs compared to normoxic SHRs (P<0.05) and remained at the normoxic WKY level. Total peripheral vascular resistance, calculated as the mean arterial pressure/cardiac output (assessed by ultrasound imaging and Doppler), was 30% lower in hypoxic than in normoxic SHRs (P<0.001) and returned to WKY levels. Interestingly, chronic hypoxia also significantly reduced systolic blood pressure in adult 12-week-old SHRs with established hypertension; blood pressure was normalized (versus normoxic WKY rats) after 4 weeks of hypoxia. Changes in hemodynamic parameters were associated with activation of proangiogenic pathways. Protein levels of vascular endothelial growth factor (VEGF)-A in the skeletal muscles were increased by 2.2-fold in hypoxic compared to normoxic SHRs (P<0.001). At the end of the hypoxic period, capillary density in the quadriceps muscle was 1.2-fold higher in hypoxic than in normoxic SHRs (P<0.001). Myocardial capillary density and VEGF-A protein contents were also 1.2- and 2.1-fold higher in hypoxic compared to normoxic SHRs (P<0.001 and P<0.05, respectively). Moreover, treatment with neutralizing VEGF-A antibody abrogated the hypoxia-induced angiogenesis and subsequently worsened arterial hypertension. Therefore, our results suggest that chronic normobaric hypoxia (1) activates VEGF-A-induced angiogenesis and thereafter (2) prevents the occurrence of hypertension in young prehypertensive SHRs and (3) normalizes blood pressure in adult SHRs with established hypertension.     

苯那普利对自发性高血压大鼠神经肽Y含量的影响

目的为探讨苯那普利对自发性高血压大鼠神经肽Ｙ（ＮＰＹ）含量的影响及其与高血压治疗的关系。方法本文选择了自发性高血压大鼠（ＳＨＲ）１６只,每８只为一组分成Ａ、Ｂ两组。Ａ组应用苯那普利进行治疗;Ｂ组作为对照组,用生理盐水治疗,４周后分别测定其血压,并测定其血浆以及重要器官组织中神经肽Ｙ的含量。结果Ａ组血压显著低于Ｂ组（Ｐ＜０．０１）。Ａ组血浆ＮＰＹ含量与Ｂ组比较显著降低（Ｐ＜０．０５）;ＮＰＹ在Ａ组的肝、肺及肾组织中的含量也明显低于Ｂ组（Ｐ分别＜０．０５,＜０．０５,＜０．０１）;而心、脑组织中ＮＰＹ略有降低,但无统计学意义（Ｐ＞０．０５）。结论苯那普利对自发性高血压大鼠体内ＮＰＹ含量变化的影响,可能与其治疗作用有关。     

花生四烯酸细胞色素p450表氧化酶基因对肺动脉高压大鼠血浆和组织中ET-1、NO、TXA2和PGI2变化的影响

目的观察野百合碱(MCT)诱导的肺动脉高压大鼠中花生四烯酸色素p450表氧化酶CYP2J2基因过表达时血浆和肺组织中内皮素-l(ET-1)、一氧化氮(NO)血栓素A2(TXA2)和前列腺素I2(PGI2)的水平及肺组织中一氧化氮合酶(NOS)活性的变化。方法成年雄性SD大鼠60只随机分为正常对照组(n=30)和MCT模型组(n=30),皮下注射MCT(60mg/kg)建立肺动脉高压模型。三周后尾静脉分别注射生理盐水和质粒分为6组:NS组,pCDNA3.1(n=10),pcDNA3.1-CYP2J2(n=10),MCT+NS(n=10),MCT+pCDNA3.1(n=10),MCT+pCDNA3.1-CYP2J2(n=10)。三周后,检测大鼠肺动脉压(mPAP),测定血浆和肺组织中ET-1和NO水平,检测肺组织中NOS和eNOS的活性,检测血浆和肺组织TXA2代谢产物TXB2和PGI2代谢产物6-酮-前列腺素1α(6-keto-PGF1α)水平及TXB2/6-keto-PGF1α的比值。结果 MCT模型组mPAP,血浆和肺组织中ET-1水平和TXB2含量和TXB2/6-keto-PGF1α比值均明显高于正常对照组(P<0.05),而pCDNA3.1-CYP2J2治疗组与MCT模型组比均显著降低(P<0.05),但仍高于正常对照组(P<0.05);MCT模型组血浆和肺组织中NO和6-keto-PGF1α含量,肺组织eNOS和NOS活性,TXB2/6-keto-PGF1α比值均明显低于正常对照组(P<0.05),而pCDNA3.1-CYP2J2治疗组均明显增高(P<0.05),但仍低于正常对照组(P<0.05)。结论花生四烯酸色素p450表氧化酶基因CYP2J2可逆转MCT诱导的肺动脉高压,其机制可能与降低肺组织和血浆中的ET-1和TXA2含量,升高PGI2含量,上调TXA2/PGI2比值,上调机体内eNOS和总NOS活性,增加体内NO水平有关。CYP2J2基因治疗对肺动脉高压有积极的治疗作用。     

The synergistic therapeutic effect of hepatocyte growth factor and granulocyte colony-stimulating factor on pulmonary hypertension in rats

Pulmonary arterial hypertension (PAH) is characterized by a progressive increase in pulmonary arterial pressure and vascular resistance. Despite advances in therapy for PAH, its treatment and prognosis remain poor. We aimed to investigate whether the transplantation of bone marrow mesenchymal stem cells (MSCs) overexpressing hepatocyte growth factor (HGF), alone or in combination with granulocyte colony-stimulating factor (G-CSF), attenuates the development of experimental monocrotaline (MCT)-induced PAH. Three weeks after MCT administration, rats were divided into the following groups: (1) untreated (PAH); (2) HGF treated; (3) MSCs administered; (4) HGF-MSCs treated; and (5) HGF-MSCs plus G-CSF treated. After 3 weeks, hemodynamic changes, histomorphology, and angiogenesis were evaluated. To elucidate the molecular mechanisms of vascular remodeling and angiogenesis, serum levels of transforming growth factor (TGF)-β and endothelin-1 (ET-1) were measured, and the gene and protein expression levels of vascular cell adhesion molecule-1 (VCAM-1) and matrix metalloproteinase-9 (MMP-9) were determined. Compared with the PAH, MSC, and G-CSF groups, the HGF and HGF+G-CSF groups exhibited significantly reduced right ventricular hypertrophy and mean pulmonary arterial pressure (P < 0.05). Histologically, vessel muscularization or thickening and collagen deposition were also significantly decreased (P < 0.05). The number of vessels in the HGF+G-CSF group was higher than that in the other groups (P < 0.05). The TGF-β and ET-1 concentrations in the plasma of pulmonary hypertensive rats were markedly lower in the HGF and HGF+G-CSF groups (P < 0.05). Furthermore, HGF induced the expression of VCAM-1, and HGF treatment together with G-CSF synergistically stimulated MMP-9 expression. Transplanted HGF-MSCs combined with G-CSF potentially offer synergistic therapeutic benefit for the treatment of PAH.     

青年大学生血清ET-1、NO水平及与中心动脉收缩压和外周血压的关系

[摘要] 目的 探讨青年大学生高血压患者血清ET-1、NO水平及与中心动脉收缩压、外周血压及相关因素的关系。 方法 分别测量高血压患者172例(男性151例,女性21例)及正常对照组198例(男性160例,女性38例)收缩压(SBP)、舒张压(DBP)、中心动脉收缩压(CSBP),测定血清ET-1、NO、血糖、胆固醇、甘油三酯、肌酐和尿素氮浓度,比较两组中心动脉收缩压水平和ET-1、NO浓度,分析ET-1和NO与外周血压、中心动脉收缩压及相关因素的相关性。结果 1.高血压组中心动脉收缩压水平(124.66±8.032mmHg)显著高于对照组水平(103.94±8.865mmHg);2. 血清ET-1水平浓度高血压组(145.66±44.07 pg/ml)显著高于对照组(114.07±16.65 pg/ml)(P<0.05);血清NO水平浓度高血压组(57.92±28.59 μmol/L)显著低于对照组(87.13±17.55 μmol/L),(P<0.05);3. 血清ET-1与SBP、DBP、CSBP呈正相关性;血清NO与SBP、DBP、CSBP呈负相关性;4. 血清ET-1与血糖、BMI呈正相关性,与NO呈负相关;血清NO与血糖、甘油三酯、胆固醇、BMI、ET-1呈负相关性; 结论 1. 血清中ET-1及NO的含量改变可能参与青年大学生高血压的发生;2. ET-1水平增高、NO水平下降及CSBP水平的升高提示[ 基金项目：科技基础性工作专项（2013FY114000） 通信作者：田建伟,E-mail:tianjianwei029@aliyun.con.王新宴,E-mail:tezhenke928041@126.com ]青年高血压患者动脉弹性功能下降、内皮功能减退;3. 青年高血压患者动脉弹性的减退与血糖、血脂、BMI水平密切相关。     

冠状动脉粥样硬化患者影像表现与冠状动脉循环血浆内皮素-1和一氧化氮水平的关系

目的　观察冠状动脉粥样硬化影像表现与冠状动脉循环血浆内皮素 - 1( ET- 1)和一氧化氮 ( NO)水平的关系。方法　 5 1例行冠状动脉造影者 ,造影前取血测定冠状静脉窦 ( CS)和冠状动脉开口 ( AO)血浆 ET- 1和 NO水平。冠状动脉腔径狭窄≥ 5 0 %者为严重冠状动脉病变组 ,反之为对照组。分析记录严重冠状动脉病变组病变血管数、狭窄病变数、闭塞病变数和病变范围积分。结果　 1.严重冠状动脉病变组 CS血浆 ET- 1水平 ( ET- 1CS)和 CS与AO的差值 ( ET- 1CS- AO)明显高于对照组 ( P<0 .0 5 ) ;严重冠状动脉病变组 ET- 1CS明显高于 AO血浆 ET- 1水平( ET- 1AO) ( P<0 .0 5 )。 2 .严重冠状动脉病变组 NOCS和 NOCS- AO明显低于对照组 ( P<0 .0 5 ) ;严重冠状动脉病变组NOCS明显低于 NOAO( P<0 .0 5 )。 3 .严重冠状动脉病变组 ,ET- 1CS- AO与冠状动脉病变范围积分呈显著正相关 ( P<0 .0 5 ) ,NOCS- AO与冠状动脉病变范围积分呈显著负相关 ( P<0 .0 5 )。结论　冠状动脉粥样硬化影响冠状动脉循环血浆 ET- 1和 NO水平 ,粥样硬化病变范围与冠状动脉循环血浆 ET- 1和 NO水平有相关关系