丹酚酸B对大鼠心肌缺血再灌注损伤内皮素及TXA2/PGI2系统的影响

目的　探讨丹酚酸 B(Sal B)对大鼠心肌缺血再灌注损伤 (MIRI)内皮素释放 (ET)及血栓素 /前列环素 (TXA2 / PGI2 )系统的影响。方法　大鼠心肌缺血 30 min后再灌注 1 2 0 min造成大鼠心肌缺血再灌注损伤模型 ,放免法测定给药前后血浆中 ET、TXB2 及 6- Keto- PGF1α的含量 ,观察 Sal B对 MIRI心肌的保护作用。结果　 Sal B可以减少 ET及 TXB2 的释放 ,提高 PGI2 的含量。结论　 Sal B可以减轻 MIRI,可能通过减少 ET的释放 ,改善 TXA2 / PGI2 系统的平衡状态 ,减轻心肌细胞的损伤。     

隐蔽性高血压患者血管活性物质的变化

目的探讨隐蔽性高血压患者血浆中血栓素A2(TXA2)、前列环素(PGI2)、神经肽Y(NPY)、降钙素基因相关肽(CGRP)水平变化并评价其对隐蔽性高血压患者血压水平的影响。方法78例研究对象分为健康对照组(A组,n=30),隐蔽性高血压组(B组,n=18)及原发性高血压组(C组,n=30)。检测各组血浆中TXA2、PGI2、NPY、CGRP水平并作比较。结果B组患者血浆中TXA2(1151.0±144.0)ng/L和NPY(138.1±16.1)ng/L水平高于A组[TXA2:(940.5±172.5)ng/L;NPY:(99.6±19.7)ng/L;P均<0.01],但是低于C组患者[TXA2:(1416.6±145.2)ng/L;NPY(169.8±26.2)ng/L;P均<0.01];而B组患者血浆中PGI2和CGRP水平低于A组[PGI2:(171.4±44.0)vsA组:(244.4±51.2)ng/L;CGRP:(56.2±15.6)vsA组:(79.8±17.9)ng/L;P均<0.01],高于C组患者[PGI2:(171.4±44.0)vsC组:(108.3±41.9)ng/L;CGRP:(56.2±15.6)vsC组:(39.2±16.6)ng/L;P<0.05或P<0.01]。经多元线性回归分析:B组患者白昼SBP水平与TXA2、NPY水平直线相关(P均<0.01);白昼DBP水平与TXA2、CGRP水平直线相关(P<0.05～0.01)。结论隐蔽性高血压病人血管活性物质如TXA2、PGI2、NPY、CGRP较正常血压的人不同,表现为收缩性血管活性因子增多,舒张性血管因子减少,提示这些血管活性物质可能参与了隐蔽性高血压的发病。     

隐蔽性高血压患者血管活性物质的变化

目的 探讨隐蔽性高血压患者血浆中血栓素A2(TXA2)、前列环素(PGI2)、神经肽Y(NPY)、降钙素基因相关肽(CGRP)水平变化并评价其对隐蔽性高血压患者血压水平的影响.方法 78例研究对象分为健康对照组(A组,n=30),隐蔽性高血压组(B组,n=18)及原发性高血压组(C组,n=30).检测各组血浆中TXA2、PGI2、NPY、CGRP水平并作比较.结果 B组患者血浆中TXA2(1151.0±144.0)ng/L和NPY(138.1±16.1)ng/L水平高于A组[TXA2:(940.5±172.5)ng/L;NPY:(99.6±19.7)ng/L;P均＜0.01],但是低于C组患者[TXA2:(1416.6±145.2)ng/L;NPY(169.8±26.2)ng/L;P均＜0.01];而B组患者血浆中PGI2和CGRP水平低于A组[PGI2:(171.4±44.0) vs A组:(244.4±51.2)ng/L;CGRP:(56.2±15.6) vs A组:(79.8±17.9)ng/L;P均＜0.01],高于C组患者[PGI2:(171.4±44.0) vs C组:(108.3±41.9)ng/L;CGRP:(56.2±15.6) vs C组:(39.2±16.6)ng/L;P＜0.05或P＜0.01].经多元线性回归分析:B组患者白昼SBP水平与TXA2、NPY水平直线相关(P均＜0.01);白昼DBP水平与TXA2、CGRP水平直线相关(P＜0.05～0.01).结论 隐蔽性高血压病人血管活性物质如TXA2、PGI2、NPY、CGRP较正常血压的人不同,表现为收缩性血管活性因子增多,舒张性血管因子减少,提示这些血管活性物质可能参与了隐蔽性高血压的发病.     

应激性胃粘膜出血与血浆血栓素、前列环素和胃泌素水平的关系

目的　探讨应激性胃粘膜出血与血浆TXA2 、PGI2 和胃泌素 (G)水平的关系。方法　 2 0只SD大鼠随机分成实验组和对照组 ,每组 10只 ,禁食 2 4小时后 ,实验组放在 2℃冰水中应激 4小时 ,对照组不给刺激。应激结束后麻醉大鼠 ,分别取血 2ml分离血浆 ,放免法测定TXB2 (TXA2 的稳定代谢物 )、6 酮 PGF1a(PGI2 的衍生物 )和G水平 ;另取大鼠胃沿小弯剪开 ,肉眼观察胃粘膜有无出血灶 ,用pH值试纸测定胃液酸碱度。结果　 8只实验鼠胃粘膜见片状出血灶 ,对照组鼠胃粘膜无出血性改变 ;两组鼠胃液pH值测定无明显差异。实验组血浆TXB2 、6 酮 PGF1a和G水平分别为 15 45 11±14 2 89、16 2 80± 42 13和 112 75± 2 3 6 8,对照组分别为 96 6 5 0± 5 18 48、3 5 6 0 0± 91 0 6和 2 47 14± 5 3 6 0 ,两组分别比较均具有显著意义 (P <0 0 1)。结论　大鼠应激性胃粘膜出血与血浆TXA2 水平升高和PGI2 水平降低有关 ;而与胃酸分泌无关。     

银杏叶制剂对老年冠心病患者血栓素及前列环素水平的影响

近年来研究证实，血栓素A2(TXA2)—前列环素(PGI2)失衡与冠心病的发生密切相关；有关研究提示银杏叶制剂可减少血栓素的释放。2001～2003年，我们将银杏叶制剂金钠多用于3D例老年冠心病患者，观察了其治疗前后血浆中TXA2的代谢产物TXB2及PGI2代谢产物6—keto—PGF1变化，现报告如下。     

血栓素A2合成酶抑制剂治疗大鼠低氧性肺动脉高压的研究

目的探讨花生四烯酸(TXA2,又称血栓素A2)合成酶抑制剂奥扎格雷钠治疗大鼠低氧性肺动脉高压的疗效及机制.方法Wister大鼠21只,随机分为3组,正常对照组7只,单纯低氧组7只,奥扎格雷钠治疗组7只.采用间断性低氧法复制大鼠低氧性肺动脉高压动物模型,观察奥扎格雷钠对低氧21天大鼠肺动脉平均压(MPAP)、右心室肥厚、血浆TXA2代谢产物血栓素B2(TXB2)和前列环素(PGI2)代谢产物6-酮-前列腺素F1α(6-K-PGF)浓度及其TXB2/6-K-PGF等的影响.结果单纯低氧组大鼠MPAP、右心室湿重、右心室湿重/(左心室 室间隔)湿重、血浆TXB2含量和TXB2/6-K-PGF均明显增加,与正常对照组相比均有显著差异(P＜0.05);奥扎格雷钠治疗组较单纯低氧组明显降低(P＜0.05～0.001),但仍高于正常对照组(P＜0.05).各组血浆6-K-PGF和体动脉平均压无显著差异.结论奥扎格雷钠可明显降低低氧大鼠肺动脉高压、减轻右心室肥厚程度,降低低氧大鼠血浆TXA2代谢产物TXB2水平和改善反应TXA2/PGI2水平的TXB2/6-K-PGF.     

非酒精性脂肪性肝病大鼠肝X受体α基因表达变化及意义

目的研究NAFLD大鼠肝X受体α(LXRα)基因表达变化及意义。方法建立高脂饮食诱导NAFLD大鼠模型后,采用RT-RCR和Western blot法动态观察NAFLD大鼠肝组织中LXRα表达变化。结果4周时模型组大鼠血清游离脂肪酸含量达(0.33±0.03)mmol/L,对照组为(0.24±0.03)mmol/L,差异有统计学意义(P<0.05),随喂养时间延长逐渐升高,12周时模型组大鼠血清游离脂肪酸含量达(0.61±0.06)mmol/L,对照组为(0.25±0.01)mmol/L,差异有统计学意义(P<0.01)。血清ALT和AST含量在8周时模型组分别为75.8 U/L和138.9 U/L,对照组分别为54.8 U/L和81.4 U/L,差异有统计学意义(P<0.01),12周时模型组分别为102.3 U/L和179.1 U/L,对照组分别为54.3 U/L和79.2 U/L,差异有统计学意义(P<0.01)。2周时模型组大鼠肝组织中LXRα基因表达相对含量为0.62,对照组为0.33,差异有统计学意义(P<0.01),随着高脂饮食喂养时间的延长表达进一步增强,12周时模型组大鼠高达1.31,对照组为0.34,差异有统计学意义(P<0.01)。模型组大鼠肝组织中LXRα蛋白表达与基因表达趋势相同,与脂肪肝进展程度一致。结论LXRα基因表达变化与NAFLD的形成密切相关。     

血栓心脉宁片对急性血瘀大鼠血浆TXA2及PGI2含量的影响

目的 观察血栓心脉宁片对急性血瘀大鼠血浆血栓素A2(TXA2)及前列环素(PGI2)的影响.方法 采用两次注射肾上腺素加冰水浴的方法 建立急性血瘀大鼠模型,观察血栓心脉宁片对大鼠血浆TXA2及PGI2含量的影响.结果 血栓心脉宁低、中、高剂量组均可使急性血瘀模型大鼠血浆TXA2含量明显降低,而使血浆PGI2含量明显升高,以中剂量组效果最为明显,与脑心通胶囊具有相似的作用.结论 血栓心脉宁片可降低急性血瘀模型大鼠血浆TXA2含量,提高大鼠血浆 PGI2含量.     

乙肝Ⅱ号方对免疫性慢性肝损伤小鼠血栓素、前列环素代谢的影响

目的 :研究乙肝Ⅱ号方对免疫性慢性肝损伤小鼠氧自由基 (OFR ) ,血栓素A2 (TXA2 )和前列环素(PGI2 )代谢的影响。方法 :将小鼠分为正常组、模型组和乙肝Ⅱ号方治疗组。对后两组小鼠用异种动物的肝提取物作为抗原 ,免疫纯系小鼠产生抗肝抗体 ,造成慢性实验性免疫性肝损伤模型。检测 3组小鼠肝组织丙二醛 (MDA)、超氧化物歧化酶 (SOD)含量及血浆TXA2 和PGI2 代谢产物的浓度。结果 :与正常组比较 ,免疫性慢性肝损伤小鼠肝组织MDA含量明显升高 ,且与血浆TXB2 变化呈正相关 (r =0 976,P <0 0 0 1)。肝组织SOD含量下降 ,血浆TXA2 明显升高 ,PGI2 明显下降 ;而乙肝Ⅱ号方治疗组小鼠肝组织MDA和血浆TXA2 较模型组低 ,SOD和PGI2 则较模型组高。结论 :乙肝Ⅱ号方对小鼠免疫性肝损伤有明显的防治作用     

血栓心脉宁片对大鼠急性心肌梗死的保护作用及其机制

目的观察血栓心脉宁片对大鼠急性心肌梗死的保护作用及其机制。方法采用大鼠结扎左冠状动脉前降支造成急性心肌梗死模型,将动物随机分为假手术组、梗死模型组、血栓心脉宁低剂量组、血栓心脉宁中剂量组及血栓心脉宁高剂量组。计算急性心肌梗死24h后的心肌梗死面积(MIS),测定血清天冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、心肌肌酸激酶同工酶(CK-MB)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量以及血浆前列环素(PGI2)及血栓素A2(TXA2)水平,并测定血小板聚集活性。结果血栓心脉宁片给大鼠连续灌胃7d,血栓心脉宁中、大剂量组与梗死模型组比较,可使急性心肌梗死24h大鼠的MIS明显缩小(P<0.01),血清AST、LDH、CK-MB活性及MDA含量明显降低(P<0.05或P<0.01),SOD及GSH-Px活性明显升高(P<0.05或P<0.01),血浆TXA2水平明显下降,PGI2水平及PGI2/TXA2比值明显增高(P<0.05或P<0.01),1min、3min、5min的血小板聚集率(PAR)及最大血小板聚集率(MPAR)明显降低(P<0.05或P<0.01)。结论血栓心脉宁片对大鼠急性心肌梗死具有明显保护作用,可能与其增强抗氧化酶活性,减少自由基对心肌的氧化损伤,纠正心肌缺血时PGI2/TXA2失衡以及抑制血小板聚集活性等机制有关。     

非酒精性脂肪性肝病大鼠肝脏解偶联蛋白2表达及其与能量贮备的关系

目的探讨非酒精性脂肪性肝病(NAFLD)大鼠肝脏线粒体解偶联蛋白2(UCP2)表达及其与能量贮备的关系。方法模型组SD大鼠给予高脂肪高胆固醇饮食饲养,分批于实验第8、12、16、24 周处死,同期设普通饮食饲养大鼠作对照。免疫组织化学和逆转录聚合酶链反应(RT-PCR)检测肝脏UCP2 mRNA转录及其蛋白表达。荧光测定法检测肝脏三磷酸腺苷(ATP)含量。结果模型组大鼠8周呈现单纯性脂肪肝,12-24周从脂肪性肝炎进展为脂肪性肝炎伴肝纤维化。免疫组织化学和RT-PCR显示,随着造模时间延长,模型组肝脏UCP2表达逐渐增强,UCP mRNA转录于24周达高峰,较对照组升高4.2倍, t=16.474,P<0.01;模型组肝脏ATP含量则随造模时间延长而逐渐减低,24周为(1.99±0.66) ×108μmol/g,对照组为(2.97±0.48)×108μmol/g,t=3.248,P<0.01。模型组肝脏UCP2 mRNA 转录的相对数值与其ATP含量呈密切负相关,r=-0.93,P<0.01。结论持续24周高脂饮食成功复制大鼠NAFLD模型,模型大鼠肝脏UCP2表达增强而ATP含量减少,两者之间关系密切。     

A study of the role of plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha in epidemic hemorrhagic fever

Plasma concentrations of Thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were dynamically measured with radioimmunoassay in 30 patients of epidemic hemorrhagic fever (EHF). It was found that the levels plasma TXB2 significantly increased and 6-keto-PGF1 alpha decreased in EHF patients as compared with those in controls. The more severe the patient's condition, the higher the level of TXB2 and the lower the level of 6-keto-PGF1 alpha. The ratio of TXB2/6-keto-PGF1 alpha was parallel with the severity of the patient's condition. Plasma TXB and TXB2/6-keto-PGF1 alpha ratio increased significantly in the hemorrhagic and shock group, while 6-keto-PGF1 alpha decreased significantly in the shock group. The results showed that there is a distinct imbalance of TXA2-PGI2 mediated through the increase of TXA2 and decrease of PGI2 in EHF. The imbalance of TXA2-PGI2 participates in the pathogenesis and pathophysiology of hemorrhage, shock and renal dysfunction.     

Sudden death induced by intracoronary platelet aggregation

Sodium arachidonate (AA, 1.5 mg/kg) was injected into the coronary arteries in 16 rabbits. Arrhythmia, marked ST-T depression and apnea appeared in all cases, and 7 cases died within 10 min after the AA. Before the injection, the thromboxane B2 (TXB2) value was 1.2 +/- 0.2 ng/ml (mean +/- SE) and the 6-keto-PGF1 alpha value was 2.1 +/- 0.4 ng/ml. Three minutes after the AA, TXB2 values were 5.0 +/- 1.1 in the surviving cases and 17.9 +/- 6.5 ng/ml in the cases which died. 6-keto-PGF1 alpha values were 47.7 +/- 4.6 in the surviving cases and 248.5 +/- 69.3 ng/ml in the cases which died. There occurred no deaths in 7 cases pretreated with aspirin (ASA) and in 11 cases pretreated with OKY-046 and 1581, which are specific inhibitors of TXA2 synthetase. TXB2 values did not change in the ASA and OKY groups after the AA injection. 6-keto-PGF1 alpha values did not change in the ASA group and increased in the OKY group after the AA injection. Histological findings of the heart showed more remarkable ischemic changes in the non-pretreated group than in the ASA and OKY groups. These results suggest a role for TXA2 in sudden death. PGI2 production was extremely enhanced, suggesting the presence of a protective mechanism against thrombogenesis in vivo.     

Intestinal prostacyclin and thromboxane production in irreversible hemorrhagic shock

Arterial and intestinal venous blood were sampled every hour for measurement of thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, stable metabolites of thromboxane A2 and prostacyclin, respectively, in dogs subjected to hemorrhagic hypotension at 32.8 +/- 1.4 mm Hg for 3 h, followed by reinfusion of the remaining shed blood. Control dogs were treated alike without hypotension. Arterial and intestinal venous TXB2 significantly increased during hypotensive and post-transfusion periods, the venous concentration being significantly higher than the corresponding arterial. The arterial and venous 6-keto-PGF1 alpha increased during hypotension but decreased during post-transfusion periods. Furthermore, arterial and venous TXB2 to 6-keto-PGF1 alpha concentration ratio increased. Intestinal TXB2 release (blood flow X arteriovenous concentration difference) increased progressively, whereas 6-keto-PGF1 alpha release decreased. No significant changes occurred in the control dogs. This study shows an imbalance in intestinal production and release of TXA2 and PGI2, in favor of TXA2 during severe hemorrhagic hypotension and after blood transfusion. The imbalance may contribute to the development of irreversible hemorrhagic shock and reperfusion injury.     

Relation of arachidonate metabolites to abnormal control of the pulmonary circulation in a child

To evaluate the role of arachidonate metabolites in regulating pulmonary vascular tone, we performed multiple studies on a 17-month-old girl with idiopathic pulmonary hypertension, systemic arterial hypoxemia (due to ventilation-perfusion mismatching), and an elevated thromboxane A2 (TXA2) to prostacyclin (PGI2) ratio due to increased TXA2 (measured as their stable metabolites, TXB2 and 6-keto-PGF1 alpha, respectively). Intravenous infusions of PGI2 reduced mean pulmonary arterial pressure (from 80 to 47 mmHg), increased cardiac output (from 3.43 to 3.97 L/min), increased systemic arterial oxygen saturation (from 60 to 72 percent), and decreased the TXB2 to 6-keto-PGF1 alpha ratio (from 5.9 to 0.2); mean systemic arterial pressure was unchanged. Pharmacologically decreasing the TXB2 to 6-keto-PGF1 alpha ratio with administration of nifedipine or diltiazem also reduced pulmonary hypertension and increased systemic arterial oxygen saturation in this patient. Nifedipine and diltiazem decreased the ratio by decreasing TXB2. Prostacyclin decreased the ratio by increasing 6-keto-PGF1 alpha. These studies support the hypothesis that the balance between TXA2 and PGI2 is an important influence on pulmonary vascular tone.     

Changes of nitric oxide and endothelin, thromboxane A2 and prostaglandin in cirrhotic patients undergoing liver transplantation

AIM: To investigate the perioperative changes of nitric oxide (NO) and endothelin (ET), thromboxane Az (TXAa) and prostaglandin (PGh) during liver transplantation in end-stage liver disease patients. METHODS: Twenty-seven patients with end-stage cirrhosis undergoing liver transplantation were enrolled in this prospective study. Blood samples were obtained from superior vena at five different surgical stages. Plasma concentrations of nitrate and nitrite were determined to reflect plasma NO levels. Plasma levels of ET-1, 6-keto-PGF1 alpha and thromboxane B2 (TXB2), the latter two being stable metabolites of PGI2 and TXA2 respectively, were measured. RESULTS: The NO level decreased significantly after vascular cross-clamping and increased significantly at 30 min after reperfusion. While the ET levels at 30 min after clamping and after reperfusion were significantly elevated. The ratio of NO/ET decreased significantly at 30 min after vascular cross-clamping and at the end of surgery. The PGI2 level and the TXA2 during liver transplantation were significantly higher than the baseline level, but the ratio of TXA2/PGI2 decreased significantly at 30 min after clamping. CONCLUSION: NO/ET and TXA2/PGI2 change during liver transplantation. Although the precise mechanism remains unknown, they may play a role in the pathobiology of a variety of liver transplant-relevant processes.     

Plasma renin activity, angiotensin II, angiotensin converting enzyme, thromboxane A2 and prostacyclin I2 levels in pigs with severe hypoxia and hypercapnea and acidosis shock]

To evaluate the role of certain plasma biosubstances on the development of pulmonary hypertension and shock during severe hypoxia, hypercapnia and acidosis, plasma renin activity (PRA), angiotensin II (ATII), angiotensin converting enzyme (ACE), TXB2 and 6-Keto-PGF1 alpha (the stable metabolites of TXA2 and PGI2) were assayed in blood from pulmonary artery and aorta in seven pigs. Pulmonary arterial pressure (PAP) was monitored via Swan-Ganz catheter. During hypoxic and hypercapnic ventilation, PaO2 dropped to 4.7 kPa, PaCO2 rose to 21.1 kPa, pH dropped to 6.82, PAP increased from 2.43 +/- 0.06 to 4.46 +/- 0.45 kPa when acidotic shock developed (all P less than 0.05). Meanwhile ATII levels rose (all P less than 0.05). PRA significantly increased during acidotic shock as compared with normal ventilation (P less than 0.02). ACE dropped significantly (P less than 0.05), TXB2 and 6-keto-PGF1 alpha showed no significant change before and after hypoxic and hypercapnic ventilation.     

Reduction of prostacyclin synthesis as a possible cause of transient flow reduction in a partially constricted canine coronary artery

Coronary blood flow decreases cyclically in a partially occluded coronary artery of anesthetized dogs. Spontaneous aggregation and deaggregation of platelet plugs in the constricted artery have been indicated to be responsible for this phenomenon. A current hypothesis is that platelet aggregation may be determined by a balance between proaggregatory platelet product, thromboxane A2 (TXA2), and antiaggregatory substance, prostacyclin (PGI2). To elucidate the relationship between the cyclical reduction of coronary flow (CRCF) and metabolic alterations of TXA2 and PGI2, we attempted to determine the plasma levels of their stable catabolites, thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), in the coronary circulation of 69 dogs. Of 40 cases, 20 cases exhibited CRCF accompanying a significant increase in TXB2 in the coronary sinus (CS) (P less than 0.05) and constant levels of 6-keto-PGF1 alpha in the CS and aorta (Ao). Another 20 cases did not exhibit CRCF that accompanied a marked increase in 6-keto-PGF1 alpha (P less than 0.05) with virtually no change in TXB2 in the CS and Ao. A higher dose of indomethacin (10 mg/kg, i.v.) was capable of evoking CRCF in cases not exhibiting CRCF spontaneously. Under these conditions, a significant decrease in 6-keto-PGF1 alpha was seen both in the CS and Ao compared with lower doses of indomethacin (1 to 3 mg/kg, P less than 0.01), that produced less pronounced reduction of 6-keto-PGF1 alpha without CRCF. Intravenous infusion of PGI2 (0.1 microgram/kg/min.) completely abolished spontaneously and indomethacin-induced CRCF with a marked elevation of 6-keto-PGF1 alpha in the CS and Ao. Although OKY-1580, a TXA2 synthetase inhibitor, relieved spontaneously-evoked CRCF with a marked increase in 6-keto-PGF1 alpha and a slight reduction of TXB2, indomethacin-induced CRCF was not abolished by this agent. These results are consistent with the hypothesis that the reduction of endogenous PGI2 synthesis in the vascular wall is related to the occurrence of CRCF after partial constriction of coronary artery and indomethacin.     

丹红注射液联合针灸治疗气虚血瘀型冠心病心绞痛患者的疗效

目的:观察丹红注射液联合针灸治疗气虚血瘀型冠心病(CHD)心绞痛患者的疗效。方法:我院146例CHD心绞痛气虚血瘀证患者被随机分为丹红注射液+针灸组(联合治疗组,74例)和丹红注射液组(72例),疗程2周。观察比较两组治疗前后主要中医症状积分、血清血管假性血友病因子(vWF)、可溶性细胞间黏附分子(sICAM)-1、内皮素(ET)-1、丙二醛(MDA)、超氧化物歧化酶(SOD)、内皮型一氧化氮合酶(eNOS)、血浆血栓素A2(TXA 2)、TXB 2、6-酮前列腺素-1α(6-Keto-PGF1α)水平,以及治疗有效率。结果:联合治疗组总有效率显著高于丹红注射液组(93.24%比80.56%),P=0.023。与丹红注射液组比较,联合治疗组治疗后胸痛[(1.83±0.44)分比(1.45±0.50)分]、胸闷[(1.86±0.45)分比(1.62±0.49)分]、气短[(1.67±0.50)分比(1.43±0.53)分]、心悸积分[(1.46±0.50)分比(1.18±0.53)分]、血清vWF[(113.08±16.00)U/L比(103.91±15.11)U/L]、sICAM-1[(0.81±0.14)mg/L比(0.69±0.13)mg/L]、ET-1[(74.57±7.48)pg/ml比(68.78±8.09)pg/ml]、MDA[(3.01±0.53)nmol/L比(2.58±0.48)nmol/L]、血浆TXA 2[(51.89±9.85)ng/L比(46.61±8.27)ng/L]和TXB 2[(105.97±18.24)ng/L比(95.21±17.19)ng/L]水平均显著降低,血清SOD[(167.26±18.82)U/L比(188.06±24.87)U/L]、eNOS[(41.58±8.83)U/ml比(47.70±9.04)U/ml]、血浆6-Keto-PGF1α水平[(83.67±18.06)ng/L比(90.33±16.43)ng/L]均显著升高,P<0.05或<0.01。结论:丹红注射液联合针灸治疗气虚血瘀型CHD心绞痛可显著提升疗效,减轻症状,改善血管内皮功能,减轻氧化应激反应,调节血小板活性,较单纯丹红注射液治疗优势更显著。     

The hypertensive response to vasopressor agents stimulates the release of thromboxane A2 in hypercholesterolaemic rabbits

The production of thromboxane A2 (TXA2) and prostacyclin (PGI2) is altered in hypercholesterolaemia. The purpose of this study was to investigate the effect of an acute rise in arterial pressure produced by pressor agents on the release of TXA2 and PGI2 in hypercholesterolaemic rabbits. Hypercholesterolaemia was induced in rabbits by feeding pellet food containing 1% cholesterol for 3 months. Administration of pressor agents (ergonovine 0.5-2.0 mg.kg-1, noradrenaline 5.0-20.0 micrograms.kg-1 and angiotensin-II 0.5-2.0 micrograms.kg-1) increased arterial pressure dose dependently, accompanied by a pressure dependent increase in the plasma concentrations of both TXB2 and 6-keto-PGF1 alpha (stable metabolites of TXA2 and PGI2) in control rabbits, but only of TXB2 in hypercholesterolaemic rabbits. In control rabbits the maximum increase in TXB2 was 51% with ergonovine, 73% with noradrenaline, and 51% with angiotensin-II; and the maximum increase in 6-keto-PGF1 alpha was 48% with ergonovine, 76% with noradrenaline, and 198% with angiotensin-II. In hypercholesterolaemic rabbits the maximum increase in TXB2 was 130% with ergonovine, 144% with noradrenaline, and 128% with angiotensin-II. The pressor induced increase in TXB2 was suppressed when the increase in arterial pressure was counteracted by the concomitant administration of vasodilators (glyceryl trinitrate 40 micrograms.kg-1.min-1 and verapamil 20 micrograms.kg-1.min-1) in both control and hypercholesterolaemic rabbits. Neither TXB2 biosynthesis nor phospholipase A2 activity in platelets was affected by ergonovine, noradrenaline or angiotensin-II in vitro. These results suggested that the acute rise in arterial pressure caused by these pressor agents increased TXA2 release in vivo and that the increase was greater in hypercholesterolaemic than in control rabbits.