局部外放射对恶性肿瘤患者外周血白细胞计数的影响

目的　分析局部外放射对恶性肿瘤患者外周血白细胞计数的影响。方法　回顾 87例接受局部外放射的恶性肿瘤患者放疗过程中 ,每周外周血白细胞总数、中性粒细胞计数、淋巴细胞计数的变化 ,进行统计学分析。其中男性 4 5例 ,女性 4 2例。年龄 19～ 6 9岁。颈部放疗 (A组 ) 2 1例 ,胸部放疗 (B组 ) 4 1例 ,腹盆部放疗 (C组 ) 2 0例 ,其他 5例。放疗剂量 2 9 5～ 70 9GY 15～ 37F。结果　放疗前外周血白细胞计数(6 2 0± 1 77)× 10 9 L ,放疗后 (4 82± 1 95 )× 10 9 L ,统计学差异无显著性意义。头颈、胸部、腹盆部不同部位的放疗对外周血白细胞计数的影响无显著性意义。腹盆部放疗组外周血淋巴细胞计数在放疗后明显低于放疗前 ,差异有显著性意义 (P <0 0 5 )。头颈部、胸部和腹盆部三组间比较 ,外周血白细胞计数、淋巴细胞计数和中性粒细胞计数的差异均无显著性意义 (P >0 0 5 )。结论　单纯常规局部放疗对患者的血象没有影响。建议单纯放疗的患者一般可以每 2周监测 1次外周血象。     

育龄妇女宫颈癌化疗后放疗36例分析

目的　探讨育龄妇女宫颈癌的综合治疗价值。方法　 36例宫颈癌化疗后行常规放疗 ,A组点剂量 >70Gy 13例 ,B组点剂量 6 0～ 70Gy 2 3例 ,全盆腔中面剂量 4 5～ 5 4Gy ,腔内放疗 4 0 0～ 5 0 0cGy/次 ,每周 1次。结果　 3年生存率 75 % (2 7/36 ) ,5年生存率 5 5 9% (19/34) ,3年局控率 86 1% ,5年局控率77 8%。放射直肠炎发生率 ,>70Gy为 31% (3年 )和 2 0 % (5年 ) ,6 0～ 70Gy为 2 6 1% (3年 )和 17 6 % (5年 )。结论　放疗前辅以化疗可提高育龄妇女宫颈癌的生存率和局控率。     

调强适形放射治疗前列腺癌

目的初步探讨调强适形放射治疗前列腺癌的临床应用价值。方法自2001年2月采用NOMOS公司调强放疗设备(孔雀系统)对10例前列腺癌实施调强放疗。5例先行全盆腔常规外照射,调强放疗剂量2.0～3.5Gy/次,每周3～5次,总剂量24.5～45.5Gy;外照射+调强放疗总量54.5～70Gy。5例全程调强放疗,剂量2.0～3.0Gy/次,每周5次,总剂量64～78Gy。结果除1例放疗前血清前列腺特异性抗原正常外,放疗后所有患者血清前列腺特异性抗原均下降。放疗后1月复查肿瘤明显缩小6例,稍微缩小或无变化4例。未发生近期严重的膀胱、直肠副反应。结论调强适形放射治疗可提高前列腺癌放疗剂量,减少膀胱、直肠副反应,是一种安全、有效的治疗手段。     

清得佳凝胶预防头颈部肿瘤患者急性放射性皮肤损伤的效果观察

目的:观察清得佳凝胶对头颈部肿瘤患者急性放射性皮肤损伤的预防效果。方法:将57例首次行放射治疗的头颈部肿瘤患者随机分为观察组、对照组各29例,放射治疗剂量50～70Gy/5～7周,常规分割,2Gy/次,1次/d,5d/周。观察组自放疗开始于每次放疗后放射野内涂抹约1mm厚清得佳凝胶,1次/d,同时放射野行常规皮肤护理,发生Ⅱ度湿性放射性皮肤损伤后常规用生理盐水或0.1%新洁尔灭清洁创面后,再涂清得佳凝胶。对照组不用清得佳凝胶,其余同观察组。结果:两组放射性皮炎、放射性疼痛、瘙痒总的发生率相比无统计学意义,但重度瘙痒的发生率两组比较P(0.05,具有统计学意义;发生I度放射性疼痛的放射剂量:观察组平均为(49±12)Gy,对照组平均为(35±16)Gy,两组比较P(0.05。发生I度瘙痒的放射剂量:观察组平均为(38±11)Gy,对照组平均为(30±15)Gy,两组比较(P(0.05),具有统计学意义。结论:清得佳凝胶的应用延缓了头颈部患者放疗过程中放射性疼痛及瘙痒的发生,降低了重度瘙痒的发生率。     

面神经轴浆快转运蛋白运输在术中对不同放疗剂量的影响

目的探讨术中放疗对面神经轴浆运输的影响,为临床术中放疗后面神经的恢复提供基础研究。方法制作腮腺区面神经术中放射预防剂量13Gy、治疗剂量15Gy、组织细胞坏死剂量17Gy动物模型,利用面神经核内微量注射标记蛋白前体结合闪烁计数技术,测量兔面神经放射损伤后不同距离段的放射活性及同一距离段不同剂量、不同时期放射活性变化的脉冲值。结果各组面神经轴浆转运蛋白放射活性脉冲值随距近心端的增加而下降,且实验组都低于对照组;在同一神经段的脉冲值:13Gy组术后4周恢复(P&;gt;0.05),15Gy组术后8周恢复(P&;gt;0.05),17Gy组术后未能恢复(P&;lt;0.01)。结论术中放疗影响神经轴浆运输,预防剂量及治疗剂量不影响面神经功能恢复,为腮腺癌手术保留面神经、术中配合放疗提供理论依据。     

含服养阴清热中药液防治急性放射性反应的效果观察

目的 探讨鼻咽癌患者放射治疗过程中含服养阴清热中药液,减轻急性放射毒副反应.方法 将116例鼻咽癌患者随机分成观察组(58例)和对照组(58例),实验组患者在放疗过程中应用养阴清热中药液,对照组患者应用消炎漱口水,观察并比较2组患者在放疗过程中出现口腔黏膜急性损伤程度及应用剂量.结果 口腔黏膜损伤中,出现损伤的放射剂量,试验组放射剂量为(41.15±11.56)Gy,对照组放射剂量为(30.32±11.03)Gy,2组比较差异有统计学意义(P＜0.05),试验组含服养阴中药液未见有任何不良反应.结论 养阴清热中药液能明显减轻放射治疗过程中放射线对口腔黏膜造成的急性损伤,且取材容易,操作方便,经济实惠,深受欢迎,值得临床推广应用.     

单细胞电泳法检测肿瘤患者化疗后淋巴细胞DNA损伤

应用单细胞电泳 (SCGE)检测肿瘤患者环磷酰胺化疗后外周血T淋巴细胞DNA损伤。在标准SCGE条件下应用彗星图象分析系统定量分析人T淋巴细胞DNA的损伤程度。彗星图象分析研究结果显示 ,肿瘤患者外周血T淋巴细胞DNA损伤明显强于正常对照组 ,肿瘤患者外周血T淋巴细胞拖尾动量为 10 42± 1 98,正常人群为 1 2 6± 0 77;两者差异极显著 (P <0 .0 1)。肿瘤患者化疗后T淋巴细胞的拖尾长度为 3 3 69± 7 56μm ,DNA损伤的百分比为 3 1 5± 5 46% ;正常人群T淋巴细胞的拖尾长度和DNA损伤的百分比分别为 16 2± 1 5μm和7 46± 1 15% ;两组数据相比差异极显著 (P <0 .0 1)。结论 :单细胞电泳可快速灵敏地检测细胞DNA损伤 ,能用于肿瘤化疗患者的流行病学观察。对于指导临床用药和预后也有指导意义     

贫血对中晚期宫颈癌放疗疗效的临床分析

目的探讨中晚期宫颈癌患者贫血程度对根治性放射治疗预后的影响。方法 128例中晚期宫颈癌患者行根治性放射治疗,体外照射总剂量50 Gy及高剂量率后装治疗总剂量42 Gy。患者均在放疗前及放疗中进行血红蛋白水平测定,了解其与宫颈癌局部控制率及远期疗效的关系。结果放疗前血红蛋白水平越低,放疗后肿瘤局部控制率及5 a生存率均越低(P<0.01);放疗中,血红蛋白水平升高组完全缓解率及5 a生存率均较降低组高(P<0.01,P<0.05)。结论血红蛋白水平影响宫颈癌的局部控制率和远期疗效,放疗前纠正贫血有助于宫颈癌患者预后。     

后程逐步递量加速超分割放射治疗局部晚期鼻咽癌的疗效分析

目的:观察后程逐步递量加速超分割治疗局部晚期鼻咽癌的近期疗效及毒副反应。方法:72例T3-4N0-1M0期鼻咽癌随机分为常规分割放疗组(对照组)及后程逐步递量加速超分割放疗组(研究组),每组各36例。对照组照射2Gy/次,5次/周,鼻咽部原发灶DT68-72 Gy/6.8-7.2周,颈部转移灶DT60-70 Gy/6-7周,预防照射DT50 Gy/5周。研究组前3.6周同对照组,然后每周分割剂量逐渐递增,即分割剂量的第1、2、3周分别为1.1Gy/次、1.2 Gy/次、1.3 Gy/次,每天2次,两次间隔时间大于6小时,每周5次,鼻咽部总剂量DT72Gy/6.6周,颈部转移灶DT60-70 Gy/6-7周,预防剂量DT50 Gy/5周。结果:放疗结束后3个月,研究组和对照组原发灶CR、PR率分别为77.8%、22.2%和55.6%、44.4%(P<0.05),两组有显著性差异,研究组急性放射性反应高于对照组,但是无统计学意义(P>0.05)。结论:后程逐步递量加速超分割放疗能提高局部晚期鼻咽癌的近期疗效,急性放射性反应患者可以耐受,远期疗效和后期放射损伤有待进一步随诊观察。     

螺旋断层放疗同步化疗对胸段食管鳞癌淋巴结跳跃性转移的临床疗效

目的:评价螺旋断层放疗同步化疗对胸段食管鳞癌伴淋巴结跳跃性转移的疗效。方法:入选86例首诊发现淋巴结跳跃性转移的胸段食管癌患者,均行螺旋断层放射治疗,每周5次。食管肿瘤原发灶治疗剂量50.0～56.0Gy,颈部淋巴结转移灶放疗剂量55.0～61.6Gy,胸部淋巴结转移灶放疗剂量50.0～56.0Gy,腹部淋巴结转移灶放疗剂量50.0～54.0Gy;全食管局部淋巴引流区预防性照射剂量45.0～50.4Gy。患者同步行紫杉醇+卡铂化疗。采用Kaplan-Meier法计算患者的生存率,用Cox回归模型分析患者的生存影响因素。结果:患者中位生存期(496±233)d。86例患者中,19例存活、56例死于食管癌原发病和淋巴结转移、6例死于治疗相关性疾病、5例死于非肿瘤性疾病。放化疗不良反应主要为Ⅰ度和Ⅱ度,其中中性粒细胞下降46例(52.3%)、急性放射性食管炎40例(46.5%)、急性放射性肺炎8例(7.4%);另有5例(5.8%)患者发生Ⅳ度食管放射性损伤。Cox模型显示,T分期和淋巴转移数目是影响患者生存的主要因素(P0.05)。结论:螺旋断层放疗同步化疗能延长胸段食管癌淋巴结跳跃性转移的患者的生存时间,患者能耐受放化疗不良反应。     

Oxidative stress, antioxidant status and DNA damage in patients with impaired glucose regulation and newly diagnosed Type 2 diabetes

Previous studies have postulated the association between oxidative stress and Type 2 diabetes. Considering the long pre-diabetic period with IGR (impaired glucose regulation) and its high risk of developing diabetes, to test this hypothesis, we have investigated oxidative stress pathways and DNA damage in patients with IGR and newly diagnosed Type 2 diabetes. The study population consisted of 92 subjects with NGT (normal glucose tolerance), 78 patients with IGR and 113 patients with newly diagnosed diabetes. Plasma MDA (malondialdehyde) and TAC (total antioxidative capacity) status, erythrocyte GSH content and SOD (superoxide dismutase) activity were determined. A comet assay was employed to evaluate DNA damage. Compared with subjects with NGT, patients with IGR had reduced erythrocyte SOD activity. Patients with diabetes had a higher plasma MDA concentration, but a lower plasma TAC level and erythrocyte SOD activity, than the NGT group. Correlation analysis revealed a strong positive association between IR (insulin resistance) and MDA concentration, but negative correlations with TAC status and SOD activity. With respect to beta-cell function, a positive association with TAC status and an inverse correlation with GSH respectively, were observed. The comet assay revealed slight DNA damage in patients with IGR, which was increased in patients with diabetes. Significant correlations were observed between DNA damage and hyperglycaemia, IR and beta-cell dysfunction. In conclusion, the results of the present study suggest that hyperglycaemia in an IGR state caused the predominance of oxidative stress over antioxidative defence systems, leading to oxidative DNA damage, which possibly contributed to pancreatic beta-cell dysfunction, IR and more pronounced hyperglycaemia. This vicious circle finally induced the deterioration to diabetes.     

Association of low repair efficiency with high hormone receptors expression and SOD activity in breast cancer patients

Objectives:To evaluate the antioxidant status and repair capacity in breast cancer patients as well as the relationship between these parameters and expression of critical proteins in breast cancer tissue.Design and methods:Blood samples were obtained from 25 female breast cancer patients and 19 healthy women. The antioxidant status was determined by the concentration of thiobarbituric-reactive substances (TBARS) and activity of superoxide dismutase (SOD) and catalase (CAT). The basal DNA damage and repair capacity in lymphocytes were evaluated by comet assay. The expression of p53, c-erbB2, Ki-67, estrogen receptor (ER) and progesterone receptor (PR) in cancer tissue was detected by immunohistochemical staining.Results:The breast cancer patients presented significantly elevated endogenous DNA damage in lymphocytes and lower susceptibility to DNA damage induced by H₂O₂ when compared to the control group. There is a negative correlation between TBARS and sensitivity to peroxide induced DNA damage in patients. The percentage of residual damage after H₂O₂ treatment followed by 3h of post-incubation is significantly higher in patients and also correlates positively with SOD activity, ER and PR expression and negatively with the basal DNA damage.Conclusions:Our results demonstrate low repair capacity in lymphocytes of breast cancer patients and suggest that the regulation of DNA repair is sensitive to cellular redox state and can be modulated by ER/PR status.     

Recombinant adenovirus shedding after intratumoral gene transfer in lung cancer patients

We conducted two phase 1 trials of direct intratumoral injection of a recombinant E1E3-deleted adenovirus (AdR) encoding either the bacterial enzyme beta-galactosidase (Ad.RSVbetagal) or interleukin 2 (IL2, AdTG5327) into primary nonsmall-cell lung cancers of 21 patients. We report here virus shedding and the duration of virus expression in the tumor after intrabronchial injection of 10(7), 10(8) or 10(9) PFU of adenovirus. The infectious AdR and the viral DNA were detected in PBL, plasma, stool and aerodigestive samples in a dose-dependent manner, since cell cultures and PCRs were found to be positive mainly for samples from patients who received the highest AdR dose (10(9) PFU). We detected beta-galactosidase activity in the tumor biopsy samples of 66% of the patients, seemingly dose related, and only low levels of IL2 mRNA could be detected in tumor biopsy samples. E1 sequences were not detected by PCR in any of the PBL and bronchial samples collected after virus delivery, except in one patient. In this patient, E1 sequences were detected in PBL as well as in tumor biopsy samples collected at days 8, 30 and 60 and were correlated with longer beta-galactosidase expression in tumor samples. PBL tested before and after virus delivery contained both E1 sequences indicating that they did not result from replication-competent adenovirus (RCA) E1 sequences present in the inoculum. In addition, only on the day of the injection was Ad.RSVbetagal also detected in E1-positive PBL, indicating that virus replication in blood was very unlikely.     

肿节风水提物抗放射诱导氧化损伤的临床观察

目的观察肿节风水提物抗氧化损伤的临床疗效。方法选择Ⅲ和Ⅳa期鼻咽癌（NPC）患者46例随机分为对照组和研究组，其中对照组25例，研究组21例。所有患者均采用放化综合治疗的方法，研究组配合单剂中药肿节风水提物20g／d口服。分,NN定治疗前后血浆总超氧化物歧化酶（SOD）活力和丙二醛（MDA）含量，并观察2组治疗后肿瘤消退情况和急性放化疗副反应。结果所有患者均完成治疗后与治疗前比较，对照组血浆总SOD活力降低，血浆MDA含量升高；而研究组二者均降低，治疗后研究组血浆总SOD活力高于对照组，MDA含量显著低于对照组，差异均有统计学意义（P〈0．05）。放疗后两组肿瘤局部控制率无差异（P〉0．05）。研究组的急性放化疗副反应出现的频率和严重度均低于对照组，差异有统计学意义（P〈0．05）。结论肿节风水提物有抗氧化损伤的作用，与放化疗结合治疗可使Ⅲ和Ⅳa期NPC肿瘤消退满意，对放化疗所致的副反应有一定消除作用。     

Evaluation of DNA damage and metabolic syndrome parameters in diabetic rabbits supplemented with antioxidants

The aim of the present study is to evaluate the extent of DNA damage in diabetes and metabolic syndrome and to assess the variations after supplementation with antioxidants. We used comet assay to measure DNA damage in freshly isolated lymphocytes from a total of 12 rabbits, distributed into four experimental groups ( n  = 3 rabbits per group): non-diabetic (control, G1), diabetic (G2), diabetic supplemented with vitamin C (G3), and diabetic supplemented with vitamin E (G4). Also their serum was isolated for estimation of parameters that contribute to metabolic syndrome. Malondialdehyde (MDA), the marker of oxidative stress was also assessed. Mean values of DNA damage (tail length, expressed as μm), lipid peroxidation and concentration of blood glucose, MDA, C-reactive protein, and triglycerides were higher in G2; whereas the mean values of concentration of high-density lipoprotein, serum paraoxonase-1 activity and small dense low-density lipoprotein oxidation time were reduced in G2 followed by G3, G4, and G1. A significant positive correlation was observed between the DNA damage and elevated parameters of metabolic syndrome ( r  = 0.66, 0.96, 0.89, 0.75, 0.88, 0.92, 0.99, P  < 0.05) and a significant negative correlation ( r  = −0.91, −0.75, −0.98, P  < 0.05) was found between the DNA damage and declined parameters of metabolic syndrome. These data indicate that the extent of DNA damage is more in diabetic rabbits as compared to the non-diabetic or antioxidant supplemented group. Abnormal metabolic parameters and their correlation with DNA damage, suggest the risk of development of metabolic syndrome in diabetic group but a possibility of repression by antioxidants because of their ability to counteract oxidative stress.     

氧化乐果长期暴露对大鼠骨骼肌氧化损伤的研究

目的探讨氧化乐果对大鼠骨骼肌组织氧化损伤的影响。方法将40只雄性Wistar大鼠随机分为4组,正常对照组,低剂量组,中剂量组和高剂量组,每组10只。低剂量组,中剂量组和高剂量组每天分别给予1/20、1/10、1/5LD50的氧化乐果,采用灌胃的途径给药,连续给药8周,检测大鼠血糖水平,骨骼肌组织中丙二醛（Malondialde-hyde,MDA）含量、超氧化物歧化酶（Superoxide dismutase,SOD）、过氧化氢酶（Catalase,CAT）和谷胱甘肽过氧化物酶（Glutathione peroxidase,GSH-Px）的活性以及骨骼肌的组织病理学检测。结果与正常对照组相比,低剂量、中剂量和高剂量组大鼠骨骼肌MDA含量显著升高（P〈0.05）,SOD、CAT和GSH-PX活性显著降低（P〈0.05）;大鼠的血糖和组织病理学检查未见异常变化。结论长期接触有机磷农药氧化乐果可导致骨骼肌出现氧化应激。     

Age-related increases in plasma malondialdehyde and protein carbonyl levels and lymphocyte DNA damage in elderly subjects

OBJECTIVES: Increased oxidative stress has been hypothesized to play an important role in the aging process. A role for oxidative damage in normal aging is supported by studies in experimental animals, but there is limited evidence in humans. To investigate the relationship between the oxidative stress and aging in humans, we determined lipid and protein oxidation in plasma as well as DNA damage in lymphocytes in young and elderly subjects. DESIGN AND METHODS: 55 healthy subjects were divided into young (21-40 years) and elderly (61-85 years) groups. Plasma malondialdehyde (MDA), protein carbonyl (PC) levels, and grade of DNA damage in lymphocytes using comet assay as well as total ferric reducing antioxidant power (FRAP) in plasma were determined in young and elderly subjects. RESULTS: Plasma MDA and PC levels were found to be increased in plasma of elderly subjects as compared to young subjects. Increases in endogenous and H2O2-induced DNA damage were also observed in lymphocytes of elderly subjects. In addition, we detected a significant decrease in FRAP values in elderly subjects. Plasma MDA, PC levels and endogenous and H2O2-induced DNA damage were positively correlated with aging, but negatively with FRAP values. CONCLUSION: We evaluated MDA, PC levels and lymphocyte DNA damage altogether in both young and elderly subjects for the first time. The results of this study strongly support the presence of increased oxidative stress in elderly subjects.     

Increased plasma malondialdehyde and protein carbonyl levels and lymphocyte DNA damage in patients with angiographically defined coronary artery disease

We investigated the oxidative modifications of lipids, proteins and DNA, three potential molecular targets of oxidative stress, in 30 patients with angiographically defined coronary artery disease (CAD) and 30 healthy control subjects. In addition, we examined relationships between these oxidative modifications and the severity of vascular lesions in patients with CAD. Malondialdehyde (MDA) and protein carbonyl (PC) levels, as well as ferric reducing antioxidant power (FRAP), were measured in the plasma. DNA damage was evaluated as single strand breaks (SSBs), formamidopyrimidine glycosylase (Fpg) and endonuclease III (E-III)-sensitive sites by the comet assay in DNA isolated from lymphocytes. MDA and PC levels increased, but FRAP values decreased, in patients as compared to controls. However, these values did not vary with the number of affected coronary vessels and were not correlated with Duke score, a parameter of the severity of vascular lesions in patients with CAD. We also found that lymphocyte DNA damage (SSBs, Fpg and E-III sites) were increased in patients. Although there were no significant differences in SSBs values in patients grouped according to affected vessel number, Fpg and E-III sites increased. We also detected significant correlations between Duke scores and SSBs and Fpg sites. Serum cholesterol, triglyceride and LDL-cholesterol levels were found to increase, but HDL-cholesterol levels decreased in CAD patients, but these lipids were not correlated with Duke scores. The results of this study reinforce the presence of increased combined oxidative modifications in lipid, protein and DNA in patients with CAD. However, lymphocyte DNA damage seems to be a more reliable assay than MDA and PC determinations to detect the severity of vascular lesions in patients.     

还原型谷胱甘肽对慢性肺源性心脏病急性加重期患者血中脂质过氧化物及抗氧化物酶活性的影响

目的:探讨还原型谷胱甘肽对慢性肺源性心脏病急性加重期患者血中脂质过氧化物及抗氧化物酶活性的影响。方法:检测27例健康成年人静脉血全血超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)的活性及血浆脂质过氧化物(LPO)和丙二醛(MDA)的浓度,与慢性肺心病急性加重期组治疗前的此5项指标进行对应比较;选择68例慢性肺源性心脏病急性加重期患者,随机分成两组,试验前均监测静脉血全血SOD、GSH-Px和CAT的活性及血浆LPO和MDA的浓度以及右室压(RVP)、平均肺动脉压(mPAP)等血流动力学指标并评价心功能。试验组在给予常规治疗的同时合并给予还原型谷胱甘肽1.2 g/d,稀释后静脉滴注,疗程2周;对照组只给予常规治疗。2周后,复测上述指标,比较各组治疗前后的变化。结果:(1)肺心病急性加重期组的全血SOD、GSH-Px和CAT的活性比对照组低,而血浆LPO及MDA的浓度比对照组高(均P<0.05)。(2)还原型谷胱甘肽组试验前后比较,全血SOD、GSH-Px和CAT活性明显增高,且血浆LPO和MDA浓度明显降低(均P<0.05);而对照组则无显著变化(P>0.05)。(3)还原型谷胱甘肽组试验前后比较,PVP、mPAP均明显下降(P<0.05);而对照组无显著变化(P>0.05)。(4)还原型谷胱甘肽组心力衰竭纠正的有效率显著高于对照组(P<0.05)。结论:慢性肺源性心脏病急性加重期患者机体的抗氧化能力降低,还原型谷胱甘肽可通过提高机体的抗氧化能力,消除氧自由基和脂质过氧化物起到降低肺动脉和右心室压力、纠正心力衰竭的作用。