氯高铁血红素对慢性肾功能衰竭大鼠的血压影响及其机制探讨

目的研究氯高铁血红素对慢性肾衰竭大鼠血压的影响,并探讨其可能机制.方法用5/6肾切除法建立CRF模型,研究分为3组(1)假手术组(sham组)、(2)慢性肾衰组(CRF组)、(3)氯高铁血红素组(hemin组).观察术后第10周(即给药后第8周)各组血清尿素氮、肌酐、尿蛋白、血红蛋白及术后第4,6,8和10周血压等指标;免疫组化方法检测肾组织中血红素氧化酶-1(HO-1)的表达和分布;双波长分光光度法测量血浆内源性CO的水平;放免法检测肾组织和血浆中内皮素-1(ET-1)的含量.结果与CRF组相比,hemin组在术后第6,8和10周均出现显著的血压下降(P＜0.05).同时,在术后第10周hemin组比CRF组血肌酐、尿素氮、尿蛋白显著降低(P＜0.05),贫血明显改善(P＜0.05);肾组织中HO-1表达明显增加,血浆中内源性CO水平明显升高,肾组织和血浆中ET-1水平明显降低(P＜0.05).结论hemin组具有延缓慢性肾功能衰竭大鼠高血压的发生和发展作用,这种作用与hemin诱导肾脏HO-1表达、增加血浆CO浓度,降低肾组织和血浆中的ET-1水平有关.     

氯高铁血红素对早期糖尿病肾病大鼠肾脏的影响

目的:观察氯高铁血红素处理不同时期糖尿病大鼠肾脏结构和功能、核转录相关因子(Nrf-2)变化.方法:选取8周SD大鼠12只作为正常对照组(A组);对另36只SD大鼠采用高糖高脂联合链脲佐菌素法诱导建立糖尿病模型,建模后再分为糖尿病组(B组,n=17)和糖尿病+氯高铁血红素组(C组,n=17).检测8～14周大鼠体质量、血糖、24 h尿微量白蛋白,第10、14周提取大鼠肾组织匀浆,分析氧化应激产物丙二醛MDA含量,Western blotting检测肾脏HO-1、Nrf-2表达,PAS染色光镜下观察肾脏结构.结果:与正常对照组比较,B、C两组体质量均增高,而B组又显著高于C组(P<0.05).B、C两组血糖、24 h尿微量蛋白也显著高于正常对照组(P<0.05).不同时期比较显示,B、C组Nrf-2表达第14周均较第10周降低,C组Nrf-2均较B组升高(P<0.05),HO-1表达也呈现相同情况.MDA含量比较显示,第14周较第10周相比各组有显著升高;第10周时C组较B组低.结论:氯高铁血红素能改善早期糖尿病肾病大鼠肾脏结构和功能,并与抗氧化因子Nrf-2、HO-1表达有关.     

氯高铁血红素对慢性肾功能衰竭大鼠的作用

氯高铁血红素(hemin)是血红素氧化酶1(HO-1)的诱导剂,它可通过诱导HO-1表达对多种肾病发挥保护作用;同时,氯高铁血红素也是一种铁络合物,在治疗缺铁性贫血方面有着其他铁剂如葡萄糖酸亚铁(FG)等不可替代的优势。本实验以FG为对照,研究氯高铁血红素在慢性肾功能衰竭(CRF)大鼠中的作用,探讨其可能的作用机制。     

高铁血红素对大鼠心肌缺血再灌注损伤的保护作用

目的探讨血红素氧合酶-1(HO-1)激动剂高铁血红素对大鼠心肌缺血再灌注损伤的保护作用及机制。方法健康雄性SD大鼠48只,随机分为4组:假手术组(SO)、缺血再灌注组(I/R)、高铁血红素预处理组(HEMI/R)、锌原卟啉IX(ZnPPIX,血红素加氧酶-1抑制剂)+高铁血红素预处理组(ZnPPIX-HEM-I/R),每组12只;后3组建立大鼠I/R模型;检测各组大鼠的心肌梗死范围、心肌酶(CK、LDH)、炎性介质(TNF-α、IL-6)、氧化应激指标(MDA、SOD)并进行比较。结果与S0组比较,I/R组血清LDH、CK、TNF-α、IL-6、MDA水平均升高,而SOD水平降低,差异有统计学意义(P均<0.05)。与I/R组比较,HEM-I/R组大鼠梗死心肌范围(35.8±2.0)%vs(51.0±2.5)%、心肌酶水平[LDH(U/L):1125.0±90.0 vs 1895.6±95.0;CK(U/L):1589.8±70.0 vs 2500.5±150.5]、炎性介质水平[TNF-α(pg/mg):27.00±0.20 vs 40.00±0.20,IL-6(pg/mg):38.80±0.25 vs 61.50±0.10]氧化应激水平[MDA(mmol/mg):7.05±0.50 vs 12.05-0.50,SOD(U/mg):170.50±5.55 vs 95.50±6.55];均显著改善,差异有统计学意义(P均<0.05)。而与HEM-1/R组比较,ZnPPIX-HEM-I/R组上述各项指标的改善均被抑制,差异有统计学意义(P均<0.05)。结论高铁血红素能显著发挥对大鼠缺血再灌注损伤的心肌保护作用,其保护作用机制可能与激动HO-1的过表达相关。     

妊娠期高血压疾病患者血清hs-CRP、sFlt-1水平变化及与妊娠结局的相关性

目的：探讨妊娠期高血压疾病（HDP）患者血清可溶性血管内皮生长因子受体-1(sFlt-1)、超敏C反应蛋白（hs-CRP）水平变化及与妊娠结局的相关性。方法：收集2022年1月—2023年2月于赣州市妇幼保健院接受治疗的HDP患者108例作为病例组,并进行回顾性分析。根据病情严重程度将病例组患者分为妊娠期高血压组（43例）、子痫前期组（35例）、子痫组（30例）,并选取同期正常妊娠的妇女82例作为对照组。分析所有研究对象中血清hs-CRP、sFlt-1水平变化情况。结果：病例组血清hs-CRP、sFlt-1水平均明显高于对照组（P<0.05）。妊娠期高血压组、子痫前期组、子痫组患者血清hs-CRP、sFlt-1水平比较差异均有统计学意义（P<0.05）,且血清hs-CRP、sFlt-1水平随病情严重程度的加重而升高（P<0.05）。不良妊娠结局组患者血清hs-CRP、sFlt-1水平均高于妊娠结局良好组（P<0.05）。血清hs-CRP、s Flt-1水平反映HDP患者妊娠结局的AUC分别为0.758、0.763。相关性分析显示,hs-CRP、sFlt-1之间呈...     

硝苯地平缓释片联合拉贝洛尔对妊娠期高血压患者血清IGF-1、sFIt-1水平及血管内皮功能的影响

目的:探究硝苯地平缓释片联合拉贝洛尔对妊娠期高血压(HDCP)患者血清胰岛素样生长因子-1(IGF-1)、人可溶性血管内皮生长因子受体1(sFIt-1)及血管内皮功能的影响。方法:将105例HDCP患者按不同治疗方案分为对照组(n=51)和实验组(n=54)。对照组接受拉贝洛尔治疗,实验组采用拉贝洛尔和硝苯地平联合治疗,两组患者均治疗两周。使用ELISA法检测血清IGF-1、sFIt-1、内皮素-1(ET-1)水平,微量一氧化氮(NO)检测仪检测NO。比较两组患者临床疗效,血清IGF-1、sFIt-1、NO、ET-1水平,母婴结局和不良反应。结果:治疗后,实验组患者总有效率(94.44%)高于对照组有效率(80.39%)(P<0.05);两组患者血清IGF-1、sFIt-1、NO水平均升高,ET-1水平均降低;实验组血清IGF-1、sFIt-1、NO水平均高于对照组(P<0.05),ET-1水平低于对照组(P<0.05)。实验组顺产率高于对照组(P<0.05),早产率低于对照组(P<0.05);两组不良反应发生率比较,差异无统计学意义(P>0.05)...     

氯化高铁血红素对人晚期内皮祖细胞数量和血红素加氧酶-1表达的影响

目的 观察氯化高铁血红素(简称血红素)在体外对人晚期内皮祖细胞(EPCs)数量和血红素加氧酶-1(HO-1)的影响.方法 从健康分娩产妇脐带静脉血中分离提取单个核细胞,体外培养诱导分化为晚期EPCsO在不同体积分数胎牛血清(FBS)条件下用血红素(10μmol/L)干预并设置对照组,干预24 h后,锥虫蓝染色计数,细胞计数试剂盒-8(CCK-8)检测细胞毒性,Western印迹法检测HO-1的表达.结果 在低体积分数(0.2%)FBS条件下,与对照组相比,血红素减少了晚期EPCs的数量,但随着FBS体积分数的逐渐提高,血红素对晚期EPCs增殖的抑制能力减弱,促增殖能力逐渐增强(P＜0.05),且诱导HO-1的表达逐渐提高.结论 细胞体外培养中,FBS体积分数在血红素对晚期EPCs数量和活性的作用方面有着重要的影响,且在高体积分数(5%)FBS条件下,血红素促进细胞增殖的效应初步推测是通过诱导HO-1高表达来实现的,但其具体机制和其中涉及的信号转导通路有待进一步探讨.     

血红素氧合酶-1对大鼠主动脉平滑肌细胞增殖的影响

目的探讨血红素氧合酶-1(HO-1)蛋白表达对大鼠主动脉平滑肌细胞(RASMC)增殖的影响。方法大鼠主动脉平滑肌细胞株经复苏、传代培养后用于实验,设置空白对照组、HO-1诱导组、HO-1抑制组,后两组分别加用血晶素、锌原卟啉Ⅸ与细胞共同孵育,用Western blot法检测HO-1表达量,并检测HO-1活力;用MTT法检测RASMC增殖能力。同时,还观察了血晶素、锌原卟啉Ⅸ的细胞毒性作用。结果上调HO-1蛋白表达及升高HO-1活力能显著抑制血清刺激的RASMC增殖,反之,抑制HO-1蛋白表达及其活力则增强血清刺激的RASMC增殖。实验浓度的血晶素、锌原卟啉Ⅸ无明显细胞毒性作用。结论 HO-1蛋白高表达能有效抑制RASMC增殖。     

血红素氧合酶在肝纤维化大鼠门静脉组织中表达的动态变化及意义

目的观察实验性大鼠肝纤维化形成过程中门静脉组织血红素氧合酶（heme oxygenase,HO）表达的动态变化,探讨H0在大鼠肝纤维化门静脉高压形成过程中的作用及意义。方法将64只SD大鼠随机分为肝纤维化模型组、对照组,每组32只。模型组皮下注射50％四氯化碳复制肝纤维化模型,0.3ml／100g,2次／周;对照组给予相同剂量的生理盐水。分别于第3、6、9、12周各组随机处死8只大鼠,观察大鼠肝脏大体及组织学变化;RT—PCR法检测大鼠门静脉组织HO-1mRNA、HO-2mRNA的表达水平。结果随着造模时间的延长,模型组大鼠肝脏变形、变小、变硬,纤维组织增生及假小叶、再生结节形成。对照组大鼠门静脉组织中有少量HO—1mRNA表达,在第3、6、9、12周分别为0．33±0.05、0．34±0．02、0．33±0．04、0．34±0．04,随着肝纤维化的形成,门静脉组织HO—1mRNA表达水平逐渐升高,分别为0．52±0．03、0．74±0．05、0．93±0.05、1.01±0.10,两组比较差异均有显著统计学意义（均P〈0．01）。模型组组内各时间点比较,第9周与第12周差异不明显（P〉0．05）,其余组间差异有显著统计学意义（均P〈0.01）。对照组与模型组HO-2mRNA的表达量差异无统计学意义（均P〉0.05）.结论随着肝纤维化／肝硬化的形成,大鼠门静脉组织中HO-1mRNA的表达逐渐增加,HO—2mRNA的表达量无明显改变,提示HO—1与肝纤维化有关,在门静脉高压形成中可能有重要作用。     

Protective effects of hemin pretreatment combined with ulinastatin on septic shock in rats

Background Urinary trypsin inhibitor inhibits the enhanced production of pro-inflammatory molecules. Hemeoxygenase-1 induction protects against ischemia/repeffusion injury, oxidative stress, inflammation, transplant rejection, apoptosis, and other conditions. However, it is unknown if a combined hemin and ulinastatin pretreatment could result in protective effects for septic shock. In this study, we investigated the role of hemin pretreatment combined with ulinastatin on septic shock in rats. Methods Eighty healthy, male Sprague-Dawley rats were randomly divided into four groups： group S, group H, group U and group HU. Groups S and U received 1 ml normal saline intraperitoneally, while groups H and HU both received 1 ml （100 mg/kg） hemin. Twenty-four hours later, 0.5 ml （10 mg/kg） E. coil lipopolysaccharide was injected intravenously to replicate the experimental model of septic shock. After an initial 25% decrease in the mean arterial pressure, corresponding to time point 0, groups HU and U received 0.5 ml 10 000 U/kg ulinastatin intravenously, and the others received 0.5 ml normal saline. Results The number of deaths in groups H and U was lower than that in the group S （P〈0.05）, and was higher than that in group HU （all P〈0.05） respectively. The mean arterial pressure （MAP） in the group S was significantly greater than that in group H （P〈0.05）, and was lower than that in group HU and group U （P〈0.05）. The plasma levels of alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, creatinine （Cr） and blood urea nitrogen （BUN）, the malondial- dehyde （MDA） of liver, kidney and lung, and the lung Evans blue （EB） contents in groups H and U, were greater than that in group HU （all P〈0.05）, and were lower than that in group S （all P〈0.05）. In contrast, the plasma levels of CO in groups H and HU were higher than that in groups S and U （all P〈0.05）, and SOD of liver, kidney and lung in groups H and U were higher than that in group S,     

Hypoxia-inducible factor-1 alpha regulates the role of vascular endothelial growth factor on pulmonary arteries of rats with hypoxia-induced pulmonary hypertension

Background Hypoxia-inducible factor-1α (HIF-1α) is one of the pivotal mediators in the response of lungs to decreased oxygen availability, and increasingly has been implicated in the pathogenesis of pulmonary hypertension. Vascular endothelial growth factor (VEGF), a downstream target gene of HIF-1α, plays an important role in the pathogenesis of hypoxic pulmonary hypertension and hypoxic pulmonary artery remodelling. In this study, we investigated the dynamic expression of HIF-1α and VEGF in pulmonary artery of rats with hypoxia-induced pulmonary hypertension. Methods Forty male Wistar rats were exposed to hypoxia for 0, 3, 7, 14 or 21 days. Mean pulmonary arterial pressure (mPAP), vessel morphometry and right ventricle hypertrophy index (RVHI) were estimated. Lungs were inflated and fixed for in situ hybridisation and immunohistochemistry. Results mPAP values were significantly higher than the control values after 7days of hypoxia ［(18.4±0.4) mmHg, P&lt;0.05］. RVHI developed significantly after 14 days of hypoxia. Expression of HIF-1α protein increased in pulmonary arterial tunica intima of all hypoxic rats. In pulmonary arterial tunica media, HIF-1α protein was markedly increased by day 3 (0.20±0.02, P&lt;0.05), reached the peak by day 7, then declined after day 14 of hypoxia. HIF-1α mRNA increased significantly after day 14 of hypoxia （0.20±0.02, P&lt;0.05）. VEGF protein began to increase markedly after day 7 of hypoxia, reaching its peak around day 14 of hypoxia (0.15±0.02, P&lt;0.05). VEGF mRNA began to increase after day 7 of hypoxia, then remained more or less stable from day 7 onwards. VEGF mRNA is located mainly in tunica intima and tunica media, whereas VEGF protein is located predominantly in tunica intima. Linear analysis showed that HIF-1α mRNA, VEGF and mPAP were correlated with hypoxic pulmonary artery remodelling. HIF-1α mRNA was positively correlated with VEGF mRNA and protein (P&lt;0.01). Conclusion HIF-1α and VEGF are both involved in the pathogenesis of hypoxia-induced pulmonary hypertension in rats.     

Flt-1、Flk-1在人年轻恒牙和成熟恒牙牙髓表达的组织学研究

目的探讨人恒牙牙髓组织不同发育阶段血管内皮生长因子受体1（VEGFR-1/Flt-1）、血管内皮生长因子受体2（VEGFR-2/Flk-1）表达的组织学特征及其在人恒牙牙根发育成熟中的可能作用。方法将因正畸治疗需要而拔除的人健康前磨牙（无畸形中央尖、牙隐裂、过度磨耗等）分为根尖开放的年轻恒牙和根尖闭合的成熟恒牙,每组各15例,采用免疫组织化学方法检测Flt-1、Flk-1蛋白的表达与定位并进行图像采集,应用Image-ProPlus 6.0和SPSS 13.0对年轻恒牙和成熟恒牙牙髓组织Flt-1、Flk-1的阳性表达进行图像和统计学分析。结果 Flt-1、Flk-1在牙髓组织血管内皮细胞免疫反应阳性;年轻恒牙牙髓VEGF、Flk-1阳性表达的平均光密度值（OD）高于成熟恒牙（P〈0.05）,而Flt-1的表达低于成熟恒牙（P〈0.05）;Flt-1、Flk-1呈显著负相关性表达（P〈0.01）。结论年轻恒牙和成熟恒牙牙髓组织Flt-1、Flk-1呈现不同特征表达,提示Flt-1、Flk-1参与了牙根的发育过程,成熟恒牙牙髓防御修复能力下降可能与Flk-1表达不足有关。     

苯丙氨酸对慢性缺氧性肺动脉高压大鼠的保护作用

目的:探讨苯丙氨酸(PHE)对慢性缺氧所致的肺动脉高压的影响及其可能机制.方法:28只雄性Wistar大鼠随机分为对照组(n=9)、缺氧组(n=10)、缺氧 PHE组(n=9).缺氧组与缺氧 PHE组每d给予缺氧处理.缺氧 PHE组每d于缺氧前腹腔注射PHE 400 mg/(kg·d),对照组与缺氧组腹腔注射等量生理盐水,共21 d.采用右心导管法测定右心室平均压(pMRV)及肺动脉平均压(pMPA),同时用多导生理记录仪测定心率和血压.测定右心室(RV)质量/(左心室(LV)质量 室间隔(S)质量)(mRV/(mLV ms))比值,并观测肺血管形态结构的变化和各组血清血管内皮生长因子(VEGF)的变化.结果:缺氧组的pMRV、pMPA、(mRV/(mLV mS)明显高于对照组(P＜0.01)与缺氧 PHE组(P＜0.05);缺氧组的肺细小动脉管壁厚度、管壁横截面积、管壁厚度占血管外径的百分比及管壁横截面积占血管横截面积的百分比均明显高于对照组与缺氧 PHE组(P＜0.01).缺氧 PHE组大鼠血清VEGF水平明显低于缺氧组(P＜0.01),但仍高于对照组(P＜0.05).结论:PHE可能是通过降低VEGF的表达而降低慢性缺氧大鼠的右心室压及肺动脉高压,逆转右心室肥厚及血管结构的重建.     

Effect of Heme Oxygenase-1 Inducer Hemin on Chronic Renal Failure Rats

The role of HO-1 inducer, hemin, in chronic renal failure (CRF) rats and its possible mechanism of action was studied. 5/6 subtotal nephrectomy was performed to establish chronic renal failure model. Rats were randomly assigned to 4 groups: sham-operated group, CRF group,ferrous gluconate group and heroin group. At the 10th week after operation, serum creatinine,BUN, RBC, HGB and HCT were measured. Renal pathologic changes were observed. RT-PCR and immunohistochemistry were used to detect the expression and distribution of HO-1. RT-PCR and radioimmunoassay was used to determine the expression of ET-1 in the kidney and plasma. The results showed that as compared with CRF group, serum creatinine and BUN in hemin group were reduced significantly and nephrogenic anemia was improved markedly. Glomerular mesangial proliferation and interstitial lesion were also ameliorated significantly. Heroin not only increased the expression of HO-1 but also reduced the expression of ET-1 in the kidney. The level of ET-1 protein in the plasma was also reduced after heroin treatment. Most of these indexes were not obviously changed in ferrous gluconate group. It was suggested that through inducing the expression of HO-1 and reducing the level of ET 1 in the kidney and plasma, heroin plays an important protective role in 5/6 subtotal nephrectomized rats.     

红藤颗粒剂对大鼠异位子宫内膜血管内皮生长因子及其受体胎肝激酶-1表达的影响

目的：观察红藤颗粒剂对子宫内膜异位症大鼠异位内膜的抑制作用以及对异位内膜血管内皮生长因子（vascular endothelial growth factor,VEGF）及其受体2胎肝激酶-1（fetal liver kinase-1,Flk-1）表达的影响。 方法：采用自体移植法建立子宫内膜异位症大鼠模型,48只SD大鼠随机分为模型组、去势组、米非司酮（5mg／kg）组和低（20g／kg）、中（40g／kg）、高（80g／kg）剂量红藤颗粒剂组。连续灌胃给药21d后处死大鼠,用电子数显卡尺测定并计算异位内膜的体积,采用免疫组织化学法检测各组异位内膜VEGF及其受体Flk—1的表达。 结果：红藤颗粒剂低剂量组异位内膜体积与模型组比较差异无统计学意义（P〉0．05）,其他组异位内膜体积均明显低于模型组,差异有统计学意义（P〈0．05）。病理组织学观察发现,除红藤颗粒剂低剂量组外,其余各组异位内膜厚度明显低于模型组,差异有统计学意义（P〈0．01）,异位内膜呈退化趋势。免疫组织化学检测发现,VEGF主要表达于异位内膜腺上皮及血管内皮细胞胞浆,散在于周围基质细胞胞浆。除红藤颗粒剂低剂量组外,各治疗组异位内膜VEGF和Flk-1平均灰度值与模型组比较,差异有统计学意义（P〈0．05,P〈0．01）。 结论：中药红藤颗粒剂可通过抑制异位内膜VEGF及其受体Flk-1的表达,阻止新血管的生成,抑制大鼠异位子宫内膜的生长并使其萎缩。     

肿瘤细胞对体外诱导人内皮细胞血管形成的影响及VEGF的作用

目的应用Matrigel建立血管形成的体外培养体系,研究肿瘤细胞对诱导人血管内皮细胞血管形成的影响及血管内皮生长因子(VEGF)的作用,进而探讨VEGF与肿瘤血管新生的关系及其作用机制。方法培养人脐静脉内皮细胞(HUVECs),应用Matrigel建立血管形成的体外培养体系;传代培养口腔鳞癌细胞株,制备肿瘤细胞条件培养液;实验分浓度效应组和时间效应组;对各实验组观察、照相后95%冰乙醇固定,CD34及激酶结构域区受体(KDR)免疫细胞化学染色;采用光镜下计数管腔数及计算机图像分析对结果进行测定并分析。结果肿瘤细胞条件培养液作用于培养的HUVECs后,培养体系的管腔数增多,且在一定范围内呈剂量和时间依赖效应(P<0.01);随培养体系的管腔数增多,血管内皮细胞KDR表达增加,在一定范围内呈剂量和时间依赖效应(P<0.01)。结论肿瘤细胞可以促进Matrigel体外诱导人内皮细胞的血管形成及KDR表达上调,并在一定范围内呈剂量及时间依赖效应。     

大鼠5/6肾切除肾脏中血红素氧合酶-1免疫组织化学及病理学研究

目的:探讨血红素氧合酶-1(HO-1)在慢性肾功能不全(CRF)大鼠肾脏中的表达、活性变化以及对肾脏病理学的影响。方法:将5/6肾切除大鼠分为假手术组、CRF组和Hemin组。第2次术后8周观察肾组织病理学改变，免疫组化方法检测HO-1在大鼠肾脏中的表达、分布，检测血清及肾组织中HO-1活性。结果:HO-1主要分布于肾皮质的近端、远端小管以及肾髓质的集合管、髓袢的上皮细胞内；HO-1在CRF大鼠肾脏中表达及活性降低。病理学检查显示，Hemin组大鼠肾小球系膜增生程度明显低于CRF组大鼠，同时肾间质炎性细胞浸润及纤维化程度也较CRF组轻。结论:HO-1在CRF大鼠肾脏中表达及活性降低，HO-1可明显减轻CRF大鼠肾脏病理学损伤，延缓肾脏病变。     

苏拉明对大鼠低氧性肺动脉高压的影响

目的 探讨血管内皮生长因子（ＶＥＧＦ）在低氧性肺动脉高压发病中的作用。方法 将３０只Ｗｉｓｔａｒ大鼠分为对照组、低氧组和低氧＋苏拉明组,以常压低氧复制大鼠肺动脉高压模型,采用微导管法测定肺动脉平均压,对肺组织切片进行图像分析。结果 经低氧３周后,大鼠形成明显的肺动脉高压、肺小动脉管壁增厚和在左心室肥厚;经苏拉明处理,可明显减轻低氧所致的肺动脉压升高、肺血管壁增厚和右心室肥厚。结论 慢性低氧导致肺动