一氧化氮对缺氧性肺血管结构重建大鼠肺动脉血小板源生长因子表达的影响

目的 探讨一氧化氮对缺氧性肺血管结构重建大鼠肺动脉中血小板源生长因子 （ＰＤＧＦ）表达的影响。方法 将大鼠随机分为４组：常氧组（６只）、低氧组（６只）、低氧＋Ｌ－精氨酸组（低氧＋Ｌ－Ａｒｇ组）（７只）及低氧＋Ｎ＾ω－硝基－Ｌ－精氨酸甲酯组（低氧＋Ｌ－ＮＡＭＥ组）（６只）。以光学显微镜观测４组大鼠肺中、小肌型动脉的相对中膜厚度（ＲＭＴ）。应用ＰＤＧＦ的单克隆抗体经免疫组织化学技术对４组大鼠肺动脉ＰＤ     

新生儿急性肾功衰竭血浆内皮素等指标水平改变

分别测定１２例新生儿急性肾功衰竭（ＡＲＦ）、２５例非ＡＲＦ和２７例正常新生儿血、尿纤维蛋白降解产物（ＦＤＰ）、血浆内皮素（ＥＴ）和Ｄ二聚体（ＤＤｉｍｅｒ，ＤＤ）。结果：ＡＲＦ组ＦＤＰ较非ＡＲＦ组和正常对照组明显增加（Ｐ＜００１）；ＡＲＦ组ＥＴ、ＤＤ较非ＡＲＦ组明显增加；ＡＲＦ组的肾功能改变（ＢＵＮ、Ｃｒ）与ＦＤＰ、ＥＰ、ＤＤ无显著相关关系。提示血管内和／或肾内凝血是ＡＲＦ的重要因素，血管内皮细胞及肾上皮细胞释放ＥＴ增加，从而影响新生儿ＡＲＦ时水电解质的代谢。     

新生儿急性肾功衰竭血浆内皮素等指标水平改变

分别测定了１２例新生急性肾功衰竭（ＡＲＦ），２５例非ＡＲＦ和２７例正常新生儿血，尿纤维蛋白降解产物（ＦＤＰ）血浆内皮素（ＥＴ）和Ｄ二聚体（Ｄ－Ｄｉｍｅｒ，ＤＤ）。结果：ＡＲＦ组ＦＤＰ较非ＡＲＦ组和正常对照组明显增加（Ｐ〈０．０１）；ＡＲＦ组ＥＴ，ＤＤ较非ＡＲＦ组明显增加，ＡＲＦ组的肾功能改变（ＢＵＮ，Ｃｒ）与ＦＤＰ，ＥＰ，ＤＤ无显著相关关系，提示血管内和／或肾内凝血是ＡＲＦ的重要因素，血管内皮细胞     

病毒性心肌炎患儿血浆内分泌素的改变及其临床意义的探讨

采用放射免疫法测定４７例急性病毒性心肌炎患儿及２０例正常儿童血浆肾素活性（ＰＲＡ）、血管紧张素Ⅱ（ＰＡⅡ）、醛固酮（ＰＡＬＤ）、心钠素（ＰＡＮＦ）的水平，以探讨病毒性心肌炎发病机制以及以上４种内分泌素在其临床中的意义。结果表明，心肌炎患儿（心功能为１和２级）与正常儿童相比，ＰＲＡ没有明显改变，ＰＡⅡ、ＰＡＬＤ及ＰＡＮＦ皆显著升高；ＰＡⅡ、ＰＡＬＤ、ＰＡＮＦ三者之间分别呈正相关关系；心肌炎组中表现为心肌缺血及心律失常的两个组间ＰＡⅡ、ＰＡＬＤ、ＰＡＮＦ没有显著差异。说明心肌炎急性期肾素－血管紧张素－醛固酮系统（ＲＡＡＳ）被激活，以维持心排血量和血压，增加血管阻力。同时，心肌细胞ＡＮＦ的合成和分泌增加，通过排钠、利尿、扩血管作用拮抗ＲＡＡＳ增加的炎症心肌的负担     

脓毒血症大鼠心肌能量代谢与超微结构变化的探讨

目的：对脓毒血症大鼠心肌葡萄糖6－磷酸酶活性及心肌腺苷酸水平的动态变化，心肌超微结构的改变进行研究，探讨脓毒血症大鼠心肌能量代谢变化在心功能障碍方面的意义。方法：Wistar大鼠随机分为内毒素注射后1h组，3h组及对照组，用酶组织化学方法检测脓毒血症大鼠心肌葡萄糖6－磷酸酶活性。高效液相色谱法测定各组大鼠心肌ATP，ADP和AMP的含量,大鼠心肌细胞进行透射电镜观察，结果：（1）注射内毒素（LPS）1h组大鼠心肌葡萄糖6－磷酸酶活性较对照组明显增强，注射LPS3h组则明显减弱（P＜0．05），（2）注射LPS1h组及LPSD3h组ATP，ADP及AMP含量均明显低于对照组（P＜0．05），注射LPS1h组ＬＰＳ３h组ＡＰ，ＡＤ冢ＡＭＰ含量差异无显著性（P＞0．05），（3）透射电镜观察可见脓毒血症大鼠心肌细胞线粒体排列紊乱，空泡变性,肌纤维水肿。结论：能量代谢障碍和线粒体结构的改变在脓毒血症心肌功能障碍发生中起到了重要作用。     

碱性成纤维细胞生长因子对新生大鼠缺氧缺血性脑损伤的保护作用

目的 探讨碱性成纤维细胞生长因子（ ｂＦＧＦ）对新生大鼠缺氧缺血性脑损伤( ＨＩＢＤ）的保护作用。方法 将 ３２只 ７日龄Ｗｉｓｔａｒ大鼠分为４组：假手术组、ＨＩＢＤ组、 ｂＦＧＦ治疗组（分大剂量组１７．５ μｇ／ｋｇ和小剂量组１０ μｇ／ｋｇ）,每组 ８只。后３组动物制成 ＨＩＢＤ模型,给予治疗组大鼠连续 ７ ｄ腹腔注射 ｂＦＧＦ, ＨＩＢＤ组腹腔注射等体积生理盐水作为对照。全部大鼠于术后１４ ｄ处死,对脑纹状体、皮质的光镜下结构、乙酰胆碱酯酶（ＡｃｈＥ）、酸性磷酸酶（ＡＣＰ）活性变化进行观察和比较。结果 新生大鼠 ＨＩＢＤ后皮质、纹状体有选择性神经元坏死及胶质细胞增生, ｂＦＧＦ治疗组上述病变明显减轻; ＨＩＢＤ后纹状体、皮质神经元 ＡｃｈＥ活性明显下降(－～＋）, ｂＦＧＦ组 ＡｃｈＥ活性（＋～＋＋）较ＨＩＢＤ组恢复快; ＨＩＢＤ后纹状体神经元 ＡＣＰ活性明显增高（＋＋＋）, ｂＦＧＦ组 ＡＣＰ活性（＋＋）变化程度小于ＨＩＢＤ组。但大、小剂量ｂＦＧＦ治疗组未见明显差异。结论 ｂＦＧＦ能通过影响受损神经元的酶物质代谢而加快ＨＩＢＤ新生大鼠神经元的修复。     

射频消融对兔心内膜单相动作电位影响的实验研究

目的探讨射频导管消融（ＲＦＣＡ）对心内膜单相动作电位（ＭＡＰ）的影响，为进一步完善ＲＦＣＡ的过程提供理论依据。方法选取健康家兔３６只，用接触电极导管监测ＲＦＣＡ前后兔心内膜的ＭＡＰ变化并观察ＲＦＣＡ不同时间（１０～６０秒）和不同温度（４０～９０℃）水平ＭＡＰ的变化。结果（１）单相动作电位振幅（ＭＡＰＡ）和０相最大上升速度（Ｖｍａｘ）随ＲＦＣＡ时间延长及温度升高而降低或下降，持续放电３０秒或温度达５０℃以后ＭＡＰＡ及Ｖｍａｘ几乎不再变化；（２）整个过程的单相动作电位时程（ＭＡＰＤ）无明显变化且未见心律失常发生。结论（１）当ＲＦＣＡ温度达５０℃心肌电活动以及心肌组织已经产生有效的损伤；ＲＦＣＡ对ＭＡＰＤ不产生影响，故不易导致心律失常（２）将ＭＡＰ记录与温度监测结合起来，对判断ＲＦＣＡ前导管心肌的接触及ＲＦＣＡ后心肌的损伤有一定的指导意义     

血小板活化因子在肾组织损伤中作用的体内外研究

观察了血小板活化因子（ＰＡＦ）受体拮抗剂ＢＮ５２０２１对阿霉素肾病大鼠、对受ＰＡＦ、溶ＰＡＦ刺激的体外培养的大鼠肾小球系膜细胞（ＧＭＣ），产生超氧化物阴离子、过氧化氢（Ｈ＿２Ｏ＿２）和胎儿ＧＭＣ产生ＰＡＦ的影响。结果表明，ＰＡＦ诱导大鼠ＧＭＣ产生和Ｈ＿２Ｏ＿２，诱导胎儿ＧＭＣ产生ＰＡＦ，但溶ＰＡＦ无此作用。ＢＮ５２０２１能减轻注射阿霉素大鼠的肾病改变和抑制ＰＡＦ上述体外刺激作用。提示ＰＡＦ是肾组织损伤的重要介质，ＰＡＦ受体拮抗剂有可能成为肾病综合征的治疗药物之一。     

病毒性肝炎T细胞亚群和几种细胞因子变化的研究

为了探讨小儿病毒性肝炎发病的细胞免疫机制，应用不标记抗体桥联酶标技术（ＡＰＡＡＰ法）检测了５６例病毒性肝炎患儿的外周血Ｔ细胞亚群及膜性白细胞介素２受体（ｍＩＬ－２Ｒ）表达率。应用酶联免疫吸附（ＥＬＩＳＡ）法分别检测了４９例病毒性肝炎患儿单个核细胞培养上清液（ＰＢＭＣｓ）中肿瘤坏死因子α（ＴＮＦα）、白细胞介素６和８（ＩＬ－６、ＩＬ－８）及α干扰素（ＩＦＮ－α）浓度。结果显示：甲型肝炎（简称甲肝）急性期、慢性乙型肝炎（简称乙肝）及丙型肝炎（简称丙肝）组与正常对照比较，ＣＤ４细胞降低，ＣＤ８细胞升高。用植物血凝素（ＰＨＡ）刺激前，甲肝急性期患儿ｍＩＬ－２Ｒ表达率明显高于其他各组，用ＰＨＡ刺激后，各组ｍＩＬ－２Ｒ表达率均显著高于刺激前，但乙肝及丙肝组ｍＩＬ－２Ｒ表达率与正常对照比较则明显降低。甲肝急性期、乙肝及丙肝患儿ＰＢＭＣｓＴＮＦα、ＩＬ－６、ＩＬ－８均较正常对照组升高，而α干扰素（ＩＦＮ－α）均较正常对照组降低。甲肝恢复期ＣＤ４、ＣＤ８和ＰＨＡ刺激前ＰＢＭＣ上ｍＩＬ－２Ｒ表达率以及上述各细胞因子水平均恢复正常。提示细胞免疫功能紊乱与小儿病毒性肝炎的发病及肝损害过程有关。     

复方丹参注射液对小鼠心肌保护作用的研究

目的　探讨复方丹参注射液对小鼠心肌的保护作用。方法　２５ 只小鼠，随机分成缺氧组，丹参治疗组和对照组，实验２ 周后，取新鲜心肌标本，测琥珀酸脱氢酶（ＳＤＨ），三磷酸腺苷（ＡＴＰ） 酶，乳酸脱氢酶（ＬＤＨ），应用光镜和电镜观察心肌病理性变化。结果　缺氧组ＳＤＨ 和ＡＴＰ酶减少，ＬＤＨ 升高，心肌间质水肿，心肌细胞线粒体肿胀，肌丝排列紊乱，丹参治疗组，心肌酶和心肌超微结构与对照组相比均无显著性差异。结论　复方丹参对小鼠心肌缺氧损伤有保护作用。     

Effect of L-carnitine supplementation on cardiac carnitine palmitoyltransferase activities and plasma carnitine concentrations in adriamycin-treated rats

Adriamycin (ADR) inhibits the carnitine palmitoyl transferase (CPT) system and consequently the transport of long-chain fatty acids across mitochondrial membranes. l-Carnitine (CARN) plays a major role in fatty acid oxidation by translocating activated long-chain fatty acids into the matrix of mitochondria. CARN has been shown to be of benefit in certain cardiac conditions including cardiomyopathy and myocardial infarction. This study was devised to investigate the effect of CARN on altered CPT I and CPT II activity in the cardiomyopathy associated with ADR therapy. We also assessed the effect of CARN on the plasma free, total, and acylcarnitine concentrations. Four groups, each consisting of four male Sprague-Dawley rats, were studied: group 1(n = 4) was not given either ADR or CARN; group 2 (n = 4) was given ADR (15 and 20 mg/kg, respectively, cumulative dose) by i.p. injections for 1 and 2 wk; group 3 (n = 4) was given the same dose of ADR with CARN (200 mg/kg); and group 4 (n = 4) was given CARN (200 mg/kg). The activities of CPT I and CPT II in heart were significantly decreased in the ADR-treated rats (p < 0.05) in a dose-dependent manner. The reduced activities of CPT I and CPT II, inhibited by ADR, were not normalized by supplementation with CARN (p < 0.05). In rats supplemented with CARN alone, the activities of CPT I and CPT II were elevated approximately 50% above those of the control rats (p < 0.05). ADR treatment resulted in elevation of plasma free and total CARN concentrations (p < 0.05). Supplementation with CARN did not effect the increased plasma CARN concentrations resulting from ADR treatment (p < 0.05). This study supports the concept that ADR toxicity results from the inhibition of both CPT I and CPT II activities and that one of the causes of ADR-induced cardiomyopathy is a result of globally impaired fatty acid oxidation.     

Apoptosis in young rats with adriamycin-induced cardiomyopathy--comparison with pirarubicin, a new anthracycline derivative.

In a previous study, we demonstrated that apoptosis in rats with adriamycin (ADR)-induced cardiomyopathy occurred through a Fas-dependent pathway. Pirarubicin, a new anthracycline derivative, seems to have a lower cardiotoxicity than ADR. To investigate whether pirarubicin has a lower chronic cardiotoxicity compared with ADR, ADR or pirarubicin were injected weekly for 8 wk into young Wister rats via the tail vein. To block the Fas-Fas ligand interaction, an anti-Fas ligand antibody (FasL) was injected with ADR 7, 8, and 9 wk after first administration of ADR. In the control group, saline was injected instead of ADR. ADR significantly induced apoptosis and left ventricular dysfunction 10 wk after the first administration of ADR. Pirarubicin also induced apoptosis, however, its apoptosis was significantly (p = 0.0069) less than that induced by ADR. Fas antigen was overexpressed in the hearts of ADR and ADR+FasL groups, however, an expression of Fas antigen in the pirarubicin group was similar to the expression of Fas antigen in the control group. Thus, pirarubicin has a significantly lower chronic cardiotoxicity compared with ADR.     

自噬基因Beclin-1和微管相关蛋白LC3在大鼠阿霉素心肌病中的表达及其意义

目的探讨自噬基因Beclin-1及微管相关蛋白LC3在大鼠阿霉素心肌病中的表达及其意义,初步证实自体吞噬(autophagy)参与了大鼠阿霉素心肌病的发病,并探讨其机制。方法雄性SD大鼠45只,随机分为3组,阿霉素(ADR)组、阿霉素(ADR)+3-甲基腺嘌呤(3-MA)组和对照组。建立大鼠阿霉素心肌病模型,电镜观察自噬体形态及数量,检测心肌组织中Beclin-1含量及LC3含量。结果ADR组大鼠心肌组织自噬体的数量较对照组及ADR+3-MA组增多;ADR组心肌组织中Beclin-1水平及LC3含量均较对照组及ADR+3-MA组增高。结论自噬性程序性细胞死亡参与了阿霉素心肌病的发病。     

黄芪甲苷保护阿霉素心肌损伤的抗氧化机制研究

目的 观察黄芪甲苷对大鼠阿霉素心肌损伤的保护作用,并探讨其抗氧化作用机制。方法 SD大鼠随机分5组,空白对照组（C组）,阿霉素组（ADR组）,阿霉素＋黄芪甲苷低剂量组（ADR＋L）,阿霉素＋黄芪甲苷中剂量组（ADR＋M）,阿霉素＋黄芪甲苷高剂量组（ADR＋H）。C组盐水,余组阿霉索腹腔注射。ADR＋L、ADR＋M、ADR＋H组不同剂量黄芪甲苷灌胃,C、ADR组羧甲基纤维素钠灌胃。观察生存率;血浆脑钠肽（BNP）浓度;心肌谷胱甘肽过氧化物酶（GsH—Px）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）活力;检测Cu-Zn—SOD蛋白水平及mRNA水平表达。结果 （1）大剂量黄芪甲苷可以保护阿霉索心肌损伤。与ADR组比较,ADR＋H组大鼠的生存率明显提高（P〈0．01）,血浆BNP浓度明显下降（P〈0．01）。（2）大剂量黄芪甲苷通过增加心肌抗氧化酶活力,增强心肌组织抗氧化酶mRNA转录水平以及蛋白质表达水平发挥其保护作用,且呈剂量依赖性。结论 黄芪甲苷从多个环节发挥其抗氧化能力,对阿霉索性心肌损伤具有保护作用,为临床治疗药物性心肌病提供新的思路。     

Serum lipid and fatty acid profiles in adriamycin-treated rats after administration of L-carnitine.

Cardiomyopathy induced by Adriamycin (ADR) is a cause of congestive heart failure. Recently, it has been suggested that ADR inhibits the carnitine palmitoyltransferase system (CPT I) and consequently the transport of long-chain fatty acids across mitochondrial membranes. This study was devised to ascertain how ADR affects serum lipid and fatty acid metabolism in rats given ADR with and without L-carnitine supplementation. Male Sprague-Dawley rats were divided into four groups. The first group was the control. The second group was given intraperitoneal injections of ADR (5 mg/kg) twice a week over a period of 2 wk. The third group received the same dose of ADR plus L-carnitine (200 mg/kg). The fourth group was injected with L-carnitine only. Serum lipids (total cholesterol, triglyceride, HDL cholesterol, and LDL cholesterol) and fatty acid levels were determined on the first, eighth, and 15th d after injection of ADR. ADR caused an increase of serum total cholesterol, triglyceride, and LDL cholesterol compared with the control group. HDL cholesterol was similar between two groups. Similarly, total fatty acids, especially C16-C18 fatty acids, were significantly elevated after injection of ADR. Striking reduction in these substances was observed when L-carnitine was added (p < 0.05). This study is the first report regarding the reversal effect of L-carnitine in connection with FFA profiles (C6-C18) in the serum of ADR-induced cardiomyopathic rats. This study also supports the view that ADR causes cardiomyopathy because it interferes with fatty acid metabolism, and we hypothesize that there is a possible protective effect of L-carnitine.     

1,6-二磷酸果糖对大鼠热性惊厥性脑损伤保护作用的研究

目的　探讨 1,6 二磷酸果糖 (FDP)对大鼠热性惊厥性脑损伤是否具有保护作用。方法　 30只雄性SD大鼠随机均分为热性惊厥组 (FS) ,盐水对照组 (NS)及果糖干预组 (FD)。水浴法建立热性惊厥模型 ;FD组于惊厥前 30min腹腔注射FDP 2 5mg/ 10 0 g大鼠体重 ;而NS组腹腔注射相同体积的 0 9%氯化钠溶液。观察各组大鼠惊厥表现并制作电镜标本以了解海马CA1区神经元、线粒体及突触超微结构变化。结果　诱发热性惊厥前腹腔注射FDP可使大鼠惊厥潜伏期延长 [FD组为(5 16± 0 88)min ,FS组为 (4 2 5± 0 98)min ,NS组为 (4 2 3± 0 87)min]、惊厥持续时间缩短 [FD组为 (47± 34)s ,FS组为 (6 6± 32 )s,NS组为 (6 6± 32 )s]、惊厥级别下降。以上 3组数据中 ,FD组与其他两组相比差异均有显著性 (P <0 0 5 )。电镜标本观察发现FDP可使大鼠海马CA1区神经元变性坏死减轻 ,神经元变性坏死百分比在FD组、FS组及NS组分别为 13%、2 8%及 30 % ,FD组与其他两组相比差异有显著性 (P <0 0 5 )。FDP防止神经突触间隙异常增宽 ,平均神经突触间隙在FD组、FS组及NS组分别为 (6 4 7± 0 37) μm、(7 6 0± 0 36 ) μm及 (7 5 3± 0 4 0 ) μm ,FD组与其他两组相比差异有显著性 (P <0 0 1)。结论　FDP可使     

1,6-二磷酸果糖对反复热性惊厥大鼠海马区超微结构损伤保护作用的研究

目的：1,6-二磷酸果糖（FDP）作为细胞代谢的能量物质已被证实在辅助治疗缺氧缺血性脑病及心肌受损性疾病方面具有重要作用。该研究探讨FDP对大鼠热性惊厥性海马超微结构损伤是否具有保护作用。方法：36只21日龄雄性SD大鼠均分为热性惊厥组（FS）,高剂量果糖干预组（HD）及低剂量果糖干预组（LD）。水浴法建立热性惊厥模型;高、低剂量果糖干预组于惊厥前30 min各腹腔注射FDP 50 mg/100 g及25 mg/100 g大鼠体重;而FS组腹腔注射相同体积的0.9%氯化钠溶液。应用透射电镜分别观察海马CA1区神经元、细胞器的病理超微结构改变和神经突触参数变化特征。结果：果糖干预组在神经元变性坏死、线粒体肿胀、内质网脱颗粒及高尔基体扩张等方面较FS组减轻,差异有显著性。果糖干预组同FS组相比,脑海马CA1区神经突触间隙缩窄（F=7.29,P<0.01）,突触后致密物质厚度增加（F=12.47,P<0.01）,突触活性带长度延长（F=14.75,P<0.01）,突触界面曲率增加（F=3.77,P<0.05）,差异有显著性。在改善上述超微结构损伤方面,HD与LD组比较差异无显著性。结论：FDP可以减轻反复热性惊厥大鼠海马区超微结构受损程度,但有效而适宜的用药剂量仍需进一步探讨。     

细胞周期蛋白D1在阿霉素诱导大鼠慢性进行性肾脏损害模型中的表达及罗格列酮干预效应

目的研究细胞周期蛋白D1(cyclin D1)在阿霉素诱导大鼠慢性进行性肾脏损害模型中的表达,以及罗格列酮(RSG)干预对其表达的影响,探讨RSG肾脏保护效应的可能机制。方法 45只2月龄SD大鼠随机分成对照组、肾损害组、RSG干预组。肾损害组和RSG干预组从尾静脉注射阿霉素(ADR)6 mg/kg建立肾病模型,对照组注射生理盐水。2周后,RSG干预组给予RSG(4 mg/kg)灌胃,对照组和肾损害组给予等量蒸馏水灌胃。模型建立当天、第14天、70天分别收集24 h尿测尿蛋白;模型建立第70天取血测肝肾功能、电解质、血糖,苏木素-伊红染色观察肾脏病理学改变,免疫组化及RT-PCR测定cyclin D1表达。结果 RSG干预组24 h尿蛋白定量、血清白蛋白、三酰甘油、胆固醇水平,系膜细胞和成纤维细胞cyclin D1蛋白及mRNA表达量与肾损害组比较,差异均有统计学意义(P均<0.05)。病理学观察,RSG干预组大鼠的肾脏损害较肾损害组轻。结论 RSG可减轻阿霉素诱导的肾损害。RSG下调肾脏系膜细胞及成纤维细胞cyclin D1表达可能是其肾保护机制之一。     

白细胞介素-18和白细胞介素-18抗体与大鼠微小病变型多柔比星肾病的关系

目的 探讨IL-18和IL-18抗体(IL-18 Ab)与大鼠微小病变型多柔比星肾病的关系.方法 将30只Wistar大鼠随机分为3组:正常对照组、非治疗组、IL-18Ab治疗组.尾静脉注射多柔比星(6.5 mg·kg<'-1>)造成微小病变型肾病综合征动物模型.其中IL-18Ab治疗组腹腔注射IL-18Ab(每只10 μg),非治疗组注射等量9 g·L<'-1>盐水,正常对照组大鼠予尾静脉注射等量9 g·L<'-1>盐水.分别于第1、14、28及42天检测其24 h尿蛋白水平,第42天心脏取血测其血清总胆固醇(TC)、三酰甘油(TG)、总蛋白(TP)、清蛋白(Alb)、BuN、SCr、IL-18、干扰素-γ(IFN-γ)及TNF-α水平,取其肾组织进行免疫组织化学分析IL-18、IFN-γ、TNF-α的表达及光、电镜病理形态.结果 24 h尿蛋白定量:非治疗组和IL-18Ab治疗组第14天开始增加,第28天达高峰;第14、28、42天非治疗组和IL-18Ab治疗组均高于正常对照组(P<,a><0.05);第28、42天IL-18Ab治疗组低于非治疗组(P<,a><0.05).非治疗组和IL-18Ab治疗组血清TC和TG均高于正常对照组(P<,a><0.05),IL-18Ab治疗组低于非治疗组(P<0.05);非治疗组和IL-18Ab治疗组血清TP和Alb低于正常对照组(P<,a><0.05),IL-18Ab治疗组高于非治疗组(P<0.05).血清IL-18、IFN-γ、TNF-α水平和肾组织IL-18、IFN-γ、TNF-α表达:非治疗组和IL-18Ab治疗组均高于正常对照组(P<,a><0.05),IL-18Ab治疗组均低于非治疗组(P<,a><0.05).肾组织光、电镜病理形态:3组光镜无明显改变,电镜:正常对照组结构正常,非治疗组病变明显,IL-18Ab治疗组病变轻微.结论 IL-18介导IFN-γ、TNF-α的产生,可能参与微小病变型大鼠多柔比星肾病蛋白尿的形成,且IL-18Ab对其有部分治疗作用.     

Coronary flow and flow reserve in children

Aortic blood pressure affects coronary blood flow, but within the normal physiological blood pressure range coronary blood flow is constant. The coronary flow is pulsatile, being maximal in the early diastole. There is a smaller systolic flow component. The low systolic pressure in the right ventricle favours systolic flow. The proportion of systolic flow is greater in the right than in the left coronary artery. Heart diseases in children cause several haemodynamic and functional changes that are likely to affect myocardial perfusion. Newborns with severe valvular aortic stenosis may have a retrograde systolic flow in the left coronary artery. Children with dilated cardiomyopathy have a reduced coronary flow related to myocardial mass. Coronary flow reserve (CFR) is defined as the ratio of maximal coronary blood flow, as induced by reactive hyperaemia or administration of vasodilators, divided by resting flow. Coronary flow can normally increase 2.5-4-fold. CFR is reduced if basal flow is increased due to myocardial hypertrophy, strain or hypoxaemia. Very low CFR values measured with positron emission tomography are reported in neonates with surgically treated congenital heart disease. Measurement of coronary flow velocity with the intracoronary Doppler guide wire may be regarded as a reference or "gold standard" in the evaluation of coronary flow velocity and CFR. Coronary flow and CFR in children is a largely unexploited field, and has vast potential for future research.