65岁以上老年患者心脏瓣膜手术中的体外循环管理

【目的】 总结65岁以上老年人心脏瓣膜置换术的体外循环管理方法。【方法】 2006年1月至2008年12月,开展了232例老年人心脏瓣膜置换术,其中男133例,女99例,年龄65～78岁(69.6±9.2)岁;体重39～81Kg（51±8.2）Kg。手术方式包括二尖瓣置换术(MVR)73例,主动脉瓣置换术(AVR)51例,三尖瓣置换( TVR)3例,二尖瓣及主动脉双瓣置换术(DVR)93例,再次二尖瓣置换术(Re-MVR)7例,再次主动脉瓣置换术(Re-AVR)3例,主动脉带瓣人造血管置换2例,同期行二尖瓣整形(MVP)21例,三尖瓣整形( TVP)66例,冠状动脉旁路移植术(CABG)12例。全部采用气管插管、静吸复合麻醉,中度血液稀释、中度低温、中高流量,冷含血停跳液进行心肌保护,全部应用超滤器。【结果】：体外循环时间46～315min(87.2±32.7)min;主动脉阻断时间25～168min(58.3±27.5)min。转流中平均动脉压维持在6O～90mm Hg,超滤量为800～8300ml,心脏自动复跳率86％,本组早期死亡10例(4.3％)。【结论】 体外循环中加强心肌保护;控制血液稀释度,使用血液超滤技术维持机体内环境的稳定;有效的组织灌注以及良好的保护等综合性措施,有助于脑、肾、肺等重要脏器的保护,有利于提高老年患者心脏瓣膜置换术中体外循环的质量,并确保手术安全     

老年心脏手术患者术中重要脏器的保护方法探讨

目的探讨老年心脏手术患者的术中重要脏器保护方法。方法 209例老年心脏手术患者,均采用气管插管、静脉复合麻醉,轻度血液稀释,浅—中度低温,高流量灌注,维持灌注压60-90 mmHg,用血液浓缩器进行超滤和改良超滤保护心、肺、脑、肾等重要脏器。心肌保护采用4：1含血停博液,采用顺行灌注、顺逆联合灌注等方法,灌注温度为温血—冷血—温血。结果本组患者手术期间心、肺、脑功能正常,手术均顺利完成,无手术死亡。结论 老年心脏手术患者应采用轻度血液稀释,浅—中度低温,高流量灌注,并用血液浓缩器进行超滤和改良超滤以保护心、肺、脑等重要脏器功能。心肌保护宜采用4∶1含血停博液,灌注温度顺序为温血—冷血—温血。     

老年心脏瓣膜病患者心脏手术过程中的体外循环管理

目的探讨老年心脏瓣膜病患者心脏手术体外循环安全及有效的管理方法。方法 2009年1月至2012年8月在体外循环下对148例60岁以上老年患者行心脏瓣膜手术,体外循环预充总量1 600～1 800 ml,维持红细胞压积(HCT)24%～30%,晶胶比0.5～0.61。全部患者均用Dideco EVO或Terumo-18膜肺,体外循环采用常温或中浅低温高流量灌注方法,4∶1冷氧合血灌注进行心肌保护。术中监测血液稀释度、平均动脉压、电解质和血糖等变化,定时进行血气分析,调节酸碱平衡,给予常规超滤与零平衡超滤,记录尿量。结果体外循环时间为31～176 min,平均(94.1±32.5)min;升主动脉阻断时间为24～130 min,平均(65.9±27.2)min;辅助时间7～75 min,平均(23.2±13.1)min;自动复跳率79%,145例血流动力学平稳,顺利停机;3例经二次辅助循环10～20 min顺利停机。4例患者在ECC停机后置入主动脉内球囊反搏泵(IABP)。术后死亡5例,死亡率为3.4%,其中4例死于严重低心排,1例死于感染后多器官衰竭。结论良好的膜式氧合器,合理的血液稀释,有效的组织灌注以及对各脏器的保护等综合性措施相结合,有利于提高老年心脏瓣膜病患者心脏手术中体外循环的质量,确保术中安全,减少术后并发症的发生。     

37例心脏移植的体外循环管理经验

目的:总结37例原位心脏移植体外循环管理经验。方法:37名患者进行了同种异体心脏移植手术,术前心脏超声检查EF值平均(24.52±4.79)%;采用中度低温、轻中度血液稀释、中高流量体外循环灌注。术中监测血气和电解质,常规使用超滤技术和白蛋白。供心保护采用HTK心肌保护液,经主动脉根部灌注冷HTK心脏停搏液,快速取下心脏,并放置于冷HTK液中低温保存。结果:供心热缺血时间(7.7±1.7)min,冷缺血时间(194.52±121.57)min,体外循环时间(110.87±29.83)min。主动脉阻断时间为(47.83±8.91)min,平均动脉压55～85mmHg。37例患者均顺利脱离体外循环机。结论:良好的供心保护,体外循环过程中保持平均动脉压在60～80mmHg及晶胶比在0.45～0.60,血气和电解质的动态监测以及超滤和白蛋白的应用是心脏移植体外循环管理的关键。     

儿童心脏瓣膜置换术的体外循环管理

目的 总结15岁以下儿童心脏瓣膜置换术中体外循环的特点，探讨最佳的体外循环方法。方法 回顾性分析2006年01月- 2016年01月上海交通大学医学院附属新华医院15岁以下61例行瓣膜置换患者临床资料。其中男39例，女性22例，年龄1-15岁。病因中先天性瓣膜发育异常36例，感染性心内膜炎9例，先天性心脏病术后13例，瓣膜成形术后3例；所有手术均使用进口中空纤维膜式氧合器。浅或中低温中高流量灌注。采用4:1冷氧合血灌注进行心肌保护。全组病人术中使用常规超滤，部分患儿术后使用改良超滤。结果 患者CPB时间（115.5±57.1） min，主动脉阻断时间（65.5±39.4） min。术中灌注压30-60mmHg，转流过程平稳，尿量满意，心脏自动复跳率96%，全部顺利脱机。全组院内死亡1例（1.6%），术后出现并发症6例(9.8% )。结论 儿童瓣膜置换手术的体外循环，合理的预充和血液稀释，良好的心肌保护，充分的组织灌注；超滤技术的应用等是降低儿童瓣膜手术后并发症，提高体外循环质量的重要方法。     

婴幼儿左向右分流型先天性心脏病合并重症肺炎的体外循环管理

目的:探讨婴幼儿左向右分流型先天性心脏病合并重症肺炎的体外循环管理方法。方法:回顾性分析2013年5月至2017年6月我院收治的78例左向右分流型先天性心脏病合并重症肺炎患儿的临床资料,患者均接受急诊或亚急诊手术。术中应用浅低温、进口膜肺进行体外循环,经主动脉根部顺行灌注康斯特保护液(HTK液)进行心肌保护,术中应用常规超滤联合改良超滤技术。结果:体外循环时间为45~68 min,平均(50.24±12.45)min,主动脉阻断时间为10~60 min,平均(23.56±10.68)min。心脏自动复跳76例(97%)。转流结束后改良超滤时间为8~15 min,平均(10.45±3.24)min。术后死亡3例(3.8%)。结论:婴幼儿左向右分流型先天性心脏病合并重症肺炎常危及患儿生命,早期手术可获得理想的治疗效果。体外循环采用常规超滤联合改良超滤技术、合适的膜式氧合器、精确的预充及血液稀释、良好的心肌保护等措施是提高手术成功率的重要保障。     

儿童瓣膜置换术体外循环74例总结

目的 总结儿童瓣膜置换术的体外循环管理。方法 回顾我院自1989年到2001年共74例儿童瓣膜置换术的体外循环情况，包括血液稀释、灌注方式、心肌保护并进行分析。结果体外循环时间51-166min，平均83min，主动脉阻断时间32-124min，平均67min；心脏自动复跳69例，占93％，电击复跳5例，占7％；全组死亡8例，死亡率10．8％，主要死因为低心排综合征、多器官衰竭、大出血和呼吸衰竭。结论 在儿童瓣膜置换术的体外循环管理中，认真作好术前准备，根据患儿的体重、病种选好相应的设备、血液稀释和灌注方法，在体外循环中保证充沛的组织灌注，注重心肺等器官的保护，心脏复跳后掌握好辅助循环的要求等综合措施，是提高手术的成功率、降低并发症和死亡率的重要方法。     

超滤法对体外循环心脏手术病理生理的影响

超滤法(ultrafiltration)是在一定跨膜压作用下,血液通过高通透膜滤器,以对流方式滤过血浆水份和中小分子物质。体外循环心脏手术超滤法能浓缩血液,逆转血液稀释的不良影响。近年来国内外已有报道本文综述超滤法的病理生理影响。一、减少体内液体潴留体外循环血液稀释具有不少优点,但它常引起体内液体潴留。Breckenridge报告:中度血液稀释体外循环心脏手术后细胞外液     

120例小儿体外循环管理体会

对120例先天性心脏病患儿行体外循环（CPB）心内直视下手术,结果CPB中末梢灌注均良好,心脏全部自动复苏108例,20W／S除颤后复跳12例,未出现低心排综合征、肺水肿及房室传导阻滞等并发症。认为维持电解质平衡和加强心肌保护是小儿心脏手术成功的重要环节;根据患儿体质量选择适宜的血液稀释和相应的灌注方法可提高手术成功率,进一步降低病死率。     

老年人长时间心内直视手术的体外循环管理

目的总结老年人长时间心内直视手术体外循环的管理经验。方法2003年9月至2005年9月老年人长时间体外循环(CPB)心内直视手术36例,其中采用深低温停循环2例、中度低温34例。使用主动脉球囊反搏(IABP)辅助7例,离心泵左心辅助循环4例,应用改良超滤(MUF)8例,心肌保护应用氧合血心肌停搏液。根据病情选用顺灌、逆灌、桥灌及顺灌逆灌间断灌注的灌注方法。实施血液保护、脑保护、心肌保护、肺保护、肾保护。结果1例冠状动脉移植合并室壁瘤切除术患者,术后因多脏器功能衰竭死亡,其余均顺利康复出院。结论体外循环中采用综合性措施是老年人长时间心内直视手术成功的保证。     

辛伐他汀对动脉粥样硬化兔不同金属基质蛋白酶动态变化的影响

目的探讨不同金属基质蛋白酶(matrix metalloproteinases,MMPs)在动脉硬化兔模型的动态变化及辛伐他汀的治疗作用。方法高脂喂食加球囊拉伤股动脉建立动脉硬化兔模型50只,分别为对照组和他汀组,每组25只,后者除高脂饮食同时服用辛伐他汀4mg/kg,两组均于拉伤后1、7、14、21、28d采血,酶联免疫吸附(ELISA)法检测MMP-1、9,组织金属蛋白酶抑制物-1(tissue inhibitors of metalloproteinases,TIMP-1),绘制各MMPs动态变化曲线,并取血管行病理检查。结果 MMP-1、9在拉伤后1d均达到峰值,延续至拉伤后7d;TIMP-1在1d达到峰值,并进行性降低;辛伐他汀分别在7、14、21d明显抑制MMP-1、MMP-9和TIMP-1浓度。结论动脉硬化兔模型的MMPs和TIMP有不同的变化规律,辛伐他汀抑制MMPs/TIMP分泌的时间也不同。     

Increased acinar damage of salivary glands of patients with Sjögren's syndrome is paralleled by simultaneous imbalance of matrix metalloproteinase 3/tissue inhibitor of metalloproteinases 1 and matrix metalloproteinase 9/tissue inhibitor of metalloproteinases 1 ratios

OBJECTIVE: Previous findings in labial salivary glands (LSGs) from patients with Sj?gren's syndrome (SS) suggest that increased activity and expression of matrix metalloproteinase 9 (MMP-9) and MMP-3 trigger the destruction of acinar structures in these glands. Tissue inhibitors of matrix metalloproteinases (TIMPs) tightly control MMP activity, and TIMP expression is an important modulator of effects attributed to MMPs. This study was undertaken to investigate the correlation between the balance of MMPs/TIMPs in the LSGs of SS patients and the degree of inflammatory infiltration and acinar structure integrity. METHODS: Three groups of SS patients classified according to focus score and residual tissue were studied. The expression of MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 was examined at the messenger RNA and protein levels. The ratio of MMP/TIMP expression (R value) was calculated. Focus score and acinar structure were evaluated by histologic analysis. RESULTS: In SS patients the MMP-3/TIMP-1 ratio was higher than 1 and the MMP-9/TIMP-1 ratio was much higher than 1 whereas the MMP-2/TIMP-2 ratio nearly equaled 1, suggesting elevated proteolytic activity due mainly to MMP-9. R values were independent of the focus score of inflammatory cells, but correlated well with the dramatic changes observed in morphologic integrity of acini, as revealed mainly by the lack of nuclear polarity. Acinar changes were more evident when R values for both MMP-9/TIMP-1 and MMP-3/TIMP-1 were higher. CONCLUSION: This study provides evidence that an altered balance between MMPs and their inhibitors is associated with acinar damage. Since salivary gland acinar cells express both MMPs and TIMPs, these cells may play an important role in extracellular matrix destruction and in the LSG pathophysiology in SS.     

Early postnatal dexamethasone influences matrix metalloproteinase-2 and -9, and their tissue inhibitors in the developing rat lung

In order to test the hypothesis that early postnatal exposure to dexamethasone (Dex) influences matrix metalloproteinases (MMP)-2 and -9, as well as their tissue inhibitors (TIMP-1 and -2) in the developing rat lung, newborn rats (3 litters/group) were treated with low Dex (0.1 mg/kg/day, IM), high Dex (0.5 mg/kg/day), or equivalent volumes of saline at 5 days postnatal age (P5), P6, and P7. Lung weight and lung MMP and TIMP levels were determined at sacrifice (7 days postinjection, P14; at weaning, P21; and at adolescence, P45, n = 10/group and time). Dex did not adversely affect lung weight or lung MMP-2 levels, which peaked in all groups at P21 and then fell by P45. In contrast, Dex decreased TIMP-2 at all time intervals, but achieved statistical significance only at P45. An imbalance in MMP-2/TIMP-2 ratio was noted at P21, with elevations occurring in the low and high Dex-treated groups. Lung MMP-9 levels remained comparable with controls during low Dex treatment. However, high Dex exposure resulted in elevated lung MMP-9 levels at P21 and P45. Lung TIMP-1 levels increased only with high Dex exposure at P14 and P21, whereas the lung MMP-9/TIMP-1 ratio was elevated at P21 in the high Dex group, and at P45 in both Dex-treated groups. These data provide evidence that early postnatal dexamethasone results in an imbalance between gelatinase-A and -B, and their tissue inhibitors in the developing rat lung. These changes may be responsible, in part, for some of the known maturational effects of steroids on lung structure in the newborn.     

Differential expression of matrix metalloproteinases during stimulated ovarian recrudescence in Siberian hamsters (Phodopus sungorus)

The matrix metalloproteinases (MMPs) are a family of extracellular matrix-cleaving enzymes involved in ovarian remodeling. In many non-tropical species, including Siberian hamsters, ovarian remodeling is necessary for the functional changes associated with seasonal reproduction. We evaluated MMPs and their endogenous inhibitors (TIMPs), during photoperiod-induced ovarian recrudescence in Siberian hamsters. Hamsters were transferred from long day (LD; 16:8) to short day (SD; 8:16) photoperiods for 14weeks, and then returned to LD for 0, 1, 2, 4, or 8weeks for collection of ovaries and plasma. Post-transfer (PT) LD exposure increased body and ovarian mass. Number of corpora lutea and antral, but not preantral follicles increased in PT groups. Plasma estradiol concentrations were lower in PT weeks 0-4, and returned to LD levels at PT week 8. No change was observed in relative MMP/TIMP mRNA levels at PT week 0 (SD week 14) as compared to LD. Photostimulation increased MMP-2 mRNA at PT week 8 as compared to PT weeks 0-1. MMP-14 mRNA expression peaked at PT weeks 1-2 as compared to LD levels, while MMP-13 expression was low during this time. TIMP-1 mRNA peaked at PT week 8 as compared to PT weeks 0-4. No changes were noted in MMP-9 and TIMP-2 mRNA expression. In general, MMP/TIMP protein immunodetection followed the same patterns with most staining occurring in granulosa cells of follicles and corpora lutea. Our data suggest that mRNA and protein for several members of the MMP/TIMP families are expressed in Siberian hamster ovaries during recrudescence. Because of the variation observed in expression patterns, MMPs and TIMPs may be differentially involved with photostimulated return to ovarian function.     

Evolution of matrix metalloprotease and tissue inhibitor expression during heart failure progression in the infarcted rat

OBJECTIVE: Characterize the timecourse of matrix metalloproteinase (MMP-1, -2, -3, -7, -9, -11, -12, -13, and -14) and endogenous tissue inhibitors of MMPs (TIMP-1, -2, -3, and -4) upregulation during left ventricular (LV) remodeling following myocardial infarction (MI) in rats. METHODS: The descending left coronary artery of male rats (Rattus norvegicus) was ligated to produce a MI. LV function and dilation were assessed from 1 day to 16 weeks post-MI. Protein and mRNA extraction was done on LV samples containing scar and myocardium together. Gelatinase activity was measured by zymography. Westerns were run on the MMPs known to cleave fibrillar collagen in the rat (MMP-8, -13, and -14) as well as TIMP-1, -2, and -4. RESULTS: Average infarct size was 38.6+/-1.1%, and produced LV dysfunction and progressive LV dilation. Thoracic ascites, a marker of congestive heart failure (HF), was not present until 12 weeks post-MI. Upregulation of MMP-2, -8, -9, -13, and -14 and TIMP-1 and TIMP-2 was detected at different timepoints during HF progression. Increased MMP protein levels occurred sometimes without a corresponding elevation in mRNA levels, and increased TIMP mRNA levels without increased protein levels. MMP-13 active form was elevated during the first 2 weeks post-MI while TIMP-1 and TIMP-2 protein levels were not significantly elevated until 2 weeks post-MI. MMP-8 and MMP-14 protein levels increased later during heart failure progression. CONCLUSION: MMP/TIMP upregulation evolves over time following infarction in the rat LV. Some MMPs were significantly elevated during the first week post-MI (MMP-13, -2, and -9) and another was not until 16 weeks post-MI (MMP-14). The dissociation between LV MMP/TIMP mRNA and protein levels shows that post-translation processing occurs in the rat heart.     

黄芪皂甙Ⅳ对大鼠心肌胶原的影响及其机制

目的研究黄芪皂甙Ⅳ(XGA)对大鼠心肌胶原代谢的影响及机制。方法采用胶原酶-胰蛋白酶消化法分离大鼠心肌成纤维细胞(FBC),建立FBC培养系统,加入不同浓度和不同作用时间的XGA后,检测Ⅰ、Ⅲ、Ⅳ型胶原,基质金属蛋白酶(MMP-1、MMP-2、MMP-9)及其组织抑制物(TIMP-1,TIMP-2)mRNA的表达水平。结扎左冠状动脉前降支制备大鼠心肌梗死模型,存活者随机分为缺血组和XGA组,另设正常组和假手术组;给予XGA组不同剂量(0.5～10.0mg/kg)和不同作用时间(7～28d)的XGA,观察血清Ⅲ型前胶原氨基端肽(P-Ⅲ-NP)、Ⅰ型前胶原羧基端肽(Ⅰ-CTP)、血管紧张素Ⅱ(AngⅡ)和内皮素(ET)的变化,Masson染色观察心肌组织胶原情况,免疫组化法观察心肌组织MMP-2、MMP-9及TIMP-1的表达。结果给予不同浓度和不同时间的XGA后,心肌成纤维细胞Ⅰ、Ⅲ、Ⅳ型胶原,TIMP-1,TIMP-2mRNA的表达水平有所下降,而MMP-1,MMP-2,MMP-9mRNA的表达水平有所上升,且随XGA剂量的增加或作用时间的延长而逐渐下降或上升。给予缺血大鼠不同剂量XGA后,血清P-Ⅲ-NP、Ⅰ-CTP、AngⅡ、ET含量均较缺血组明显下降(0.5mg/kg剂量组除外);同时5,10mg/kg剂量组心肌MMPs/TIMP比值较缺血组明显增加;且随XGA剂量的增加,上述变化逐渐增加。给予缺血大鼠XGA10mg/kg,除血清ET水平和心肌MMPs/TIMP比值在治疗7d后与缺血组变化不大外,余各组血清指标较缺血组明显下降,心肌MMPs/TIMP比值较缺血组明显增加,且随用药时间的延长,上述变化逐渐增大。结论 XGA可减少心肌胶原的形成,其机制可能为抑制胶原的合成、增加胶原的降解。     

Matrix metalloproteinases in isolated hypercholesterolemia.

AIM: Levels of circulating matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are altered in subjects with atherosclerosis. We hypothesized that also otherwise healthy hypercholesterolemic subjects will have altered MMP/TIMP concentrations. To validate this hypothesis, we compared MMPs/TIMPs in patients with moderate isolated hypercholesterolemia before and after atorvastatin therapy and in healthy normolipidemic controls. METHODS: Twenty-seven otherwise healthy subjects with isolated hypercholesterolemia (total cholesterol 8.3+/-0.3 mmol/L) and 29 healthy normolipidemic controls were included. Patients were treated by atorvastatin for 10 weeks. We studied plasma levels of MMPs (MMP)-2, -3, and -9 and of their TIMPs (TIMP)-1 and -2. RESULTS: Patients differed from controls by significantly lower MMP-3 [11.6 (5.7-21) vs 18.4 (12-22) ng/mL, P<10-4 (median, range 25-75%)] and TIMP-2 [13.3 (8.8-30.5) vs 22.1 (10.8-39) ng/mL, P=0.02] and by higher TIMP-1 [496 (461-538) vs 483 (456-500) ng/mL, P=0.004]. Atorvastatin decreased significantly TIMP-1 [from 496 (461-538) to 476 (451-525) ng/mL]. CONCLUSIONS: Isolated hypercholesterolemia per se is associated with similar alterations of circulating MMPs and TIMPs as developed symptomatic atherosclerosis. Most consistent link to serum lipids was observed in case of TIMP-1. MMP and TIMP levels probably reflect the atherogenic process in its early stages in these subjects.     

Tissue inhibitor of metalloproteinase-1 levels in bronchoalveolar lavage fluid from asthmatic subjects.

Airway remodeling is a well-recognized feature in patients with chronic asthma. The accumulation in the submucosa of fibrous proteins that are substrates of matrix metalloproteinases (MMP), and the demonstration of increased levels of MMP-9 in bronchoalveolar lavage fluid, prompted us to determine whether there was an imbalance between MMPs and tissue inhibitors of metalloproteinase (TIMP) in such patients. We investigated the presence of TIMPs and other MMPs. TIMP levels were compared with those of all MMPs and inflammatory cytokines. Adults with stable asthma, either untreated or treated with glucocorticoids (GCs), were enrolled. Healthy nonsmokers served as a control population. MMPs and TIMPs were identified through zymography or immunoblotting. TIMPs, MMPs, and cytokines were measured with enzyme immunoassays. TIMP-1 levels were significantly higher in untreated asthmatic subjects than in GC-treated subjects or controls (p < 0.0001), and were far greater than those of MMP-1, MMP-2, MMP-3, and MMP-9 combined. TIMP-2 was undetectable. TIMP-1 levels were correlated with levels of interleukin-6 (p < 0.012) and the number of alveolar macrophages recovered (p < 0.005). This observation has important implications, since an excess of TIMP-1 could lead to airway fibrosis, a hallmark of airway remodelling in patients with chronic asthma.     

血清基质金属蛋白酶9和组织基质金属蛋白酶抑制剂1与急性脑梗死的临床关系

目的探讨脑梗死患者血清基质金属蛋白酶9(MMP-9)和组织基质金属蛋白酶抑制剂1(TIMP-1)的动态变化及对临床预后的影响。方法选择急性脑梗死患者60例,按照TOAST分型方法将脑梗死患者分为3组,心源性脑栓塞(CE)组,大动脉粥样硬化性卒中(LAA)组,腔隙性脑梗死(SA)组,每组20例;另选健康体检者20例作为对照组,分别测定急性脑梗死患者发病24 h内,第5、10天的血清MMP-9、TIMP-1含量,记录患者入院时的美国国立卫生研究所脑卒中量表(NIHSS)评分;记录发病1、6个月时的Barthal指数(BI)来评价顸后。结果发病后24 h内,脑梗死各组患者血清MMP-9、TIMP-1含量较对照组均明显升高(P<0.05),其中,CE组和LAA组MMP-9、TIMP-1含量持续至第5天仍未下降.而SA组已逐渐降至正常水平。发病后24 h内血清MMP-9含量与相应时间段NIHSS评分呈正相关。近期预后较好患者发病24 h内血清MMP-9含量明显低于预后较差患者(P<0.05)。结论MMP-9与病情的严重程度有关。脑梗死后24 h内的血清MMIP-9含量是预后的独立预测因素。     

Relationship of Matrix Metalloproteinases 2 and 9 in the Wall of Abdominal Aortic Aneurysms

This study examines the pathogenesis of abdominal aortic aneurysms (AAAs) with respect to pathological characteristics and expressions of matrix metalloproteinases (MMP)-2, MMP-9 and tissue inhibitor of metalloproteinases (TIMP)-1, in Tottori University Hospital, Japan. Thirty-four consecutive patients were operated on for (AAAs). During surgery, the anterior wall of the aneurysmal aorta was resected from the site of maximal diameter throughout the wall. AAA specimens consisted of the aneurysmal aortas, while control specimens consisted of the undulated aortas of autopsy cases. The expression of MMP-2, MMP-9 and TIMP-1 was evaluated by immunohistochemistry, Western blotting and competitive polymerase chain reaction (C-PCR). Immunohistochemistry showed MMP-2-positive cells and TIMP-1 positive cells mainly in the intima, and MMP-9-positive cells in the intima and adventitia. Western blotting revealed the expression of MMPs and TIMP-l variably in all the cases examined. C-PCR showed significantly higher elevation of MMP-2 mRNA in the small-diameter AAAs (30–45 mm), plus higher MMP-9 mRNA expression in both the small-diameter and the medium-large-diameter AAAs (45 < mm), than in controls. The ratio of MMP-2 to TIMP-1 mRNA levels in the small-diameter AAAs, and the ratio of MMP-9 to TIMP-1 mRNA levels in both the small-diameter and medium-large-diameter AAAs were significantly higher than in controls. The mRNA levels were significantly correlated between MMP-2 and MMP-9, between MMP-2 and TIMP-1, and between MMP-9 and TIMP-1 in the AAAs. This study demonstrates that increases in mRNA imbalanced expression of MMPs/TIMP, as well as increases of MMP-2 and MMP-9 expression, may play crucial roles in the development and growth of AAAs, and TIMP-1 may play an important rule of preventing the aortic expansion.