前列腺素E_1在酸吸入性急性呼吸窘迫综合征中的肺保护作用

目的　研究静脉注射前列腺素E1(PGE1)能否阻止酸吸入性急性呼吸窘迫综合征(ARDS)的发生。方法　 2 0只新西兰兔在稀HCl经右支气管滴入后随机分成两组 :(1)损伤组 (n =10 )在酸滴入后维持机械通气 ,未行其它治疗 ;(2 )治疗组 (n =10 )在酸滴入后即刻缓慢静注PGE1并维持。在基础状态及酸滴入后记录血气、气道压力并抽动脉血测定 6 K PGF1α、TXB2 、NO-2 /NO-3 和ET 1,动物处死后测定右肺的湿干比 (W /D)值及测定右肺支气管肺泡灌洗液 (BALF)中总蛋白 (TP)的水平 ,并作肺组织形态学观察。结果　治疗组在酸滴入后血氧分压 (PaO2 )显著高于损伤组。治疗组血浆 6 K PGF1α和NO-2 /NO-3 水平显著高于损伤组 ,而血浆TXB2 和ET 1水平显著低于损伤组 ,治疗组右肺W/D和TP显著低于损伤组。损伤组右肺呈弥漫性炎性损伤 ,而治疗组则见损伤呈局灶性 ,且其病理损伤程度较损伤组明显减轻。结论　 (1)酸吸入后即刻应用PGE1可减轻ARDS的范围和严重程度 ;(2 )PGE1保护了肺血管内皮细胞 ,使内源性PGI2 /TXA2 和NO /ET 1的产生保持平衡 ,有利于减轻ARDS。     

甘遂对重症急性胰腺炎大鼠胰腺环氧合酶-2表达的影响

目的探讨甘遂对重症急性胰腺炎（SAP）大鼠胰腺组织环氧合酶-2（COX-2）表达的影响及意义。方法将SD大鼠随机分为假手术组（S组）、SAP组、甘遂治疗组（K组），每组40只。建立SAP模型后K组立即给予甘遂灌胃（200mg／kg体重），每8h1次。各组动物在术后2、6、12、24h检测胰腺组织的COX-2mRNA和蛋白表达、血浆TXB2和6-Keto-PGF1α水平、胰腺光镜和电镜检查。结果SAP组COX-2mRNA和蛋白表达、血检查B2（TXB2）、6-酮-前列腺素F1α（6-Keto—PGF1α）水平及TXB2／PGF1α比值均显著高于S组（P〈0．01）。K组6，12hCOX-2mRNA表达显著低于SAP组（P〈0．05）；6、12、24hCOX-2蛋白表达、TXB2及TXB2／PGF1α比值均显著低于SAP组（P〈0．01）。TXB2／PGF1α比值与COX-2蛋白表达呈显著正相关（r=0．851，P〈0．01）。K组胰腺组织损害较SAP组减轻，微血管内血栓较SAP组明显减少。结论SAP时有COX-2的高表达，甘遂可以下调COX-2的表达，减轻炎症反应，并可能通过纠正TXA2和PGI2之间的失衡改善胰腺微循环。     

甘利欣对兔肺缺血/再灌注时肺内皮素-1生成的影响

目的 研究甘利欣对缺血／再灌注肺脏内皮素－1（ET－1）生成的影响。方法 20只家兔随机分为缺血－再灌注组（Ⅰ组）和缺血－再灌注＋甘利欣组（Ⅱ组）。丙组动物均于麻醉后呼吸机控制呼吸，右侧开胸，右肺门阻断60min后，再开放60min。其中Ⅱ组动物在阻断右肺门前30min静脉输注甘利欣30mg/kg。检测Ⅰ组和Ⅱ组中断右肺门前即刻、开放右肺门后1min、5min右房血和股动脉血中内皮素－1值。开放右肺门后60min取左右肺组织作电镜观察。结果 Ⅰ组中，股动脉血和右房血中ET－1值在缺血／再灌注后1min显著升高（P＜0.01），并且股动脉血中ET－1值显著高于右房血中ET－1值（P＜0.01）。Ⅱ组中，股动脉血和右房血ET－1值在缺血／再灌注前后没有显著性差别（P＞0.05）。结论 肺脏缺血／再灌注损伤可以引起肺脏局部ET－1的合成和分泌增加，甘利欣预先输注可以抑制缺血肺脏局部ET－1的生成。     

血栓素/前列环素与小儿肾病综合征白色微血栓关系

目的：探讨血栓素／前列环素（TXA2／PGI2）与原发性肾病综合征（PNS）外向微循环白色微血栓发生的关系。方法：采用WS－9型体表微循环观察仪检测甲皱微循环,根据有无白色微血栓将71例PNS患儿分为无白色微血栓组（1组,50例）和有白色微血栓组（2组,21例）。用放免法测定两组患儿和尿中血栓素A2（TXA2）和前列环素（PGI2）代谢终产物血栓素B2（TXB2）及6－酮前列环素F1a（6－K－PAF1a）。正常对照 组31例。结果：2组血清TXB2明显高于1组和对照组（P＜0．01）。2组TXB2／6－K－PGF1a比值明显高于1组（P＜0．05）;1组TXB2／6－K－PGF1a比值高于对照组（P＜0．05）。2组尿TXB2和TXB2／6－K－PGF1a比值明显高于1组和对照组（P＜0．01）。结论：血栓素／前列环素失衡在小儿肾病综合征白色微血栓形成和肾损伤中起重要作用。     

吲哚美辛对门静脉高压症术后免疫功能影响的临床研究

目的：探讨吲哚美辛（消炎痛）栓剂对门静脉高压症术后病人免疫功能的影响。方法：观测14例应用吲哚美辛的门静脉高压症（A组）和13例对照组病人（B组）手术前后IgG,IgM,C3,C4,T细胞亚群,NK细胞,PGE2（前列腺素E2）,TXB2（血栓素B2）,6－K－PGF1α（6酮前列腺素F1α）的变化及吲哚美辛的毒副作用。结果：术后A组PGE2,TXB2,6－K－PGF1α均显性低于B组,CD4,NK细胞均显性高于B组,未见明显的毒副作用。结论：吲哚美辛有助于改善门静脉高压症病人术后的免疫功能,短期经直肠给药,不会引起不良反应。     

体外循环中氨甲苯酸对血小板的保护作用

目的：探讨氨甲苯酸（AMBA）在心肺转流（CPB）中对血小板的保护作用及其临床意义。方法：测定AMBA组和对照组血小板数量出血量和输血量以及CPB前后血浆α－颗粒膜蛋白（GMP－140），血栓烷B2（TXB2）和6－酮－前列腺素F1α（6－K－PGF1a)的浓度变化。结果：CPB术后，AMBA组血小板计数明显高于对照组，出血量明显少于对照组，AMBA组GMP－140和TXB2上升幅度小，而对照组上升幅度大（P＜0．05）。结论：氨甲苯酸在CPB术中可以起到保护血小板，减少术后出血的作用。     

前列腺素E1对大鼠肝脏缺血再灌注损伤的保护作用

目的 探讨前列腺素E1（PGE1）对肝脏 因再灌注损伤的保护作用。方法 制作常温下大鼠部分肝叶缺血再灌注模型，于缺血前经门静脉给予PGE1，45min后恢复血流灌注，并于1h后取门静脉血测定血清谷草转氨酶（GOT）、谷丙转氨酶（GPT）、乳酸脱氢酶（LDH）、肿瘤坏死因子－α（TNF－α）及内皮素1（ET－1），同时取缺血肝叶行病理组织学检查。结果 缺血再灌注组GOT、GPT、LDH及TNF－α和ET－1均明显高于正常对照组，PGE1组则明显低于缺血再灌注组。PGE1组的肝脏病理组织学改变明显轻于缺血再灌注组，并接近正常对照组。结论 PGE1对肝缺血再灌注具有保护作用。     

甘遂对重症急性胰腺炎大鼠胰腺组织微循环的影响及其机制

目的： 探讨甘遂对重症急性胰腺炎（SAP）大鼠胰腺组织微循环的影响及其机制。方法：SD大鼠随机分为假手术组（S组）、SAP组和甘遂治疗组（K组），每组40只。检测各组手术后2，6，12，24h的血清淀粉酶水平，胰腺组织TXB2和6-Keto-PGF1α含量、COX-2mRNA和蛋白表达水平、光镜和电镜观察胰腺组织结构，以及术后72h死亡率。结果：（1）胰腺组织TXB2，6-Keto-PGF1α水平及TXB2/PGF1α比值：SAP组在各时间点均较S组显著升高（P<0.01）；K组TXB2及TXB2/PGF1α比值在6，12，24h点均较SAP组显著降低（P<0.01），但仍高于S组（P<0.01）。(2)COX-2mRNA和蛋白表达：S组COX-2mRNA和COX-2蛋白表达均极弱；SAP组表达均明显；K组COX-2mRNA表达6，12h明显弱于SAP组（P<0.05），COX-2蛋白表达6，12，24h均显著低于SAP组（P<0.01）。(3)胰腺组织TXB2/PGF1α比值与COX-2蛋白表达呈显著正相关（r=0.867,P<0.01）。(4)光镜和电镜观察：S组胰腺组织结构正常；SAP组胰腺组织有出血坏死，微血管内大量血栓形成；K组胰腺组织损害较SAP组减轻，微血管内血栓明显减少。（5）72h死亡率：S组为0%，K组为12.5%，两者均明显低于SAP组（62.5%）（均P<0.05）。结论：重症急性胰腺炎时有COX-2 的高表达和TXA2/PGI2之间的失衡，甘遂可以下调COX-2的表达，纠正TXA2/PGI2之间的失衡，而改善胰腺微循环。这可能是其治疗大鼠SAP的作用机理之一。     

川芎嗪在大鼠肾脏缺血再灌注损伤中的作用

目的：探讨川芎嗪对大鼠肾脏缺血再灌注损伤的保护作用。方法：观察川芎嗪注射液对大鼠肾脏缺血再灌注损伤后血浆超氧化物歧化酶（SOD）、脂质过氧化物丙二醇（MDA）、内皮素－1（ET－1）的作用及肾小管损伤形态学的影响。结果：川芎嗪治疗组大鼠血浆SOD水平较缺血再灌注组显著升高（P＜0.05)，MDA和ET－1水平显著性下降（P＜0.05)，肾小管损伤的病理分级显著减轻（P＜0.05)。结论：川芎嗪对肾脏缺血再灌注性损伤具有保护作用。     

山莨菪碱在大鼠胰腺移植中的保护作用

目的通过建立大鼠胰腺移植模型，探讨山莨菪碱对胰腺移植缺血再灌注（I／R）损伤的保护作用。方法建立大鼠胰腺移植模型。Wistar大鼠随机分成3组。假手术组只行开腹手术；对照组只做大鼠胰腺移植模型；实验组给受体大鼠静脉注射山莨菪碱5mg／kg，其余同对照组。各组不同时段采血，检测血淀粉酶、血栓烷素B2（TXB2）、6酮前列腺素F1α（6-K）的水平，取胰腺组织观察病理学改变。结果术后2h对照组血淀粉酶、TXB2、6-K均升高，4hTXB2／6-K比值上调，移植胰腺组织病理损伤明显。实验组血淀粉酶、TXB2较对照组降低（P〈0．05），TXB2／6-K比值趋于正常，胰腺组织病理损伤减轻。结论山莨菪碱对大鼠胰腺移植组织有保护作用，作用机制可能与抑制TXB2生成、缓解TXB2／6-K比值失调、改善微循环，减轻移植胰腺I／R损伤有关。     

Complement partially mediates acid aspiration-induced remote organ injury in the rat

Background: Acid aspiration into one lung is known to cause both a local as well as remote organ injury characterized by neutrophil sequestration and subsequent edema. This study investigated the role of the complement cascade in the development of acid aspiration-induced local lung and remote organ injuries using K-76 COONa (K76), an anticomplement agent that inhibits the complement pathway at the C5 step, and its usefulness as a treatment drug. Methods: Anesthetized rats underwent tracheostomy and insertion of a cannula. K76 was intraperitoneally administrated prior to or immediately after the instillation of 0.1 ml of HC1 (0.1N) or phosphate buffer solution (PBS) into the left lung. Inflammatory responses were evaluated by tumor necrosis factor a (TNFa) in the plasma and the bronchoalveolar lavage fluid (BALF) (n=4), tissue myeloperoxidase (MPO), wet-to-dry weight ratio (W/D ratio)(n=6), and protein concentration in the BALF (n=6). Results: Acid instillation caused an increase in the plasma TNFa, which was significantly attenuated by the administration of K76 prior to or after the acid instillation. Acid instillation to the left lung resulted in an increase of MPO and W/D ratios of the left lung, the right lung, and the small intestine. The administration of K76 inhibited the increase of MPO in these organs. K76 inhibited the increase of W/D ratios of the right non-in-stillated lung and the small intestine. Acid instillation led to increased protein concentration in the BALF of the left lung, which was not inhibited by K76. K76 administrated after the acid instillation had the same effects. TNFa in the BALF was not detected in all groups. Conclusion: These results suggest that localized acid aspiration induces, through the C5a step of the complement system-dependent mechanisms, TNFa formation and neutrophil sequestration, which caused the increase of endothelial permeability of the systemic organs. K76 is effective as a treatment drug in modulating some of the injuries caused by the acid instillation, but further investigation is warranted as to its potential as a therapeutic agent.     

肺表面活性物质对盐酸吸入性肺损伤肺渗出的影响

目的：探讨外源性ＰＳ盐权吸入性损伤家兔肺组织渗出的影响。方法：健康家兔２０只复制盐酸吸入肺损伤模型后随机分为二组,Ａ组（ｎ＝１０）为ＰＳ治疗组,Ｂ组（ｎ＝１０）为对照组,气管内分别注入３７℃ＰＳ１００ｍｇ／ｋｇ和生理盐水（ＮＳ）,对比观察ＰＳ治疗对肺水、ＢＡＬＦ蛋白浓度及肺组织形态学改变。另设Ｃ（ｎ＝８）组,未行盐酸吸入,而在相应时间注入同等体积的ＮＳ作为ＰＳ疗效的对照。结果：Ａ、Ｂ组各尿参数明显     

Effect of NO donor sodium nitroprusside on lipopolysaccharide induced acute lung injury in rats

Nitric oxide (NO) donor-sodium nitroprusside (SNP) mitigates acute lung injury (ALI), but the mechanism of this protection is incompletely known. We investigated the effect of SNP on lipopolysaccharide (LPS)-induced ALI in rats. Forty-eight male Wistar rats were randomly assigned into six groups: the sham-operation group (S group), the LPS instillation group (LPS group), the haemin, a haeme oxygenase-1 (HO-1) inducer, pretreatment group (HM group), the haemin pretreatment plus LPS instillation group (HM+LPS group), the SNP alone and SNP plus LPS treatment groups. Macroscopic and histopathological examinations and immunohistochemistry analysis were performed for the lung specimens 8h after LPS instillation. Intratracheal administration of LPS induced significant expressions of the inducible isoform of NO synthase (iNOS) and HO-1, while both haemin pretreatment and SNP treatment increased the expression of HO-1 and prevented the expression of iNOS. In the LPS group, the wet-dry weight ratio (W/D), bronchoalveolar lavage fluid (BALF) protein, and lung malondialdehyde (MDA) content were significantly higher than those in the sham-operation group, which were reversed by the pretreatment with haemin or administration of SNP. These results suggest that HO-1 plays a protective role against LPS-induced acute lung injury, which may be achieved at least in part, via inactivating the iNOS/NO system that is involved in the pathophysiological process of LPS-induced acute lung injury. The nitric oxide (NO) donor-SNP ameliorates LPS-induced ALI, which may be related to the induction of HO-1 and the subsequent inhibition of iNOS.     

Neutrophil Elastase Inhibitor, ONO-5046, Modulates Acid-induced Lung and Systemic Injury in Rabbits

Background: Acid instillation leads to direct lung and to secondary systemic organ injury, probably via activated macrophages and neutrophils. This study investigated the effects of neutrophil elastase on organ injury after unilateral lung acid instillation by administrating a specific neutrophil elastase inhibitor, ONO-5046, before acid instillation.

Methods: Three groups of anesthetized rabbits (n = 12 in each group) underwent tracheostomies, and instillations were made into their right lower lobe airspaces with either phosphate buffered saline (pH, 7.4; volume, 1.2 ml/kg; n = 12) or HCl (pH, 1.25; volume, 1.2 ml/kg; n = 24). In half of the acid-instilled rabbits, ONO-5046,10 mg/kg, was given intravenously 15 min before the HCl instillation, and then 10 mg [center dot] kg sup -1 [center dot] h sup -1 of the drug was continuously infused throughout the experiment. The other groups of animals received the vehicle intravenously. Anesthesia and mechanical ventilation was continued for 8 h, whereas arterial blood gases were sampled intermittently. Eight hours after saline or acid instillation, the animals were killed, and their lungs, heart, kidneys, liver, and small intestines were harvested. Wet-to-dry weight ratios (W/D) and myeloperoxidase (MPO) assays of these organs were done, and elastase assays on the bronchoalveolar lavage fluids (BALF) obtained from each lung also were performed.

Results: Pretreatment with ONO-5046 attenuated the physiologic changes seen in the vehicle-treated animals. Significant decreases in W/D of the noninstilled lungs and of the small intestine and normalization of the oxygenation of the experimental animals occurred. The ONO-5046 pretreatment did not affect the neutrophil sequestration in the lungs or in the other organs as determined by neutrophil counts in BALF and by the MPO assays.     

p38MAPK/iNOS/HO-1信号通路在赤芍减轻大鼠内毒素性急性肺损伤中的作用

目的 评价p38MAPK/iNOS/HO-1信号通路在赤芍减轻大鼠内毒素性急性肺损伤(AL1)中的作用.方法 健康清洁级雄性Wistar大鼠40只,随机分为5组(n=8):生理盐水对照组(C组)、内毒素组(L组)、赤芍组(R组)、赤芍预处理组(PR组)和SB203580组(S组).气管内滴注脂多糖(LPS)制备大鼠ALI模型.L组气管内滴注1 ml LPS溶液(2.5 mg/kg);C组滴注等容量生理盐水;R组、PR组分别于气管内滴注LPS后、滴注前2 h,经股静脉输注赤芍注射液15 mg·kg-1·h-1 2 h;S组于气管内滴注LPS前3 h,经股静脉输注SB203580溶液2.5 μmol·kg-1·h-1 3 h.于气管内滴注LPS后6 h时,经颈动脉采血样2 ml,行血气分析及测定血清NO浓度;颈动脉放血处死大鼠,测定支气管肺泡灌洗液蛋白浓度,计数中性粒细胞及细胞总数,检测肺组织MDA含量,p38MAPK、HO-1及iNOS的表达.观察肺组织病理学结果 .结果 与C组比较,其余各组肺组织p38MAPK、iNOS及HO-1表达上调,支气管肺泡灌洗液中性粒细胞计数比、蛋白浓度、肺组织MDA含量及血清NO浓度升高.PaO2和HCO1浓度降低(P<0.01);与L组比较,R组、PR组和S组p38MAPK及iNOS表达下调,HO-1表达上调.支气管肺泡灌洗液中性粒细胞计数比、蛋白浓度、肺组织MDA含量及血清NO浓度降低,PaO2和HCO3-升高(P<0.05);R组、PR组和S组肺组织损伤程度较L组减轻.结论 赤芍可减轻大鼠内毒素性急性肺损伤,可能与抑制p38MAPK/iNOS/HO-1信号通路有关.     

单肺通气诱发兔急性肺损伤模型的建立

目的 建立单肺通气诱发兔急性肺损伤模型.方法 清洁级健康新西兰白兔16只,体重2.3～2.7 kg,采用随机数字表法,将兔随机分为VT 6 ml/kg组(Ⅰ组)和VT 12 ml/kg组(Ⅱ组),每组8只.气管切开插入单腔气管导管行右侧单肺通气,Ⅰ组和Ⅱ组VT分别为6、12 ml/kg,余通气参数均为FiO2 50%.通气频率40次/min,I∶E为1∶2.于单肺通气前即刻(T0)、单肺通气1、2、3 h(T1-3)时记录气道峰压,采集动脉血行血气分析,计算氧合指数;于单肺通气3 h时处死动物,取肺组织,观察病理学结果,行肺损伤评分,计算肺湿/干重比,测定左、右支气管肺泡灌洗液蛋白浓度,计数中性粒细胞.结果 与T0时比较,Ⅱ组T1～3,时气道峰压升高,两组T2,3时氧合指数降低(P＜0.05);与左肺比较,两组右肺湿/干重比和肺损伤评分降低(P＜0.05);与Ⅰ组比较,Ⅱ组T1～3,时气道峰压升高,T3时氧合指数降低,右肺湿/干重比、支气管肺泡灌洗液蛋白浓度、中性粒细胞计数及肺损伤评分升高(P＜0.05).结论 采用VT 12 ml/kg单肺通气3 h成功建立了兔急性肺损伤模型.

Abstract：

Objective To establish a rabbit model of acute lung injury induced by one-lung ventilation (OLV) .Methods Sixteen New Zealand white rabbits weighing 2.3-2.7 kg were randomly divided into 2 groups (n=8 each):conventional tidal volume(VT) group (group Ⅰ) and high VT group (group Ⅱ).All the rabbits were tracheostomized and a tracheal tube was inserted into the right bronchus for right lung ventilation in the two groups. VT was set at 6 ml/kg in group Ⅰ and at 12 ml/kg in group Ⅱ and the other ventilatory parameters were the same in the two groups (FiO2 50% , RR 40 bpm, I∶E=1∶2). Immediately before OLV(T0) and at 1, 2 and 3 h of OLV (T1-3), peak airway pressure was measured and arterial blood samples were taken for blood gas analysis and oxygenation index (OI) was calculated. The animals were sacrificed at 3 h of OLV and lung tissues obtained for microscopic examination.The lung injury was scored. W/D lung weight ratio was calculated. Bron-choalveolar lavage fluid (BALF) was collected for measurement of protein concentrations and neutrophil counts. Results The peak airway pressure was significantly higher at T1-3 in group Ⅱ and OI was significantly lower at T2,3 in the two groups than those at T0(P＜0.05) .W/D lung weight ratio and lung injury scores of the right lung were significantly lower than those of the left lung in the two groups(P＜0.05).The peak airway pressure was significantly higher at T1-3, OI was significantly lower at T3, and W/D lung weight ratio, protein concentrations and neutrophil counts in BALF and lung injury scores of the right lung were significantly higher in group Ⅱ than in group Ⅰ(P＜0.05). Conclusion OLV with VT of 12 ml/kg for 3 h can successfully establish a rabbit model of acute lung injury.     

L-精氨酸对兔库血输注模型微循环状态的影响

目的观察L-精氨酸(L-Arg)对兔库血输注模型微环境状态的影响。方法大白兔20只用于制备库血,另40只随机均分为四组:输血组(T组)、L-Arg组(L组)、输血+L-Arg组(TL组)以及空白对照组(C组)。分别于放血前后及输血前后行动脉血气分析,并测量血浆一氧化氮(NO)、内皮素(ET)-1含量。结果 T组的NO和ET-1均于放、输血后升高,而NO/ET-1和pH下降(P<0.05)。TL组出现类似的变化,但其相应时点的NO、ET-1及乳酸含量均低于T组,而NO/ET-1和pH高于T组(P<0.05)。结论补充外源性L-Arg可升高NO水平并抑制ET-1的合成和分泌,且对维持内环境稳定有重要意义。     

氟比洛芬酯对大鼠机械通气所致肺损伤的影响

目的 探讨氟比洛芬酯对大鼠机械通气所致肺损伤的影响.方法 健康成年雄性SD大鼠40只,体重300～350 g,随机分为4组(n=10),常规潮气量通气组(TV组,潮气量8 ml/ks)、大潮气量通气组(HV组,潮气量40 ml/ks)、大潮气量通气+氟比洛芬酯5 ms/kg组(HV+F1组)和大潮气量通气+氟比洛芬酯10 mg/kg组(HV+F2组).HV+F1组和HV+F2组于机械通气前15 min时分别静脉注射氟比洛芬酯5、10 mg/ks.于机械通气4 h时处死大鼠,测定支气管肺泡灌洗液(BALF)肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、血栓素B2(TXB2)和总蛋白浓度,计数白细胞及计算肺组织湿/干重比(W/D),光镜下观察肺组织病理学结果.结果 与TV组相比,HV组BALF TNF-α、IL-6、TXB2、总蛋白浓度、白细胞计数和肺组织W/D升高(P<0.05),肺组织发生病理学损伤;与HV组相比,HV+F1组和HV+F2组BALF TNF-α、IL-6、TXB2、总蛋白浓度、白细胞计数和肺组织W/D降低(P<0.05),肺组织病理学损伤减轻;HV+F2组BALF TNF-α和TXB2浓度低于HV+F1组(P<0.05),其余指标差异均无统计学意义(P>0.05).结论 氟比洛芬酯可通过抑制炎性反应减轻大鼠机械通气所致肺损伤.     

The effects of platelet-activating factor (PAF) and a PAF antagonist (CV-3988) on smoke inhalation injury in an ovine model.

The role of platelet-activating factor (PAF) in inhalation injury was studied in sheep, using CV-3988, a PAF antagonist. Following smoke exposure, 15 sheep were divided into three groups of five. Group I animals were untreated; group II animals were treated with CV-3988 before and after exposure; group III animals were treated only after exposure. In group I, platelet and WBC counts were markedly changed within 6 hours (p less than 0.05); in the treated groups, alteration of cell counts was not obvious. Blood malondialdehyde (MDA) levels were increased significantly only in group I. Blood PGE2 and TXB2 levels did not differ among the groups. Mean tissue MDA and mean bronchoalveolar lavage fluid (BALF) MDA concentrations were significantly increased in group I (p less than 0.01); mean BALF TXB2 levels were significantly decreased in group I (p less than 0.01). These data suggest that PAF affects inhalation injury through modulation of lipid oxygenation and that PAF antagonists may offer therapeutic benefit in the management of this injury.     

塞来昔布对鼻内镜手术患者的术后镇痛效应

目的 评价术前和术后口服塞来昔布对鼻内镜手术患者的术后镇痛效应.方法 拟在全麻下行鼻内镜手术患者120例,ASA分级Ⅰ或Ⅱ级,年龄18～64岁,性别不限,随机分为3组(n=40):对照组(C组)、塞来昔布200 mg组(CEL1组)和塞来昔布400 mg组(CEL2组).麻醉前1 h时,CEL1组口服塞来昔布200 mg,CEL1组口服塞来昔布400 mg,C组不给予任何处理.静脉注射咪达唑仑、异丙酚、瑞芬太尼和罗库溴铵行麻醉诱导,气管插管后行机械通气.静脉输注异丙酚和瑞芬太尼维持麻醉.术毕送入麻醉恢复室(PACU),当VAS评分≥3分时,静脉注射芬太尼25μg/次,间隔5～10 min,直至VAS评分＜3分.返回病房后,CEL1组和CEL2组口服塞来昔布200 mg,2次/d,连续5 d.当VAS评分≥4分时,口服羟考酮5 mg/次,直至VAS评分＜4分.记录PACU期间芬太尼的使用情况、术后6 h内、6～24 h、2～5 d羟考酮的使用情况和术后不良反应的发生情况.术后5 d时评价患者镇痛满意情况,计算镇痛满意率.于术毕、术后6、48 h时,采集肘静脉血样,采用放射免疫法测定血浆前列腺素E2(PGE2)、6-酮-前列腺素F1α(6-k-PGF1α)和血栓烷素B2(TXB2)的浓度,计算TXB2/6-k-PGF1α.结果 与C组比较,CEL1组和CEL2组PACU期间芬太尼使用率和术后6 h内、6～24 h羟考酮使用率降低,患者镇痛满意率升高,术后48 h时血浆PGE2浓度降低(P＜0.05或0.01);CEL1组和CEL2组各指标比较差异无统计学意义(P＞0.05).各组各时点TXB2/6-k-PGF1α比较差异无统计学意义(P＞0.05).C组术后有1例患者发生恶心呕吐,CEL1组和CEL2组未见不良反应的发生.结论 术前和术后口服塞来昔布可减轻鼻内镜手术患者术后疼痛,其机制与降低血液PGE2浓度有关.