氨基胍对烟雾吸入性肺损伤的影响

目的探讨诱导型一氧化氮合酶(iNOS)抑制剂氨基胍(aminoguanidine,AG)对大鼠烟雾吸入性肺损伤的影响。方法40只SD雄性大鼠随机分为正常对照组(n=8)、烟雾吸入组(n=16)和AG治疗组(n=16)。建立烟雾吸入性肺损伤模型,AG治疗组于致伤后立即腹腔注射AG50mg/kg。正常对照组及烟雾吸入组腹腔注射等容量生理盐水。分别于2、6、12、24h时相点进行动脉血气分析,并分批处死大鼠,取肺组织测肺含水量,制备肺组织匀浆检测超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、各型一氧化氮合酶(NOS)活性及一氧化氮(NO)含量。制作肺组织病理切片,光镜下观察病理变化。结果与烟雾吸入组相比,AG治疗组动脉血氧分压显著升高(P<0.05),肺组织含水量降低(P<0.05),肺组织中SOD活性及CAT活性升高(P<0.05),iNOS活性及NO含量降低(P<0.05)。结论AG能够升高动脉血氧分压,提高烟雾吸入性肺损伤肺组织抗氧化能力,减轻肺组织氧化性损伤,减轻肺水肿,并减轻组织炎性浸润,对烟雾吸入性肺损伤有较好的保护作用。     

吸入一氧化氮对犬烟雾吸入性损伤ACE活性的影响

目的，血管紧张素转换酶（ACE）已作为肺毛细血管内皮细胞受损的指示性指标，本研究旨在评价吸入一氧化氮（NO）对吸入性损伤后肺血管内皮细胞的影响。方法，21只犬随机分为3组，烟雾吸入后，对照组（n=8）单纯吸氧（FiO2，0．45），治疗组（n=9）吸氧（FiO2，0．45）＋0．0045％（45PPm）NO，连续监测12h动脉血ACE活性变化；正常组（n=4）不致伤，用于建立组织学对照。动脉血数据行多个样本均数间方差分析，支气管肺泡灌洗液（BALF）和肺组织ACE活性行两样本均数t检验。结果，治疗组血浆ACE活性比对照组降低（P＜0．05）；BALF和肺组织中，治疗组ACE活性也明显低于对照组（P＜0．01）。结论，吸入NO对犬烟雾吸入性损伤肺毛细血管内皮细胞有一定减轻损害作用。     

烟雾吸入伤大鼠肺组织α1—AR的变化与哌唑嗪保护作用的实验研究

目的 探讨α1肾上腺素受体（α1-AR）在烟雾吸入伤大鼠肺组织变化与哌唑嗪对烟雾吸入伤的保护作用。方法 采用大鼠烟雾吸入伤模型致伤大鼠，干湿重法测定肺组织含水量，伊文斯蓝法测定肺微量血管通透性（PMVP），放射受体分析法测定肺组织α1-AR的变化。结果 烟雾吸入致伤后大鼠PMVP增大，2h达显著水平，6h达高峰，24h仍显著高于正常，肺含水量伤后2h明显升高,6h达非常显著水平，24h达高峰，肺组织α1-AR密度于烟雾致伤后2、4、6及24h显著升高，但亲和力除伤后2h升高之外，无明显变化。相关分析显示，肺组织α1-AR密度的升高与PMVP增大呈显著正相关，腹腔给予α1- AR阻断剂哌唑嗪0.5、1.5及3.0mg/kg能明显降低PMVP及肺水含量，减轻肺损伤。结论 大鼠烟雾吸入性肺损伤的发病机制与α1-AR密度升高有关，哌唑嗪对烟雾吸入伤具有一定保护作用。     

7-硝基吲唑在烟雾吸入性肺损伤中的作用

目的 探讨神经型一氧化氮合酶（nNOS）抑制剂7-硝基吲唑（7-NI）在烟雾吸入性肺损伤中的作用。方法 40只SD雄性大鼠被随机分为正常对照组（n=8）、烟雾吸入性肺损伤模型组（n=16）和7-NI治疗组（n=16），建立烟雾吸入性肺损伤模型。7-NI治疗组在致伤后立即腹腔注射7-NI 20mg／kg（溶于2ml花生油中）；正常对照组及模型组腹腔注射2ml花生油。分别于伤后2、6、12和24h时间点监测动脉血气分析；并分批处死大鼠，取肺组织测肺含水量，制备肺组织匀浆检测超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、各型一氧化氮合酶（NOS）活性及肿瘤坏死因子-α（TNF—α）和一氧化氮（NO）含量。光镜下观察肺组织病理学变化。结果 与模型组比较，7～NI治疗组各时间点动脉血氧分压均显著升高（P均〈0．05），肺组织含水量显著降低（P〈0．05），肺组织中SOD及CAT活性均明显升高（P均〈0．05），nNOS活性及NO含量均明显降低（P均〈0．05）。治疗组2h和6h肺组织中TNF—α含量均较模型组降低（P均〈0．05）。光镜下7-NI治疗组较模型组损伤程度减轻，炎性细胞浸润减少，肺间质内未见点状出血。结论 7-NI对烟雾吸人性肺损伤有较好的保护作用，可提高动脉血氧分压，减轻肺水肿程度，增加组织抗氧化能力，并减轻组织炎性细胞浸润。     

一氧化氮对吸入性损伤犬肺功能的改善作用及机制

目的：评价吸入一氧化氮（ＮＯ）对烟雾吸入性损伤犬肺功能的改善效果，并验证其作用机制。方法：２１只犬随机分为３组，烟雾吸入后的对照组（８只）给予单纯吸氧（ＦｉＯ２０．４５）；治疗组（９只）吸氧（ＦｉＯ２０．４５）＋０．００４５％ＮＯ，连续监测１２小时血气变化；正常组（４只）不致伤，用于建立组织学对照。数据行多个样本均数间方差分析。结果：治疗组肺氧合功能明显改善（Ｐ均＜０．０５），肺通气功能也明显改善（Ｐ均＜０．０５）；动脉血和肺组织环磷酸鸟苷（ｃＧＭＰ）明显升高（Ｐ均＜０．０１）。结论：吸入ＮＯ能明显改善肺功能，其作用机制为提高平滑肌细胞内ｃＧＭＰ水平。推荐临床应用吸入ＮＯ作为吸入性损伤的综合治疗方法。     

吸入一氧化氮对烟雾吸入性损伤犬肺组织含水量的影响

目的：观察吸入一氧化氮（ＮＯ）对烟雾吸入性损伤犬肺组织含水量的影响。方法：２１只犬随机分为３组：烟雾吸入后单纯吸氧〔氧浓度（ＦｉＯ２）０．４５〕为对照组（８只）；吸氧（ＦｉＯ２０．４５）＋０．００４５％ＮＯ为治疗组（９只），按时相点采血标本；正常组（４只）不致伤，用于建立组织学对照。动脉血浆胶体渗透压（ＣＯＰ）行多个样本均数间方差分析；支气管肺泡灌洗液（ＢＡＬＦ）中ＣＯＰ和蛋白质含量行两样本均数ｔ检验。结果：吸入ＮＯ治疗组血浆ＣＯＰ比对照组升高（Ｐ＜０．０５）；ＢＡＬＦ中ＣＯＰ比对照组略降低（Ｐ＞０．０５），而ＢＡＬＦ中蛋白质含量比对照组明显降低（Ｐ＜０．０５）；肺组织含水量略低于对照组（Ｐ＞０．０５）。结论：吸入ＮＯ对烟雾吸入性损伤犬肺组织含水量有减轻趋势，但尚无显著的效果，对其病理转归的影响仍难以定论，有待进一步深入研究。     

烟雾吸入伤大鼠肺组织α_1-AR的变化与哌唑嗪保护作用的实验研究

目的　探讨α1肾上腺素受体 (α1-AR)在烟雾吸入伤大鼠肺组织变化与哌唑嗪对烟雾吸入伤的保护作用。方法　采用大鼠烟雾吸入伤模型致伤大鼠 ,干湿重法测定肺组织含水量 ,伊文斯蓝法测定肺微量血管通透性 (PMVP) ,放射受体分析法测定肺组织α1-AR的变化。结果　烟雾吸入致伤后大鼠PMVP增大 ,2h达显著水平 ,6h达高峰 ,2 4h仍显著高于正常 ;肺含水量伤后 2h明显升高 ,6h达非常显著水平 ,2 4h达高峰 ;肺组织α1-AR密度于烟雾致伤后 2、4、6及 2 4h显著升高 ,但亲和力除伤后 2h升高之外 ,无明显变化。相关分析显示 ,肺组织α1-AR密度的升高与PMVP增大呈显著正相关。腹腔给予α1-AR阻断剂哌唑嗪 0 5、1 5及 3 0mg/kg能明显降低PMVP及肺水含量 ,减轻肺损伤。结论　大鼠烟雾吸入性肺损伤的发病机制与α1-AR密度升高有关 ,哌唑嗪对烟雾吸入伤具有一定保护作用。     

烟雾吸入性损伤大鼠肺泡巨噬细胞吞噬功能与炎症消散关系研究

目的：探讨烟雾吸入性损伤大鼠肺泡巨噬细胞吞噬功能与炎症消散关系。方法：建立大鼠烟雾吸入损伤模型后于伤后2、6、12、24h及2、3、4、5d各时相点动态观察（1）肺泡巨噬细胞体外对鸡红细胞吞噬功能；（2）肺泡巨噬细胞体内对凋亡中性粒细胞吞噬功能。结果：（1）致伤后2－6h肺泡巨噬细胞对鸡红细胞吞噬率、吞噬指数下降，12h后逐渐恢复正常，2－5d仍保持较高的吞噬功能。（2）肺泡巨噬细胞对凋亡中性粒细胞吞噬在伤后2h即开始逐渐升高，24h达峰值，然后逐渐下降。结论：（1）烟雾吸入伤早期（2－6h）肺泡巨噬细胞吞噬功能受损害，然后逐渐恢复正常，并保持较高吞噬活性，它有利于清除异物、细菌等。（2）肺内中性粒细胞发生凋亡，然后被巨噬细胞吞噬参与了恢复期肺内炎症消散的过程。     

肺保护性通气对肺内外不同源性急性呼吸窘迫综合征犬外周血和肺泡灌洗液中炎性递质的影响

背景：肺保护性通气策略和呼气末正压作为近些年来治疗急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS）有效通气方式在临床得到广泛的应用，但对其疗效一直有很大的争议。 目的：观察在肺保护性通气条件下ARDS模型犬氧合指数以及外周血和肺不同部位（肺上区、肺下区腹侧和肺下区背侧）支气管肺泡灌洗液中炎性递质的变化。 设计：随机对照动物实验。 单位：解放军总医院呼吸科。 材料：取健康成年雄性杂种犬24只。单纯随机分为肺内源性ARDS实验组、肺内源性ARDS对照组、肺外源性ARDS实验组和肺外源性ARDS对照组。每组6只。 方法：采用静脉注射油酸0．1～0．15mg／kg形成肺外源性ARDS动物模型；应用十六烷磺基丁二酸钠盐气管内吸入形成肺内源性ARDS动物模型。实验组肺损伤后进行肺保护性通气（潮气量：8mL/kg。呼气末正压：0.981kPa）3h。对照组继续进行大潮气通气（潮气量：14-17mL／kg。呼气末正压：0kPa）3h。 主要观察指标：①各组犬氧合指数的变化。②动态观察肺保护性通气条件下各组犬外周血和肺不同部位（肺尖叶、肺心叶和肺膈叶）支气管肺泡灌洗液中炎性递质（肿瘤坏死因子α，白细胞介素1β和白细胞介素6）的变化。 结果：24只犬全部进入结果分析。①肺损伤后各组犬氧合指数均显著下降。应用肺保护性通气治疗后实验组氧合指数明显高于对照组（P〈0．05）；肺保护性通气后2h和3h肺外源性ARDS实验组氧合指数咀显高于肺内源性ARDS实验组（P〈0．05）。②肺损伤后各组外周血中炎性递质明显升高。应用肺保护性通气治疗后。炎性递质水平有不同度下降。但肺内源性ARDS实验组的治疗效果不如肺外源性ARDS实验组。③肺内源性ARDS模型犬肺尖叶和肺心叶支气管肺泡灌洗液中炎性递质水平明显高于肺外源性ARDS模型犬。 结论：肺外源性和肺内源性急性呼吸窘迫综合征模型犬肺的不同部位炎性递质释放和氧合指数改善均具有明显的差异。而肺保护性通气模式对肺外源性急性呼吸窘迫综合征模型犬具有良好的效果，对肺内源性急性呼吸窘迫综合征模型犬疗效较差。     

犬烟雾吸入性损伤吸入一氧化氮肺脏病理改变与肺能量代谢的变化

目的：评价犬烟雾吸入性损伤吸入一氧化氮（ＮＯ）肺脏病理改变与肺组织能量代谢的变化。方法：２１只犬随机分为３组，烟雾吸入损伤后，对照组（ｎ＝８）单纯吸氧（ＦｉＯ２，０．４５），治疗组（ｎ＝９）吸氧（ＦｉＯ２，０．０４５）＋０．００４５％（４５ｐｐｍ）ＮＯ，正常组（ｎ＝４）不致伤，用于建立病理和组织学对照。实验终点进行肺组织学和病理形态学检测。结果：对照组ＡＴＰ含量和能量负荷（ＥＣ）显著低于正常和治疗组（Ｐ＜０．０１），ＡＤＰ和ＡＭＰ含量明显低于正常组（Ｐ＜０．０５），而与治疗组相比无显著差别（Ｐ＞０．０５）；肺脏光镜和电镜病理所见，治疗组病理性改变程度较对照组轻。结论：在烟雾吸入性损伤犬模型中，吸入ＮＯ可不同程度改善肺组织能量代谢，肺脏病理形态改变也有一定程度减轻，表明治疗方法有一定效果     

Effects of manganese superoxide dismutase nebulization on pulmonary function in an ovine model of acute lung injury

Smoke inhalation injury is a major cause of morbidity and mortality in thermally injured individuals. There is evidence of increased oxygen free radical activity, e.g., superoxide, in association with smoke inhalation injury. Because superoxide dismutase converts the reactive superoxide radical to peroxide, we hypothesized that nebulization of manganese superoxide dismutase (Mn-SOD) into the airway might attenuate pulmonary dysfunction secondary to smoke inhalation injury. The present study was designed as a prospective, controlled, and randomized laboratory experiment to determine the effects of aerosolized Mn-SOD on lung fluid balance, as indexed by changes in pulmonary microvascular permeability, lung lymph flow (Q(L)), and gas exchange in an established and clinically relevant ovine model of smoke inhalation injury. Fifteen female Merino sheep were chronically instrumented with a femoral arterial, a Swan-Ganz, and a left atrial catheter. In addition, the right caudal mediastinal lymph node was cannulated to measure Q(L) (mL.h(-1)). Pneumatic occluders were placed around the right pulmonary veins for the determination of the reflection coefficient (sigma). After 7 days of recovery, sheep were randomly allocated to (a) an untreated control group (4 groups of 12 breaths of cotton smoke), (b) an injured group treated with nebulized Mn-SOD (5 mg/kg), and (c) an injured group that received only the vehicle (nebulized saline). Nebulization was performed 1 h and 12 h after smoke inhalation. Mn-SOD nebulization attenuated the increase in both filtration coefficient and sigma and significantly decreased lung tissue conjugated dienes. However, there were no differences in Q(L), PaO2/FiO2 ratio, and bloodless lung wet/dry weight ratio between groups. Although Mn-SOD nebulization attenuated the loss of protein, it failed to improve lung edema and pulmonary gas exchange, thereby limiting its clinical use.     

部分液体通气对吸入性损伤犬肺组织病理学的影响

目的 研究部分液体通气(PLV)对吸入性损伤犬肺组织病理学的影响。方法 将16只犬经蒸气吸入造成吸入性损伤模型，并随机分为对照组和治疗组。所有动物行机械通气，伤后1．5h PLV治疗组给予氟碳，剂量为12mL／kg，伤后3h放血致死动物，取肺组织分别进行光镜和电镜下的组织病理学观察。结果 与对照组比较，PLV治疗组肺组织充血、水肿、中性粒细胞浸润明显减轻，血管内皮细胞和肺泡细胞损伤轻。结论 PLV能减轻吸人性损伤的肺组织损伤，具有抗炎作用。     

Selective tracheal gas insufflation during partial liquid ventilation improves lung function in an animal model of unilateral acute lung injury.

OBJECTIVE: During unilateral lung injury, we hypothesized that we can improve global lung function by applying selective tracheal gas insufflation (TGI) and partial liquid ventilation (PLV) to the injured lung. DESIGN: Prospective, interventional animal study. SETTING: Animal laboratory in a university hospital. SUBJECTS: Adult mixed-breed dogs. INTERVENTIONS: In six anesthetized dogs, left saline lung lavage was performed until PaO(2)/FiO(2) fell below 100 torr (13.3 kPa). The dogs were then reintubated with a Univent single-lumen endotracheal tube, which incorporates an internal catheter to provide TGI. In a consecutive manner, we studied 1) the application of 10 cm H(2)O of positive end-expiratory pressure (PEEP); 2) instillation of 10 mL/kg of perflubron (Liquivent) to the left lung at a PEEP level of 10 cm H(2)O (PLV+PEEP 10 initial); 3) application of selective TGI (PLV+TGI) while maintaining end-expiratory lung volume (EELV) constant; 4) PLV+TGI at reduced tidal volume (VT); and 5) PLV+PEEP 10 final. MEASUREMENTS AND MAIN RESULTS: Application of PLV+PEEP 10 initial did not change gas exchange, lung mechanics, or hemodynamics. PLV+TGI improved PaO(2)/FiO(2) from 189 +/- 13 torr (25.2 +/- 1.7 kPa) to 383 +/- 44 torr (51.1 +/- 5.9 kPa) (p <.01) and decreased PaCO(2) from 55 +/- 5 torr (7.3 +/- 0.7 kPa) to 30 +/- 2 torr (4.0 +/- 0.3 kPa) (p <.01). During ventilation with PLV+TGI, reducing VT from 15 mL/kg to 3.5 mL/kg while keeping EELV constant decreased PaO(2)/FiO(2) to 288 +/- 49 torr (38.4 +/- 6.5 kPa) (not significant) and normalized PaCO(2). At this stage, end-inspiratory plateau pressure decreased from 19.2 +/- 0.7 cm H(2)O to 13.6 +/- 0.7 cm H(2)O (p <.01). At PLV+PEEP 10 final, measurements returned to those observed at previous baseline stage (PLV+PEEP 10 initial). CONCLUSIONS: During unilateral lung injury, PLV with a moderate PEEP did not improve oxygenation, TGI superimposed on PLV improved gas exchange, and combination of TGI and PLV allowed a 77% reduction in VT without any adverse effect on PaCO(2).     

A novel animal model of sepsis after acute lung injury in sheep

OBJECTIVE: Patients with acute lung injury after smoke inhalation often develop pneumonia subsequently complicated by sepsis. This often is a fatal complication. The aim of this study was to develop a standardized and reproducible model of hyperdynamic sepsis after smoke inhalation in sheep. DESIGN: Prospective, experimental study in sheep. SETTINGS: Experimental laboratory in a university hospital. SUBJECTS: Twenty-one female Merino ewes. INTERVENTION: Animals were anesthetized and surgically prepared for this chronic study. After a week of recovery, baseline data were collected. After tracheostomy was performed, sheep were connected to a volume-controlled ventilator. Acute lung injury was produced by insufflating the lungs with 48 breaths of cotton smoke. During halothane anesthesia, live bacteria suspended in a 30-mL saline solution containing 2-5 x 10(11) colony-forming units were instilled through a bronchoscope into the right lower and middle lung lobes (10 mL each) and left lower lung lobe (10 mL; n = 10). Eleven sheep were given smoke but not bacteria. After injury and the bacterial challenge, the animals were ventilated mechanically with 100% oxygen. The animals were monitored for 48 hrs. was detected in blood cultures after 14-48 hrs. MEASUREMENTS AND MAIN RESULTS: The sheep developed a hyperkinetic cardiovascular response concomitant with a decrease in Pao similar to severe sepsis in human patients who meet the criteria for acute respiratory distress syndrome (PaO2 /FIO2 <200). These changes were more severe than in animals exposed to smoke inhalation alone. Mean arterial pressures at 48 hrs in the smoke-alone and the smoke + sepsis group were 85.5 +/- 5.2 and 68.1 +/- 7.6 mm Hg, respectively (mean +/- se, p<.05). CONCLUSION: This animal model closely resembles hyperdynamic sepsis in humans and may be of great value for studies of sepsis with smoke inhalation.     

肺表面活性物质稀释剂延迟肺灌洗治疗烟雾吸入性损伤

目的 探讨外源性肺表面活性物质(PS)稀释剂延迟肺灌洗对大鼠严重烟雾吸入伤后内源性PS功能障碍和急性呼吸衰竭的治疗效果.方法 90只Wistar大鼠随机分为5组:Ⅰ组,正常对照(n=14);Ⅱ组,烟雾吸入(n=27);Ⅲ组,烟雾+PS灌洗+机械通气(MV),n=21;Ⅳ组,烟雾+盐水灌洗+MV,n=10;V组,烟雾+MV,n=18.伤后2 h经气管插管注入含PS(100ms/ks)的等渗盐水30 ml/kg或等量盐水行肺灌洗,MV 4 h,观察24 h;检测动脉血气、肺水量、静态肺顺应性(Cst)、支气管肺泡灌洗液(BAIF)蛋白含量、BALF表面张力特性和24 h病死率等.结果 致伤动物伤后立即出现严重缺氧和一氧化碳中毒;Ⅱ组发生急性呼吸衰竭、高通透性肺水肿和PS功能障碍;Ⅲ组Cst和BALF表面张力特性显著改善(P<0.05),但氧合能力、肺水量和BALF蛋白含量无明显好转(P>0.05).Ⅳ、V组疗效不佳.结论 外源性PS稀释剂延迟肺灌洗可一定程度恢复烟雾吸入所致内源性PS功能抑制,改善肺功能,但不能显著减轻高通透性肺水肿和呼吸衰竭,不能降低早期病死率.     

两种剂量氟碳部分液体通气对吸入伤犬铜蓝蛋白及肺内血浆蛋白外漏的影响

目的 :对比观察两种剂量氟碳 (PFC)部分液体通气 (PL V)对吸入性损伤 (INI)犬血丙二醛 (MDA)、铜蓝蛋白 (CP)及肺泡灌洗液 (BAL F)和肺匀浆中铜蓝蛋白、血浆蛋白的影响。方法 :制作 15条犬蒸气 INI模型并分成 PFC 6 m l/ kg组 (PFC 6组 )和 12 ml/ kg组 (PFC 12组 )。将 PFC(C1 0 F1 8,英国产 )缓慢注入肺内 ,实施PL V,于治疗 2小时后抽静脉血测 MDA、CP;并测 BAL F、肺匀浆中 CP、总蛋白 (TP)、白蛋白 (AL B)、球蛋白(GL B)及白球比 (A/ G)。结果 :PL V后 2小时 ,PFC 6组与 PFC 12组血 MDA、CP比较均无显著性差异(P均 >0 .0 5 ) ,但均较各自的致伤前明显下降 (P均 <0 .0 5 )。 BAL F中 ,PFC 12组的 TP、AL B、GL B及 A/ G均较 PFC 6组明显降低 (P均 <0 .0 5 ) ,而 CP无明显改变。肺匀浆中 ,PFC 12组的 TP、AL B、GL B及 A/ G均较 PFC 6组明显降低 (P均 <0 .0 5 ) ,而 CP则明显增高 (P<0 .0 5 )。结论 :PL V可能通过抗脂质过氧化等作用而减少血浆蛋白外漏 ,降低肺水肿的发生 ,并呈现剂量效应趋势。     

Combined smoke inhalation and scald burn in the rat

The combination of burn injury with smoke inhalation from fires significantly increases mortality. The mechanism of increased mortality is poorly understood but has been associated with multiple organ dysfunction syndrome, including cardiac dysfunction. Impaired cardiac function correlates with decreased survival in burn patients. We investigated smoke inhalation from burning cotton combined with a 40% body surface area, third-degree burn during the first 4 hours after injury in rats. In the early phase after injury, burn caused a significant rise in lung neutrophil infiltration but no increase in lung water. Smoke led to a rise in lung water but only a mild increase in neutrophil infiltration. Combined smoke and burn did not increase neutrophil accumulation or lung water above that which occurred with either injury alone. Only in combined smoke and burn was there a drop in cardiac output and stroke volume with pulmonary edema and lung neutrophil influx.     

山莨菪碱对兔肺缺血-再灌注损伤保护作用的实验研究

目的 :探讨山莨菪碱对肺缺血再灌注损伤的保护作用及其作用机制。方法 :建立兔单肺原位温缺血再灌注模型。 30只日本大耳白兔随机分成 3组 ,每组 10只。对照组不行缺血再灌注处理 ;缺血再灌注组行左肺缺血再灌注处理 ;山莨菪碱组行左肺缺血再灌注处理 ,并静脉给予山莨菪碱 (8mg/kg)。各组进行肺组织湿/干质量比 (W/D)、丙二醛 (MDA )、髓过氧化物酶 (MPO)活性和肺毛细血管通透指数 (L PI)的测定 ,并进行肺组织光镜、电镜的观察及肺组织损伤 (L TD)程度的定量评价。结果 :经 90 min缺血、12 0 m in再灌注后 ,缺血再灌注组的 W/D、L PI、MDA、MPO活性及 L TD程度较对照组均显著升高 (P均 <0 .0 1) ,肺组织病理损伤明显。山莨菪碱组可降低上述指标的水平 (P均 <0 .0 1)和病理损伤。结论 :山莨菪碱对肺缺血再灌注损伤有明显的保护作用 ,其作用机制与抑制中性粒细胞在肺内积聚、减轻氧自由基造成的肺损伤有关。