15-F2t-isoprostane在大鼠肠缺血再灌注损伤中的作用

目的 评价异构前列腺素15-F2t-isoprostane在大鼠肠缺血再灌注损伤中的作用.方法 健康雄性SD大鼠32只,体重230 ～ 255 g,采用随机数字表法,将其随机分为4组(n=8):假手术组(S组)、肠缺血再灌注组(I/R组)、血栓烷A2(TXA2)受体拮抗剂SQ-29548组(SQ组)和二甲基亚砜组(DMSO组).采用阻断肠系膜上动脉60 min,再灌注120 min的方法制备肠缺血再灌注损伤模型.SQ组及DMSO组分别于夹闭肠系膜上动脉前30 min腹部皮下注射SQ-29548或二甲基亚砜2μmol/kg.于再灌注120 min时取肠段,观察肠粘膜形态学,并行Chiu评分,取肠粘膜组织,检测髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)、乳酸(LD)含量;采集动脉血样,检测血清二胺氧化酶( DAO)活性及15-F2t-isoprostane、内皮素-1(ET-1)和血栓烷B2(TXB2)浓度.结果 与S组比较,其余各组Chiu评分、DAO活性、15-F2t-isoprostane及TXB2浓度均升高(P＜0.05),SQ组LD和MDA含量、MPO和SOD活性及ET-1浓度差异无统计学意义(P＞0.05);与I/R组比较,SQ组Chiu评分、LD含量、DAO和MPO活性及ET-1浓度降低,SOD活性升高(P＜0.05).结论 15-F2t-isoprostane可通过激活TXA2受体,增加ET-1生成及促进中性粒细胞在肠粘膜聚集参与大鼠肠缺血再灌注损伤过程.     

Protective effects of glucagon-like peptide 2 on intestinal ischemia-reperfusion rats

Our objective was to evaluate the protective effects of glucagon-like peptide 2 (GLP-2) on intestinal ischemia/reperfusion (I/R) rats. Thirty-two rats were randomly assigned to four experimental groups, each of 8: Group A, sham rats underwent laparotomy only, without superior mesenteric artery (SMA) occlusion; Group B, I/R animals underwent laparotomy and occlusion of the SMA for 60 minutes followed by 120 minutes of reperfusion; Group C, I/R animals underwent intestinal I/R, and received pretreatment with GLP-2 for 3 days preoperatively; and Group D, I/R animals underwent intestinal I/R, received pretreatment with GLP-2 as above, and during the reperfusion phase were injected intravenously with GLP-2. After the reperfusion of intestinal ischemia, samples of intestinal mucosa, mesenteric lymph nodes (MLN) and blood were prepared for determination. In the pretreatment rats with GLP-2 (group C), Chiu's scores, bacterial colony counts, serum D-lactate, intestinal mucosal MDA and ET-1, and serum endotoxin, TNF-alpha and IL-6 were significantly reduced compared with intestinal I/R rats (group B). Administration of GLP-2 during the reperfusion phase following pretreatment (group D) showed further protective effects in comparison with the pretreatment rats (group C). We conclude that treatment with GLP-2 attenuates intestinal I/R injury, reduces bacterial translocation, inhibits the release of oxygen free radicals and ET-1, and may well inhibit the production of proinflammatory cytokines.     

小剂量氯胺酮预处理对大鼠肠缺血再灌注损伤的影响

目的 探讨小剂量氯胺酮预处理对大鼠肠缺血再灌注损伤的影响.方法 清洁级健康雄性SD大鼠48只,体重230～270 g,随机分为6组(n=8):假手术组(S组)、氯胺酮+假手术组(KS组)、肠缺血再灌注组(I/R组)、氯胺酮预处理组(K组)、锌原卟啉Ⅸ+氯胺酮预处理组(KZ组)和锌原卟啉Ⅸ组(Z组).采用夹闭肠系膜上动脉根部1 h后再灌注的方法 制备肠缺血再灌注模型.于麻醉前30 min时,S组腹腔注射生理盐水2 ml,K组和KS组均腹腔注射氯胺酮10 mg/kg,KZ组依次腹腔注射氯胺酮10 ms/kg和锌原卟啉Ⅸ5 mg/kg,Z组腹腔注射锌原卟啉Ⅸ5 mg/kg.S组、KS组仅分离肠系膜上动脉,不结扎.于再灌注6 h时处死大鼠,取肠组织测定丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性、血红素加氧酶-1(HO-1)及诱导型一氧化氮合酶(iNOS)的表达,光镜下观察肠组织病理学结果 并采用Chiu评分评价损伤程度.结果 与S组比较,I/R组、KZ组和Z组肠组织MDA含量升高,SOD活性降低,K组MDA含量升高(P<0.05或0.01),SOD活性差异无统计学意义(P>0.05),I/R组、K组、KZ组和Z组肠组织HO-1和iNOS表达上调(P<0.05或0.01),肠组织病理学损伤加重;与I/R组比较,K组肠组织MDA含量降低,SOD活性升高,肠组织HO-1表达上调,iNOS表达下调(P<0.05),肠组织病理学损伤减轻,KZ组和Z组以上指标差异无统计学意义(P>0.05).结论 小剂量氯胺酮预处理可减轻大鼠肠缺血再灌注损伤,可能与氯胺酮上调肠组织HO-1表达,下调iNOS表达有关.     

细胞穿透肽PEP-1介导血红素加氧酶-1对大鼠肠缺血再灌注损伤的影响

目的 评价细胞穿透肽PEP-1介导血红素加氧酶-1(HO-1)对大鼠肠缺血再灌注损伤的影响.方法 雄性SD大鼠18只,周龄7～9周,体重210～260 g,采用随机数字表法,将大鼠随机分为3组(n=6):假手术组(S组)、肠缺血再灌注组(IR组)和融合蛋白PEP-1/HO-1+肠缺血再灌注组(HO组).采用夹闭肠系膜上动脉45 min,恢复灌注120 min的方法制备大鼠肠缺血再灌注损伤模型.HO组夹闭肠系膜上动脉前30 min,左侧髂静脉注射融合蛋白PEP-1/HO-1 0.5 mg,S组不夹闭肠系膜上动脉,余操作同IR组.于再灌注120 min时处死大鼠取小肠组织,称重后计算肠湿/干重比,测定丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和HO-1活性,免疫组化法检测肠组织HO-1蛋白的表达,光镜下观察肠组织结构并进行损伤评分.结果 与S组比较,IR组和HO组肠湿/干重比和MDA含量升高,SOD活性降低,HO-1活性和蛋白表达水平升高,损伤评分升高(P＜0.05);与IR组比较,HO组肠湿/干重比、MDA含量降低,SOD活性升高,HO-1活性和蛋白表达水平升高,损伤评分降低(P＜0.05).HO组大鼠肠组织病理学损伤较IR组减轻.结论 细胞穿透肽PEP-1可将HO-1成功导人大鼠肠组织中的细胞并减轻肠缺血再灌注损伤.

Abstract：

Objective To investigate the effects of heme oxygenase-1 (HO-1) mediated by cell penetrating peptide PEP-1 on intestinal ischemia/reperfusion (I/R) injuiy in tats. Methods Eighteen male SD rats aged 7-9 weeks weighing 210-260 g were randomly divided into 3 groups (re = 6 each): sham operation group (group S) , I/R group and PEP-1/HO-1 + I/R group (group HO) . To establish a model of intestinal I/R injury, intestines were exteriorized and the superior mesenteric artery was exposed and occluded for 45 min ischemia, and then the clamp was removed for 120 min reperfusion. The PEP-1/HO-1 fusion protein 0.5 mg was injected via the left iliac vein 30 min prior to ischemia in group HO. The superior mesenteric artery was exposed but not occluded in group S. At the end of reperfusion, the rats were sacrificed and intestinal tissues obtained to determine the intestinal wet/ dry ratio, malondialdehyde (MDA) level, activities of superoxide dismutase (SOD) and HO-1, and HO-1 protein expression. The histological changes in the intestinal mucosa were examined and the injuiy was scored. Results Compared with group S, the intestinal wet/dry ratio, MDA level, HO-1 activity, HO-1 protein expression and injury score were significantly increased, while the SOD activity was significantly decreased in groups I/R and HO ( P ＜ 0.05) . Compared with group I/R, the intestinal wet/dry ratio, MDA level and injury score were significantly decreased, while the SOD activity, HO-1 activity and HO-1 protein expression increased in group HO ( P ＜ 0.05) . The pathologic changes were significantly attenuated in group HO compared with group I/R.Conclusion HO-1 protein can be successfully delivered into intestinal tissues by PEP-1 and has protective effects against intestinal I/R injury.     

The effect of colchicine and low-dose methotrexate on intestinal ischemia/reperfusion injury in an experimental model

Aim

Intestinal ischemia/reperfusion (I/R) injury is a serious clinical condition. Colchicine and low-dose methotrexate have anti-inflammatory features. An experimental model was conducted to investigate the effect of colchicine and methotrexate on intestinal I/R injury.

Methods

Twenty-four rats were included. Only laparotomy was done in control group (CG, n = 6). In experimental groups, superior mesenteric artery was occluded. After 1 h ischemia, reperfusion (1 h) was started by de-occlusion. 30 min before reperfusion, saline in sham group (SG, n:6), colchicine (1 mg/kg) in colchicine group (CNG, n:6), and methotrexate (0.1 mg/kg) in methotrexate group (MTXG, n:6) were infused intraperitoneally. Small intestines were harvested for evaluation of intestinal mucosal injury (Chiu score) and oxidative stress markers (nitric oxide: NO, malondialdehyde: MDA, superoxide dismutase: SOD).

Results

Biochemically, MDA levels were significantly low in CG compared to SG, CNG, and MTXG (p < 0.05). NO levels were significantly low and SOD levels were significantly high in CG compared to MTXG (p < 0.05). Histopathologically, Chiu score was significantly low in CG compared to SG, CNG, and MTXG (p < 0.05), and significantly high in MTXG compared to SG and CNG (p < 0.05).

Conclusion

The present experimental model caused I/R injury in rat intestines. Contrary to literature, it was found that methotrexate worsens and colchicine does not attenuate intestinal I/R injury.     

硝苯地平对大鼠肾缺血再灌注损伤的影响

目的 探讨硝苯地平对大鼠肾缺血再灌注损伤的影响.方法 健康雄性SD大鼠42只,体重220～250 g,随机分为3组(n=14):假手术组(S组)、缺血再灌注组(IR组)和硝苯地平组(N组).IR组和N组采用夹闭双侧肾动、静脉45 min后恢复灌注的方法制备大鼠肾缺血再灌注模型,S组不夹闭双侧肾动、静脉.N组于夹闭前15 min和再灌注前15 min分别尾静脉注射硝苯地平0.1 mg/kg,IR组分别尾静脉注射等量溶剂.于再灌注6和24 h时留尿,测定尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG)活性;抽取腹主动脉血,测定血清肌酐(Cr)、MDA和一氧化氮(NO)浓度,然后处死大鼠取肾,采用流式细胞仪检测肾皮质细胞凋亡情况、热休克蛋白70(HSP70)的表达,免疫组化法测定内皮素-1(ET-1)的表达.结果 与S组比较,IR组血清Cr和MDA浓度、尿NAG活性、HSP70和ET-1表达水平及肾皮质细胞凋亡率均升高(P＜0.05),血清NO浓度差异无统计学意义(P＞0.05);与IR组比较,N组血清Cr和MDA浓度、尿NAG活性、ET-1表达水平及肾皮质细胞凋亡率降低,血清NO浓度升高(P＜0.05),HSP70表达水平差异无统计学意义(P＞0.05).结论 硝苯地平可减轻大鼠肾缺血再灌注损伤,可能与其抑制ET-1表达有关.     

Thiopental improves renal ischemia–reperfusion injury

Ischemia/reperfusion (I/R) occurs in a number of pathological conditions, including myocardial infarction, stroke, aortic surgery, cardiopulmonary bypass surgery, organ transplantation, resuscitation, and critical care. Massive and abrupt release of oxygen-free radicals after reperfusion triggers oxidative damage. Before critical operations or after resuscitation, it would be wise to find a suitable prophylactic treatment to avoid I/R damage. We aimed to determine whether several commonly used intravenous anesthetics protect against renal I/R injury. Methods: Animals were randomly divided into seven groups, each consisting of six animals: sham group, control group, thiopental group, propofol group, intralipid group, etomidate group, and ketamine group. At the end of the 60-min ischemic period, 60 min reperfusion was established and the materials administered 15 min before the reperfusion. At the end of the reperfusion period, the samples of blood and tissue were reaped for biochemical and serological evaluation. Results: I/R procedure significantly increased malondialdehyde (MDA) levels, decreased catalase (CAT) activities, and superoxide dismutase (SOD) levels. The lowest MDA mean level was in the thiopental group and the highest MDA mean level was in control group. The lowest CAT mean level was in the intralipid group and the highest CAT mean level was in the etomidate group. The lowest SOD mean level was in the control group and the highest SOD mean level was in the propofol group. Conclusion: Thiopental and propofol, especially thiopental, are more effective to protect renal I/R injury.     

缺血预处理-后处理对大鼠肠缺血再灌注损伤的影响

目的 评价缺血预处理.后处理对大鼠肠缺血再灌注损伤的影响.方法 清洁级成年雄性SD大鼠40只.体重225～275 g,随机分为5组(n=8):假手术组(S组)仅分离肠系膜上动脉(SMA),不夹闭;肠缺血再灌注组(IIR组)采用夹闭SMA 60 min,再灌注60 min的方法制备肠缺血再灌注损伤模型;缺血预处理组(IPr组)夹闭SMA 10 min,再灌注10 min,余同IIR组;缺血后处理组(IPo 组)夹闭SMA 60 min后,再灌注30 s,缺血30 s,反复3次,再灌注60 min;缺血预处理.后处理组(IPr-IPo组)先行缺血预处理,再行缺血后处理,操作过程同IPr组和IPo组.于再灌注60 min时各组取肠粘膜组织,观察肠粘膜形态并行Chiu评分,检测丙二醛(MDA)含量,超氧化物歧化酶(SOD)及髓过氧化物酶(MPO)活性,同时采集动脉血样检测血浆肿瘤坏死因子α(TNF-α)及白细胞介素6(IL-6)浓度.结果 与S组比较,其余各组Chiu评分、MDA含量、MPO活性、血浆TNF-α与IL-6浓度升高,SOD活性降低(P<0.05).与IIR组比较,IPr组、IPo组及IPr-IPo组Chiu评分、MDA含量、MPO活性、血浆TNF-α和IL-6浓度降低.SOD活性升高(P<0.01).与IPr组和IPo组比较,IPr-IPo组Chiu评分和MDA含量降低,SOD活性升高(P<0.05).IPr组与IPo组各指标比较差异无统计学意义(P>0.05).结论 缺血预处理-后处理可减轻大鼠肠缺血再灌注损伤,较单独应用时效果好.     

Effects of Intravenous Anesthetics on Renal Ischemia/Reperfusion Injury

Background. Renal ischemia/reperfusion (I/R)-induced tubular epithelial cell injury, called ischemic acute renal failure, is associated with high mortality in humans. Protecting the kidney against I/R injury is very important during complicated renal operations, transplantation surgery, and anesthesia. Aim. The purpose of this study was to investigate and compare the efficiency of ketamine, thiopental, propofol, etomidate, and intralipid in reducing the injury induced by free radicals in a rat model of renal I/R. Method. Forty-two Wistar rats were divided into seven groups in our study. Rats in the sham group underwent laparotomy and waited for 120 minutes (min) without ischemia. Rats in the control group were given nothing with ischemia-reperfusion. Rats in the I/R groups were given ketamine (20 mg/kg), thiopental (20 mg/kg) propofol (25 mg/kg), etomidate (10 mg/kg) and 10% intralipid (250 mg/kg) intraperitoneally 15 min prior to the ischemia for 60 min, followed by reperfusion for 60 min. The blood samples and kidney tissues of the rats were obtained under anesthesia at the end of the reperfusion period. Biochemical malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), blood urea nitrogen (BUN), creatine (Cr), aspartate aminotransferase (AST) were determined, and histopathological analysis was performed with these samples. Results. MDA level was increased significantly in the control group (p < 0.05). Histopathological findings of the control group confirmed that there was renal impairment by tubular cell swelling, interstitial edema, medullary congestion, and tubular dilatation. MDA levels were lower in the ketamine, thiopental, and propofol groups compared to the control group (p < 0.05). In the thiopental and propofol groups, the levels of histopathological scores were significantly lower than control and etomidate groups in ischemia-reperfusion. Conclusion. Our results demonstrated that I/R injury was significantly reduced in the presence of propofol and thiopental. The protective effects of these drugs may belong to their antioxidant properties. These results may indicate that propofol and thiopental anesthesia protects against functional, biochemical, and morphological damage better than control in renal I/R injury.     

丙泊酚对2型糖尿病大鼠心肌缺血-再灌注时自噬的影响

目的探讨丙泊酚对2型糖尿病大鼠心肌缺血-再灌注时自噬的影响及雷帕霉素靶蛋白(m TOR)信号在其中的作用。方法健康成年雄性SD大鼠6~8周龄,体重200~220 g,共42只,随机分为六组(n=7):假手术组(CC组)、心肌缺血-再灌注组(CI组)、心肌缺血-再灌注+丙泊酚组(CI+P组)、糖尿病假手术组(DC组)、糖尿病心肌缺血-再灌注组(DI组)、糖尿病心肌缺血-再灌注+丙泊酚组(DI+P组)。高糖高脂饲料(HFD)喂养8周联合腹腔注射链脲佐菌素(STZ)30 mg/kg诱导2型糖尿病大鼠模型。CC、DC组只穿线不结扎;CI、DI组以3 ml·kg-1·h-1静脉泵注生理盐水10 min后结扎左冠状动脉左前降支30 min,再灌注120 min。CI+P、DI+P组以6 mg·kg-1·h-1静脉泵注丙泊酚10 min后结扎左冠状动脉左前降支30 min,再灌注2 h。于结扎前、缺血30 min及再灌注2 h记录HR、左心室压(LVSP)、左心室内压最大上升及下降速率(±dp/dtmax);于再灌注2 h采血检测NO、内皮素(ET-1)活性;并取病变区域心肌,Western blot法检测LC3Ⅱ、m TOR、p-m TOR表达水平。结果五组结扎前HR、LVSP、±dp/dtmax差异无统计学意义;缺血30 min以及再灌注2 h,除DC组外,其它各组血流动力学指标均明显低于CC组(P0.05),NO、p-m TOR表达水平均明显低于CC组(P0.05),c Tn T、ET-1、LC3Ⅱ、m TOR表达水平明显高于CC组(P0.05);CI+P组NO、p-m TOR表达水平明显高于CI组,c Tn T、ET-1、LC3Ⅱ及m TOR表达水平明显低于CI组(P0.05);DI+P组NO、p-m TOR表达水平明显高于DI组,c Tn T、ET-1、LC3Ⅱ及m TOR表达水平明显低于DI组(P0.05)。结论丙泊酚可能通过上调自噬抑制蛋白p-m TOR表达,下调自噬激活蛋白m TOR表达,减轻正常大鼠和2型糖尿病大鼠心肌缺血-再灌注损伤。     

Effects of in vivo freezing and mannitol in intestinal ischaemia-reperfusion injury

PURPOSE: The main purpose of this study was to investigate whether in vivo freezing and mannitol administration can protect the small intestine against ischaemia-reperfusion (I-R) injury. METHODS: Fifty male Sprague-Dawley rats (200-225 g) were divided into 5 groups each containing 10 rats; group SO, sham operation group; group I, mesenteric ischaemia group; group R, ischaemia-reperfusion (I-R); group FR, I-R plus in vivo freezing; group MR, I-R plus mannitol treatment. Intestinal ischaemia for 30 min and reperfusion for 60 min were applied. Ileum specimens were obtained to determine the tissue levels of malondialdehyde (MDA) and histological changes. RESULTS: The mucosal injury scores of group R were significantly higher than those of the group I (P<0.0001). The mucosal injury scores in the groups FR and MR were significantly lower than the group R (P<0.0001 and P<0.0001, respectively). In the group FR, mucosal injury scores were not significantly different from those of group I (P=0.123). However, mucosal injury scores of group MR were significantly less when compared to those of group I (P=0.01). Mean MDA levels of group R were significantly higher than those of the group I (P<0.0001). Mean MDA levels of groups FR and MR were significantly lower than those of group R (P<0.0001 and P<0.0001, respectively). In addition, MDA levels of group FR were significantly higher than those of group MR (P<0.0001). CONCLUSION: In conclusion, these observations suggest that the in vivo freezing of SMA and the pre-treatment with mannitol before reperfusion period may be useful in preventing intestinal reperfusion injury.     

Protective effects of pretreatment with Radix Paeoniae Rubra on acute lung injury induced by intestinal ischemia/reperfusion in rats

Objective： To investigate the effect of pretreatment with Radix Paeoniae Rubra （RPR） on acute lung injury induced by intestinal ischemia/reperfusion in rats and its protective mechanism.
Methods： Thirty-two Wistar rats were randomly divided into four groups： Sham-operation group, ischemla/ reperfusion group （I/R group ）, RPR-pretreatment group and hemin group. The model of intestinal ischemia/ reperfusion was established by clamping the superior mesenteric artery for 1 hour followed by 2-hour reperfusion. The effect of RPR on the expression of heme oxygenase-1 （HO-1） in lung tissues was detected by immunohistochemistry and morphometry computer image analysis. Arterial blood gas analysis, lung permeability index, malondialdehyde （MDA） and superoxide dismutase （SOD） contents in lungs were measured. The histological changes of lung tissue were observed under light microscope.
Resalts： The expression of HO-1 in RPR-pretreatment group and hemin group was obviously higher than that in sham-operation group and I/R group （ P 〈 0.01 ）. The level of MDA and lung permeability index in RPR-pretreatment and hemin group were significantly lower than those in I/R group （P〈0.01 or P〈0.05）, while the activity of SOD in RPR-pretreatment and hemin group was obviously higher than that in I/R group （P〈0.01）. Under light microscope, the pathologic changes induced by I/R were significantly attenuated by RPR.
Conclusion： Intestinal ischemia/reperfusion may result in acute lung injury and pretreatment with RPR injection can attenuate the injury. The protective effect of RPR on the acute lung injury is related to its property of inducing HO-1 expression and inhibiting lipid peroxidation.     

失血性休克再灌注对早期肠黏膜显微结构的影响

目的观察失血性休克再灌注后肠黏膜屏障功能损伤及其病理改变和超微结构变化。方法16只家兔随机分为2组（n=8）：假手术组（A），休克再灌注组（B）。采用失血性休克再灌注模型。检测灌注后0．5、2、4h血清磷脂酶A2（PLA2）、一氧化氮（NO）和丙二醛（MDA）值；实验结束后取回肠末端黏膜测MDA和组织钙含量；分别通过光镜和电镜观察肠黏膜结构的变化。结果B组血清NO相对A组降低明显。而PLA2、MDA显著升高。B组肠黏膜MDA和组织钙含量有明显升高（P〈0．05）；光镜和电镜观察表明B组肠黏膜损伤明显重于A组。结论失血性休克再灌注使肠道经历缺血缺氧和再灌注损伤，导致肠黏膜生理结构被破坏。     

Protective effects of propofol against ischemia/reperfusion injury in rat kidneys

Aim: The purpose of this study was to investigate and compare the efficiency of propofol in the reduction of injury induced by free radicals in a rat model of renal ischemia/reperfusion (I/R). Method: Twenty-four Wistar rats were divided into four groups in our study. Rats in the sham group underwent laparotomy and were made to wait for 120 min without ischemia. Rats in the control group were given nothing with ischemia–reperfusion. Rats in the I/R groups were given propofol (25 mg/kg) and 10% intralipid (250 mg/kg) ip, respectively, 15 min before the ischemia for 60 min followed by reperfusion for 60 min. The kidney tissues of the rats were taken under anesthesia at the end of the reperfusion period. Evaluation of biochemical malondialdehyde (MDA), superoxide dismutase, and catalase activities and histopathological analysis were performed with these samples. Results: I/R significantly increased MDA levels (p < 0.05). Histopathological findings of the control group confirmed that there was renal impairment by tubular cell swelling, interstitial edema, medullary congestion, and tubular dilatation. MDA levels were lower in the propofol group compared to control group (p < 0.05). In the propofol group, the level of histopathological scores is significantly decreased than control and intralipid groups in ischemia–reperfusion. Conclusion: Our results demonstrate that I/R injury was significantly reduced in the presence of propofol. The protective effects of propofol may be due to their antioxidant properties. These results may indicate that propofol anesthesia protects against functional, biochemical, and morphological damage better than control in renal I/R injury.     

肝素对顿抑心肌功能影响的实验研究

目的：探讨肝素化剂量肝素对在体家兔短暂缺血－再灌注顿抑心肌的功能的影响。方法：23只雄性家兔，分为实验（A）组和对照（B）组，建立在体心肌短暂缺血（15min）－再灌主（60min）损伤模型。A组于前降支阻断前20min给予肝素（700U／kg）。分别于给药前、缺血前、再灌注期间，检测2组NO、ET－1、MDA、SOD水平，测定血流动力学指标变化，对心肌超微结构做定性观察。结果：A组在给药后20min，NO含量即较给药前明显升高（P＜0．05），且在整个再灌注期较B组有显著性差别（P＜0．05），心功能、超微结构明显改善。结论：肝素参与短暂缺血－再灌注顿抑心肌功能的保护，机制可能是通过药物性预适应，增强内皮源性NO的产生，从而减轻心肌缺血－再灌注损伤。     

不同剂量异丙酚对大鼠小肠缺血再灌注后肺损伤超微结构的影响

目的 探讨不同临床剂量异丙酚对大鼠小肠缺血再灌注后肺损伤肺组织钙离子含量变化和肺组织超微结构改变的影响及其保护作用。方法 雄性SD大鼠40只,随机分为假手术对照组(Ⅰ组)。小肠缺血再灌注组(Ⅱ组)及分别给予异丙酚4mg·kg-1·h-1、8mg·kg-1·h-1、10mg·kg-1·h-1(Ⅳ、Ⅳ、Ⅴ)5组;制作小肠缺血再灌注模型。实验结束即刻取部分肺组织固定于2.5％戊二醛行透射电镜检查肺组织超微结构,部分肺组织用原子吸收分光光度法测钙离子含量。结果IIR后Ⅱ组、Ⅲ组肺组织钙离子含量明显升高,与Ⅰ组、Ⅳ组、Ⅴ组相比均有非常显著差异(P<0.01),Ⅳ组、Ⅴ组与Ⅰ组相比无统计学差异,同时Ⅱ组、Ⅲ组肺组织钙离子含量相比显著差异(P<0.05)。Ⅱ组肺组织超微结构明显受损,异丙酚用药组肺组织超微结构均明显改善,尤其Ⅳ组、Ⅴ组两组除线粒体结构轻微改变外基本接近正常。结论 钙离子在大鼠小肠缺血再灌注后肺损伤中有重要作用,临床剂量异丙酚可明显降低肺组织钙离子含量,并对肺组织超微结构产生保护作用。     

异丙酚联合机体低氧预处理对大鼠肺缺血再灌注损伤的影响

目的 探讨异丙酚联合机体低氧预处理对大鼠肺缺血再灌注损伤的影响.方法 健康雄性SD大鼠90只,体重250～320 g,随机分为5组(n=18):假手术组(S组)、肺缺血再灌注组(IR组)、异丙酚组(P组)、机体低氧预处理组(WBHP组)和异丙酚联合机体低氧预处理组(PW组).IR组采用阻断左肺门45 min后再灌注的方法制备大鼠单肺缺血再灌注损伤模型,P组夹闭左肺门前30 min持续静脉输注异丙酚30 mg·kg-1·h-1;WBHP组夹闭左肺门前先行机体低氧预处理;PW组夹闭左肺门前30 min持续静脉输注异丙酚30 mg·kg-1·h-1和机体低氧预处理.分别于再灌注0.5、1、4 h时测定肺组织TNF-α、IL-1、IL-6和MDA的含量,SOD活性,计算肺湿干重比(W/D).结果 与S组比较,IR组、P组、WBHP组和PW组T1～3时肺组织TNF-α、IL-1、IL-6和MDA的含量及W/D升高,SOD活性降低(P＜0.05);与IR组比较,P组、WBHP组和PW组T1～3时TNF-α、IL-1、IL-6和MDA的含量及W/D降低,SOD活升高(P＜0.05);与P组和WBHP组比较,PW组T2,3时TNF-α和IL-6的含量及W/D降低,SOD活性升高,T3时IL-1和MDA的含量降低(P＜0.05).P组与WBHP组各指标差异无统计学意义(P＞0.05).结论 异丙酚联合机体低氧预处理减轻肺缺血再灌注损伤的作用较单独应用时强,可能与联合应用时抑制炎性反应的作用增强和抗氧化能力提高有关.     

生脉注射液对肠粘膜再灌注损伤保护作用机制的实验研究

目的探讨生脉注射液(SM)对休克再灌注期间肠粘膜的保护作用及机制.方法利用兔休克复苏模型,21只家兔随机分为SM组(A组)、单纯复苏组(B组)和对照组组(C组).分别于实验前(S0)、休克1h(S1)、及再灌注1h(R1)、3h(R3)观察乙状结肠粘膜内pH(pHi)、肠氧摄取率(ERO2)、肠粘膜一氧化氮(NO)、丙二醛(MDA)及钙(Ca2+)含量、肠粘膜病理病理形态学变化.结果A组R1和R3时肠pHi及肠ERO2明显高于B组相应值,肠粘膜NO、MDA及Ca2+含量低于B组(均为P＜0.05),而B组复苏期间肠pHi维持在S1时的低水平状态,肠ERO2显著降低,肠粘膜NO、MDA及Ca2+含量均明显高于A组和C组;光镜下肠粘膜损伤A组显著轻于B组且病理分级与肠pHi负相关(r=-0.841,P＜0.05).结论SM对休克再灌注期间肠粘膜的保护作用机制为增加肠粘膜灌注及氧合、抑制肠粘膜NO活性、清除氧自由基及减轻钙超载.     

Propofol and tourniquet induced ischaemia reperfusion injury in lower extremity operations

BACKGROUND AND OBJECTIVE: Extremity surgery with tourniquet to provide a bloodless field may be a good human model for ischaemia reperfusion (IR) injury. The aim of this study was to investigate the effects of three different modes of propofol use on tourniquet induced IR injury in lower extremity operations. METHODS: Thirty-three consecutive ASA Grade I and II patients were randomized into three groups of 11 patients each. In the spinal group (Group S), after intrathecal anaesthesia, sedation was given with a propofol infusion at 2 mg kg-1 h-1 after a 0.2 mg kg-1 bolus dose and fentanyl 100 microg. In the general (Group G) and TIVA (Group T) groups, general anaesthesia was induced with propofol 2 mg kg-1 with fentanyl 100 microg and maintained with inhalation of halothane or infusion of propofol respectively. Venous blood samples were obtained at different time points for measurements of plasma malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels. RESULTS: Plasma MDA levels were increased significantly in the Group G at 1 min before tourniquet release and 5 and 20 min after tourniquet release compared with before induction of general anaesthesia (baseline). Before intrathecal anaesthesia and before induction of general anaesthesia significantly decreased levels of MDA were observed both before and after tourniquet release compared to baseline. Plasma SOD and CAT concentrations were decreased significantly only at tourniquet release in the Group G compared with baseline. In the Groups S and T these enzymes were not changed significantly. Plasma GPx levels were not altered in any groups. CONCLUSION: Propofol administration may inhibit lipid peroxidation and restore antioxidant enzyme levels in extremity surgery requiring tourniquet application.