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1.
本实验发现大鼠体表面积20%Ⅲ°烧伤后,皮肤内产生了大量丙二醛(MDA),第二天达最高,第七天有第二高峰,血浆和红细胞(RBC)MDA第三天达最高,血浆和RBC维生素E(VE)于伤后第二天后迅速下降,RBC溶血第三天最甚。对皮肤MDA、血浆MDA、RBCMDA、血浆VE、BBC VE、1%H_2O_2溶血进行相关分析后发现在不同时相,有不同的相关关系,但基本遵循烧伤皮肤MDA增加、血浆MDA增加、RBC MDA增加、血浆和RBC VE降低,溶血增加的规律。文中讨论了RBC损伤的机制。  相似文献   
2.
大鼠背部20%光辐射Ⅲ度烧伤7天后的焦痂提取液及1:4、1:8稀释液能对正常大鼠肝线粒体呼吸产生明显的抑制作用,相同方法制成的正常皮提取液只呈轻度抑制,1:4稀释液已无抑制作用,两者丙二醛含量相差悬殊,丙二醛含量与抑制率呈相关,但进一步分析表明这种相关为共存现象,丙二醛含量增高不是呼吸率下降的直接原因。丙二醛增高与膜脂双层的破坏有关,内膜能化作用实验表明,当膜脂受到一定程度破坏时,能化作用受到抑制。然而在能化作用未表现异常时,呼吸率已呈一定程度抑制,故呼吸率抑制还受到提取液其他组分的影响。  相似文献   
3.
Endogenousformationofnitricoxide(NO)invarioustisuesplaysanimportantroleincelfunctionandcelcommunicationbothinhealthanddiseas...  相似文献   
4.
Extract of the eschar tissue taken from the rat which had been given full-thickness burn of20% TBSA was found to be inhibitory to the respiratory function of the mitochondria and theenergization of the inner membrane. The inhibition was also demonstrated by the 1: 2 and 1: 4and 1: 8 dilutions of the eschar extract. The extract of normal skin only showed weak inhibitory cf-fect. The 1: 4 dilution of normal skin had no (?) on mitochondrial functions. There is a widegap between the malonaldehyde (MDA) contents of these two kinds of extracts. An apparent posi-tive correlation was found between MDA content and degree of inhibition. However, on close ex-amination, it was found that the MDA content is not the direct cause of the decrease of therespiratory control ratio (RCR). The increase of MDA content is probably related to the destruc-tion of the lipid bilayer of the mitochondria. Data from the energization experiment show that theenergization process is compromised when the destruction of the membrane has proceeded to a cer-tain degrce. The inhibition of mitochondrial respiratory function becomes evident when encrgizationfunction is still normal. Therefore at least two mechanisms are operating in the inhibition process.Further work is needed to elucidate the problem.  相似文献   
5.
烧伤焦痂脂溶性毒性物质提取物(D1)诱发大鼠肝脏亚线粒体颗粒化学发光作用。结果:正常大鼠皮肤脂溶性提取物(D'1)和D1均能诱导鼠肝亚线粒体颗粒产生化学发光作用,其化学发光积分值随D1和D'1的剂量增大而增高,但在剂量相同时D1的作用显著大于D'1。超氧化物歧化酶(SOD)和β胡萝卜素对D1诱导的化学发光均有显著的抑制作用,在一定的剂量范围内(SOD<10μg/ml,β胡萝卜素<3.2mmol/L),随SOD和β胡萝卜素的剂量增加其抑制化学发光的作用显著增强。提示D1与亚线粒体作用时发生了自由基反应,且在此过程中有超氧阴离子和单线态氧的产生。  相似文献   
6.
一氧化氮对离体心脏功能的影响   总被引:2,自引:0,他引:2  
目的:初步探讨一氧化氮对心脏功能的作用及其可能机制。方法:本实验利用Langendorf离体工作心脏灌流装置及技术,观察了NO供体SIN-1、硝普钠灌流心脏后心功能及心肌某些生化指标的改变情况。结果:心脏功能多项指标明显下降,以LVSP,±dp/dtmax为甚。伴之心肌cGMP含量的升高及心肌细胞膜Na+-K+-ATP酶活性的下降。结论:一氧化氮通过调控心肌cGMP的合成及肌膜Na+-K+-ATP酶活性而影响心肌功能。  相似文献   
7.
Protectiveeffectsofverapamilonmyocardialmitochondrialrespiratoryfunctionafter combinedradiation-burninjuryinratsXiongYe(熊业);C...  相似文献   
8.
大鼠5Gy~(60)Coγ射线全身照射复合15%TBSAⅢ度光辐射烧伤后:(l)对外周血中性粒细胞(PMN)数量和血清C_3调理活性抑制作用较小,而对PMN本身的吞噬功能抑制作用较大;(2)PMN吞噬功能降低可能是由于PMNC_3受体表达减少,还原型辅酶Ⅱ(NADPH)氧化酶和髓过氧化物酶(MPO)活性降低及SOD活性增高等因素所致;(3)PMNMDA含量显著增高,并与PMN-CL降低显著相关,提示PMN功能损伤与脂质过氧化的损伤作用有关;(4)两伤复合后第14天对PMN吞噬功能的抑制作用具有加重效应;而伤后第21天,复合伤组PMN吞噬功能显著高于放射损伤组,提示两伤复合后,烧伤对复合伤PMN功能恢复有刺激作用.  相似文献   
9.
Abnormalcalciumtransportofmyocardialmitochondriaduringtheearlystageofcombinedradiation-burninjuryinrats¥(熊业)(陈宗荣)XiongYe;Chen...  相似文献   
10.
Male mice were subjected to 6 Gy total body irradiation,20% TBSAfull-thickness burns,or combined radiation-burn injury and lipid peroxides(LPO),vita-min E,sulfhydryl group,respiratory control ratio(RCR),ADP/O ratio,and cytochromeoxidase activity of the liver mitochondria were determined in the first 9 d postinjury.Theresults are as follows:(1)LPO level increased in the early postinjury stage after combinedradiation-burn injury,on the 5th-7th day after irradiation and on the 7th day postburn.(2)Vitamin E level decreased significantly in the two groups of radiation and burn inju-ries but showed no significant decrease after combined injury.(3)The sulfhydryl groupshowed a tendency to increase in all the 3 groups.(4)The activity of cytochrome oxidaseincreased significantly on the 7th day after radiation but decreased considerably in theburn and combined injury groups.(5)RCR and ADP/O ratio decreased more significantlyin the combined injury group than in either the radiation group or the burn group.These facts suggest that the respiratory dysfunction of the liver mitochondria results mostprobably from the damage on the mitochondrial membrane due to lipid peroxidation.  相似文献   
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