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热射病时中枢神经系统变化研究进展.pdf

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1、D8 h H w *“dMZ张水文( + u9D, 100700)null nullK1null 中暑是环境高温或剧烈体力劳动时,因热的作用引起的一组急性热致疾病,其中,最严重的一种是热射病b为探讨热射病的发生机理,在复习有关外国文献的基础上,重点综述了以下四个问题: (1)单胺类介质是热射病时下丘脑体温调节的物质基础; (2)细胞因子的研究展示了热射病治疗的光辉前景; (3)脑缺血a缺氧是热射病的主要病理生理基础; (4)凋亡null 热射病时脑细胞可能的又一死亡形式b本文对热射病的研究前景提出了展望bnull null null null1oM: null h, null w *“dnul

2、l null null null nullms |:R135.3 null nullDS M :B null nullcI|:1001- 5248(2000) 04- 0307- 03null null/ 8 H,y T7 BF$ %h, B h( heatstroke), qr17% 80%b h v+: ( 1)8, (2) # 2,(3) w *“db *“d iC * h1o,7 O *“d R, hh n5VC *b “ w *“d MF , M 9 ,/ Z sYF8 b1 null h H/ m 78$null null w *“d y ,Cabanac v 7K s 40. 5

3、 nullb/ m7Y ,/ m 7 T V V ,8Kr46. 5 null ,y/ m 7 8 w, “ -,v s 8b M YV, 8 w.1 %“b 48 , 8Ab*60 M, VonEuler / m 7 J / F (NE)5- ( 5- HT) i1 7 = u Y L,4 8T,“Myers1971 M4 #8 *8L , 5- HT P8 6,NE P8/b at/ m 7NE5-HT s8T Myers4null1null,TangriNE5- HT 7 iT9Mnull2nullb , “ / F 5-HT s8sasa ?a# ,?C * Tbs8Tnull3nul

4、l,/ m 7 / F s8null2anull s8,8p/ m 78T null2 s8,null s8i8 wTb5- HT s88 wTG s87 ,5- HT2 s84: 8 , V 34 G 8 6,7T V$ F4 null4null,# 5- HT2 s88 6,MQ5- HT1A s848- OH-DOPA(8-) 8/,i O8/ V$5- HT1A s8 F4, 9 L5- HT1A4Ipspirone V 88/b7 hV,/ m 7a8)a5- a J / F ( 6, 7 null307nullb +Dnull 2000 M818 4 null J Prev Med

5、 Chin PLA null August 2000 null Vol.18No.4a 7 “1Tnull5null, 6-a5. 7-= 7 =a5- ? h 7 7 *% ,T 6, 79 6,i HWAnull6nullb2 null%y0Z U h ; -null null Linnull5null?C h7 7 * V,/ m 7a8%a5- a J / F A 6,7IL- 1aIL- 6 ? y0(TNF)c 9 6, L, hv i q 7a5- HTh H A 6,7 OIL- 1 s8 F4,i HW9A, 7 a * 9h bHammami?C hV, ? y0 s8(s

6、TNFR60asTNFR80)IL- 6 s8 (A 6, P 9 ?M ? y0 s8 i,4UB ? et%y0Qnull7nullbyN, F4 ? h, ? P 6, ,7 O X 39 V4, 7 * ,i HWnull8nullb Chiunull9nullv h, a ,IL- 1 s8E4i HW17s( S/ H HW),89F275%, IL- 1 s8E4i HW91s,9/204%b 9F4%,i HW Vr10l H, T IL- 1 s8E4 “ - hKrZEBb “ -n “5, rT),7 OIL- 1 s8NL, “5 k4 3b3 null 7 a h1h

7、 3 $null null 7 a 7 a 7 h1h 3$,837 42 nullW H,8L ,8V 5 f, 9F, 9F40%b8r42 null H, l h , 9 y/, 1yb/B, AY 7 b 6, 7 75,5 = %n, 7 = / F s8ya5- i 67 75l ,BF 7 b “ 7 h ,7F ? v? 3p, ATP,%Na+ - K+,p, Na+ ?, , =Na+ iv 6, 1i9 6, s% % b H 7F V,9F, c 9F, pH/, 7 pYi9F,y7 7F%W sc 99F,%W b 7 TQV 75,Y 7 b7 A 7 b 6BZ

8、 ,8 ,9F;ApHM, wLM,Ya ; 6, h, 8F PVBt M# Vp, 7F q, y 8TV7 P 7F ? A/bMustafa233 hh S s, 94 (40%) , c V15ml/dc, 67 hh , F q0%b 7 V ? h1yb 7F T ? ? 3p,L 8 r q, ?h , ATP, Na+ - K+, ?p,QV % = , 5,Y b9, y MM,Y, N0b4nullnull h H 7% V ?B Tnull nullv 7 B a K 2, / b # , y a * a aL 8L a1 aNO b“ - y YT, w *% b 7

9、1VKerr 4% Q,V B Tnull nullnull4 G, O sD jb MBtV : 7 % H# onull10null,- 7null308nullb +Dnull 2000 M818 4 null J Prev Med Chin PLAnull August 2000null Vol. 18 No. 4 ?C ISEL%,/9%VCnull11nullb 7 |Bt%1+ yyM9F, bcl- 2EBaTNFEBnull12nullbB : , null13nullb%7, _4 T,y Kv uY Q,“ VE ? 3,i M“ %b hy, l, P-815%43-

10、44 null H? 3,46 nullH v % ,yN|% 1o null14null, 84045 nullW, 7% V ?vnull15nullb 7 h w *M1h 3 $,7 %-$ LbyN, h H T,F hVNOnull16nullTNFnull17null 69 V%, hV V ?%? 3bZnull null h KB T,1998 M F VC A, T = , qb kX “ a%y0# F4a 7 a%# e ,M h “1il -b IDnull 1 null Quan N, XinL, Ungar AL, et al . Preoptic norepin

11、ephrine-induced hypothermia is mediated by alpha2null adrenoceptors.Am J physiol,1992,262( 3): R407null 2 null TangriKK,Gupta SK,Vrat S, et al , A study of effects of punulltative transmitter injected into the lateral cerebral ventricle ofman. Prog Neuropsychopharmacol Biol Psychiatry, 1993, 17(5) :

12、731null 3null Quan N, Xin L,Bletteis CM.Microdialysis of norepinephrineinto preoptic area of guinea pigs: characteristics of hypothernullmic effect. Am J physiol,1991,261:R378null 4 null Gudelsky GA,Koening JI, Meltzer HY.Thermoregulatory renullsponses to serotonin( 5- HT) receptor for opposing role

13、s of 5- HT2 and 5- HT1A receptors. Neuropharmacology, 1986,25:1307null 5null LinMT.Heatstroke- induced cerebral ischemia and neuronaldamage.Involvement of cytokines and monoamines.Ann- N- Y- Acad- Sci,1997,813:572null 6null Kao TY,Lin MT. Brain serotonin depletion attenuates heatnullstroke- induced

14、cerebral ischemia and cell death in rats. JAppl physiol,1996,80( 2) :680null 7null Hammami MM,Bouchama A,Shail E, et al. Concentrationsof soluble tumor necrosis factor and interleukin- 6 receptorsin heatstroke and heatstress. Crit Care Med 1997, 25( 8):1263null 8null Yang YL,Lu KT,Tsay- HT, et al. H

15、eat shock protein exnullpression protects against death following exposure to heatnullstroke in rats. Neurosci- Lett,1998,252( 1) :9null 9 null Chiu WT, Kao TY, Lin MT. Increased survival in experinullmental rat heatstroke by continuous perfusion of interleukin- l receptor antagonist.Neurosci- Res,1

16、996,24(2):159null 10 null Li Y, Chopp M, Zhang ZG, et al . P53- immunoreactiveprotein and P53 mRNA express after transient middle cerenullbral artery occulusion in rats.Stroke 1994,25: 849null 11 null Lslam N,Aftabuddin M,Moriwaki A, et al. Neurosci Lett,1995,188: 159null 12null Hara A, Lwai M, Niwa

17、 M, et al. Immunohistochemical denulltection of Bax and Bcl- 2 proteins in gerbil hippocampusfollowing transient forebrain ischemia. Brain Res 1996, 711(1 2): 249null 13null BurschM.Trends pharmacol.Sci 1992,13:245null 14null Li Y.Induction of DNA fragmentation after 10 to 120 minnullutes of focal c

18、erebral ischemia in rats. Stroke, 1995, 26:1252null 15null Fairbairn DW,Walburger DK.Key morphologic changes andDNA strand breaks in human lymphoid cells discriminatingapoptosis from necrosis.Scanning,1996,6:407null 16 null Canini F, Bourdon L, Cespuglio R, et al. Voltametric asnullsessment of brain

19、 nitric oxide during heatstroke in rats.Neunullrosci- Lett,1997,231(2) :67null 17null Dbaibo GS,Perry DK, Gamard CJ, et al. Cytokine responsemodifier inhibits ceramide formation in response to tumornecrosis factor(TNF) - alpha: CrmA and Bcl- 2 target disnulltinct components in the apoptotic pathway. J Exp,1997,185:481( l:1999- 05- 18null:1999- 10- 25)null309nullb +Dnull 2000 M818 4 null J Prev Med Chin PLA null August 2000 null Vol.18No.4

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