Differential effects of prolonged septicemia on isolated pulmonary arteries and veins from sheep

被引:9
作者
Nelson, SH [1 ]
Ehardt, JS [1 ]
Lingnau, W [1 ]
Dehring, DJ [1 ]
Traber, L [1 ]
Traber, D [1 ]
机构
[1] UNIV IOWA,COLL MED,IOWA CITY,IA 52242
来源
SHOCK | 1996年 / 5卷 / 06期
关键词
D O I
10.1097/00024382-199606000-00009
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Isolated third-order pulmonary arteries and veins from sheep were examined for the effects of septicemia on norepinephrine-induced contractions, nitric oxide INO)-mediated dilation, and basal cyclic GMP levels. The groups studied were as follows: control sheep (n = 7); sheep given live Pseudomonas aeruginosa (Ps, n = 6) for 48 h; and sheep given N-G-mono-methyl-L-arginine during the last 24 h of Ps infusion (Ps-L-NMMA, n = 4). The norepinephrine-induced contractions were significantly greater (p < .05) in arteries from septic (Ps and Ps-L-NMMA) sheep. Basal cyclic GMP levels were similar in all of the arteries. The norepinephrine-induced contractions were significantly depressed (p < .05) in veins from septic (Ps and Ps-L-NMMA) sheep. Basal cyclic GMP levels in veins from Ps sheep were markedly elevated (p < .01). N-omega-nitro-L-arginine methyl ester (L-NAME) ex vivo decreased cyclic GMP in both arteries and veins. Removal of endothelium enhanced contractions and decreased cyclic GMP in arteries and veins only from control sheep. The results show that septicemia differently affects the pulmonary artery and vein. The enhanced vasoconstriction of the artery is due to decreased endothelium-dependent NO release; the attenuated vasoconstriction of the vein is associated with NO-mediated increased cyclic GMP levels.
引用
收藏
页码:440 / 445
页数:6
相关论文
共 33 条
[1]  
AUGUET M, 1990, ARCH MAL COEUR VAISS, V83, P1187
[2]   ENDOTHELIUM-DEPENDENT RELAXATION OF CORONARY-ARTERIES BY NORADRENALINE AND SEROTONIN [J].
COCKS, TM ;
ANGUS, JA .
NATURE, 1983, 305 (5935) :627-630
[3]  
DEHRING DJ, 1989, CIRC SHOCK, V29, P245
[4]   INDUCIBLE BUT NOT CONSTITUTIVE PRODUCTION OF NITRIC-OXIDE BY VASCULAR SMOOTH-MUSCLE CELLS [J].
FLEMING, I ;
GRAY, GA ;
SCHOTT, C ;
STOCLET, JC .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1991, 200 (2-3) :375-376
[5]   EVIDENCE THAT AN L-ARGININE NITRIC-OXIDE DEPENDENT ELEVATION OF TISSUE CYCLIC-GMP CONTENT IS INVOLVED IN DEPRESSION OF VASCULAR REACTIVITY BY ENDOTOXIN [J].
FLEMING, I ;
JULOUSCHAEFFER, G ;
GRAY, GA ;
PARRATT, JR ;
STOCLET, JC .
BRITISH JOURNAL OF PHARMACOLOGY, 1991, 103 (01) :1047-1052
[6]   THE OBLIGATORY ROLE OF ENDOTHELIAL-CELLS IN THE RELAXATION OF ARTERIAL SMOOTH-MUSCLE BY ACETYLCHOLINE [J].
FURCHGOTT, RF ;
ZAWADZKI, JV .
NATURE, 1980, 288 (5789) :373-376
[7]   NITRIC-OXIDE FROM ENDOTHELIUM AND SMOOTH-MUSCLE MODULATES RESPONSES TO SYMPATHETIC-NERVE STIMULATION - IMPLICATIONS FOR ENDOTOXIN-SHOCK [J].
GONZALEZ, C ;
FERNANDEZ, A ;
MARTIN, C ;
MONCADA, S ;
ESTRADA, C .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1992, 186 (01) :150-156
[9]   LOSS OF VASCULAR RESPONSIVENESS INDUCED BY ENDOTOXIN INVOLVES L-ARGININE PATHWAY [J].
JULOUSCHAEFFER, G ;
GRAY, GA ;
FLEMING, I ;
SCHOTT, C ;
PARRATT, JR ;
STOCLET, JC .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (04) :H1038-H1043
[10]   REVERSAL OF ENDOTOXIN-MEDIATED SHOCK BY NG-METHYL-L-ARGININE, AN INHIBITOR OF NITRIC-OXIDE SYNTHESIS [J].
KILBOURN, RG ;
JUBRAN, A ;
GROSS, SS ;
GRIFFITH, OW ;
LEVI, R ;
ADAMS, J ;
LODATO, RF .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 172 (03) :1132-1138