Systemic fatty acid responses to transient focal cerebral ischemia: influence of neuroprotectant therapy with human albumin

被引:74
作者
de Turco, EBR
Belayev, L
Liu, YT
Busto, R
Parkins, N
Bazan, NG
Ginsberg, MD
机构
[1] Univ Miami, Sch Med, Dept Neurol, Cerebral Vasc Dis Res Ctr, Miami, FL 33101 USA
[2] Louisiana State Univ, Hlth Sci Ctr, Sch Med, Neurosci Ctr Excellence, New Orleans, LA USA
关键词
arachidonic acid; brain ischemia; docosahexaenoic acid; human albumin; middle cerebral artery occlusion; neuroprotection;
D O I
10.1046/j.1471-4159.2002.01121.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Human albumin therapy is highly neuroprotective in focal cerebral ischemia. Because albumin is the main carrier of free fatty acids (FFA) in plasma, we investigated the content and composition of plasma FFA in jugular vein (JV), femoral artery (FA) and femoral vein (FV) of rats given intravenous human albumin (1.25 g/kg) or saline vehicle (5 mL/kg) 1 h after a 2 h middle cerebral artery occlusion (MCAo) or sham surgery. Arachidonic acid was the only FFA significantly increased by MCAo in all plasma samples prior to albumin administration, remaining at the same level regardless of subsequent treatments. Albumin treatment induced in both MCAo- and sham-groups a 1.7-fold increase in total plasma FFA (mainly 16:0, 18:1, 18:2n-6) during 90-min reperfusion. MCAo selectively stimulated the albumin-mediated mobilization of n-3 polyunsaturated fatty acids (PUFA), with an early increase in 22:5n-3 and 22:6n-3 in the FA prior to detectable changes in the JV. In the MCAo-albumin group, the lower level of FFA in JV as compared with FA and FV suggests an albumin-mediated systemic mobilization and supply of FFA to the brain, which may favor the replenishment of PUFA lost from cellular membranes during ischemia and/or to serve as an alternative source of energy, thus contributing to albumin neuroprotection.
引用
收藏
页码:515 / 524
页数:10
相关论文
共 54 条
[1]  
Bazan N G, 1980, Adv Neurol, V28, P197
[2]  
Bazan NG, 1996, PHARMACOLOGY OF CEREBRAL ISCHEMIA 1996, P173
[3]   MEDIATORS OF INJURY IN NEUROTRAUMA - INTRACELLULAR SIGNAL-TRANSDUCTION AND GENE-EXPRESSION [J].
BAZAN, NG ;
DETURCO, EBR ;
ALLAN, G .
JOURNAL OF NEUROTRAUMA, 1995, 12 (05) :791-814
[4]  
Bazan NG, 1996, RETINAL DEGENERATION AND REGENERATION, P89
[6]  
BAZAN NG, 1992, AM OIL CHEM SOC, P107
[7]  
BAZAN NG, 1990, NUTR BRAIN, P1
[8]  
BAZXAN NG, 2001, NEUROPROTECTION BASI, P196
[9]   Middle cerebral artery occlusion in the rat by intraluminal suture - Neurological and pathological evaluation of an improved model [J].
Belayev, L ;
Alonso, OF ;
Busto, R ;
Zhao, WZ ;
Ginsberg, MD .
STROKE, 1996, 27 (09) :1616-1622
[10]   HU-211, A NOVEL NONCOMPETITIVE N-METHYL-D-ASPARTATE ANTAGONIST, IMPROVES NEUROLOGICAL DEFICIT AND REDUCES INFARCT VOLUME AFTER REVERSIBLE FOCAL CEREBRAL-ISCHEMIA IN THE RAT [J].
BELAYEV, L ;
BUSTO, R ;
ZHAO, WZ ;
GINSBERG, MD .
STROKE, 1995, 26 (12) :2313-2319