Oxidized low-density lipoproteins and microvascular responses to ischemia-reperfusion

被引:18
作者
Liao, LX [1 ]
Harris, NR [1 ]
Granger, DN [1 ]
机构
[1] LOUISIANA STATE UNIV, MED CTR, DEPT PHYSIOL & BIOPHYS, SHREVEPORT, LA 71130 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1996年 / 271卷 / 06期
关键词
vascular permeability; leukocyte adhesion; mast cell degranulation; arterial hypertension;
D O I
10.1152/ajpheart.1996.271.6.H2508
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The objective of this study was to determine whether ischemia and reperfusion (I/R) and/or chronic arterial hypertension potentiates the leukocyte-endothelial cell adhesion (LECA) and microvascular dysfunction elicited by oxidized low-density lipoproteins (ox-LDL). Mast cell degranulation, leukocyte adherence adn emigration, and albumin leakage were monitored in postcapillary venules of rat mesentery. Intra-arterial infusion of copper-oxidized LDL (Cu-LDL), at a concentration that does not directly affect the microvasculature, significantly enhanced the I/R-induced recruitment of adherent and emigrated leukocytes but does not affect the increased albumin leakage and mast cell degranulation responses normally observed after I/R. Infusion of a higher concentration of Cu-LDL in nonischemic mesentery of either normotensive Wistar-Kyoto or spontaneously hypertensive rats elicited significant yet similar increases in LECA, mast cell degranulation, and albumin leakage. These findings indicate that 1) ox-LDL act synergistically with I/R to promote leukocyte recruitment in postcapillary venules but without an accompanying exacerbation of albumin leakage, and 2) ox-LDL do not elicit a more intense inflammatory response in the microvasculature of hypertensive versus normotensive animals.
引用
收藏
页码:H2508 / H2514
页数:7
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