Liao L, Harris N R, Granger D N
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
Am J Physiol. 1996 Dec;271(6 Pt 2):H2508-14. doi: 10.1152/ajpheart.1996.271.6.H2508.
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 and 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.
本研究的目的是确定缺血再灌注(I/R)和/或慢性动脉高血压是否会增强氧化型低密度脂蛋白(ox-LDL)引发的白细胞-内皮细胞黏附(LECA)和微血管功能障碍。在大鼠肠系膜毛细血管后微静脉中监测肥大细胞脱颗粒、白细胞黏附和迁移以及白蛋白渗漏情况。动脉内输注铜氧化型低密度脂蛋白(Cu-LDL),其浓度不会直接影响微血管,显著增强了I/R诱导的黏附和迁移白细胞募集,但不影响I/R后通常观察到的白蛋白渗漏增加和肥大细胞脱颗粒反应。在正常血压的Wistar-Kyoto大鼠或自发性高血压大鼠的非缺血肠系膜中输注更高浓度的Cu-LDL,会引起LECA、肥大细胞脱颗粒和白蛋白渗漏显著但相似的增加。这些发现表明:1)ox-LDL与I/R协同作用,促进毛细血管后微静脉中的白细胞募集,但不会伴随白蛋白渗漏加剧;2)与正常血压动物相比,ox-LDL不会在高血压动物的微血管中引发更强烈的炎症反应。