Oliver M G, Specian R D, Perry M A, Granger D N
Department of Cellular Biology, Louisiana State University Medical Center, Shreveport.
Inflammation. 1991 Oct;15(5):331-46. doi: 10.1007/BF00917350.
Intravital microscopic studies of the mesenteric microcirculation have demonstrated that leukocyte adherence and emigration in postcapillary venules are a characteristic feature of tissues exposed to ischemia-reperfusion. The objectives of this study were to determine whether: (1) neutrophils are the predominant leukocytes that adhere and emigrate in postischemic mesenteric venules, and (2) leukocyte adherence and/or emigration are a prerequisite for reperfusion-induced increases in venular permeability. Leukocyte kinetics in cat mesenteric venules (25-35 microns diameter) were evaluated using both intravital microscopy and quantitative morphometry. The intestine and mesentery were exposed to 60 min of ischemia, followed by 60 min reperfusion. Some animals were pretreated with a monoclonal antibody (MoAb IB4) against the leukocyte adhesion glycoprotein, CD11/CD18. Vessels observed by intravital microscopy and adjacent venules of similar diameter were excised and processed for light (LM) and electron microscopy (EM). Horseradish peroxidase (HRP), administered intravenously, was used to assess vascular permeability by EM. By LM, the control (nonischemic) mesentery is sparsely populated by plasma cells, mast cells, and leukocytes; 30-50% of the resident population is neutrophils. Ischemia-reperfusion led to a significant increase in the number of extravascular cells, with neutrophils accounting for greater than 80% of the total cell population. Control and ischemic venules demonstrated no leakage of HRP into the interstitium. However, venules exposed to ischemia and reperfusion demonstrated HRP leakage between endothelial cells and into the surrounding interstitium; neutrophils were adherent to the luminal surface of the endothelium, transmigrating the vessel wall, and in the surrounding interstitium. Animals pretreated with MoAb IB4 presented the same cell profile as nonischemic controls, with no adherent or transmigrating neutrophils. However, some HRP leakage was noted following reperfusion in venules treated with MoAb IB4. The results of this study indicate that: (1) neutrophils are the predominate leukocytes that adhere and emigrate in postischemic venules, and (2) inhibition of leukocyte adhesion does not completely prevent the venular dysfunction associated with ischemia-reperfusion.
对肠系膜微循环进行的活体显微镜研究表明，毛细血管后微静脉中的白细胞黏附和游出是缺血再灌注组织的一个特征性表现。本研究的目的是确定：（1）中性粒细胞是否是缺血后肠系膜微静脉中黏附和游出的主要白细胞，以及（2）白细胞黏附和/或游出是否是再灌注诱导的微静脉通透性增加的先决条件。使用活体显微镜和定量形态学评估猫肠系膜微静脉（直径25 - 35微米）中的白细胞动力学。将肠和肠系膜暴露于60分钟的缺血，随后再灌注60分钟。一些动物用针对白细胞黏附糖蛋白CD11/CD18的单克隆抗体（MoAb IB4）进行预处理。通过活体显微镜观察的血管以及直径相似的相邻微静脉被切除并进行光镜（LM）和电镜（EM）处理。静脉注射辣根过氧化物酶（HRP），通过电镜评估血管通透性。光镜下，对照（非缺血）肠系膜中浆细胞、肥大细胞和白细胞分布稀疏；常驻细胞群体的30 - 50%是中性粒细胞。缺血再灌注导致血管外细胞数量显著增加，中性粒细胞占总细胞群体的80%以上。对照和缺血微静脉未显示HRP漏入间质。然而，经历缺血和再灌注的微静脉显示HRP在内皮细胞之间漏出并进入周围间质；中性粒细胞黏附在内皮细胞的管腔表面，穿过血管壁，并存在于周围间质中。用MoAb IB4预处理的动物呈现出与非缺血对照相同的细胞分布，没有黏附或游出的中性粒细胞。然而，在用MoAb IB4处理的微静脉再灌注后，观察到一些HRP漏出。本研究结果表明：（1）中性粒细胞是缺血后微静脉中黏附和游出的主要白细胞，以及（2）抑制白细胞黏附并不能完全预防与缺血再灌注相关的微静脉功能障碍。
