ROLE OF LEUKOCYTES IN RESPONSE TO ACUTE MYOCARDIAL-ISCHEMIA AND REFLOW IN DOGS
ROLE OF LEUKOCYTES IN RESPONSE TO ACUTE MYOCARDIAL-ISCHEMIA AND REFLOW IN DOGS
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DOI：
10.1152/ajpheart.1986.251.2.h314
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发表时间：
1986-08-01
影响因子：
--
通讯作者：
SCHMIDSCHONBEIN, GW
中科院分区：
文献类型：
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作者：
ENGLER, RL;DAHLGREN, MD;SCHMIDSCHONBEIN, GW
最近的证据表明，白细胞（LEU）是大，硬，粘性细胞，自然粘附到血管内皮。它们在急性缺血的早期心肌微血管反应中的广泛作用由以下因素表明：（1）白细胞毛细血管堵塞在无复流现象中的作用，（2）LEU输注引起骨骼肌阻力增加，（3）抗LEU药物挽救缺血心肌。我们在匹配的受控条件下用全血或去除粒细胞的全血灌注冠状动脉循环。在1小时的缺血（左前降支闭塞）回旋灌注压伺服控制到一个恒定的值。在全血灌注的心脏中，通过放射性标记的微球方法测量的流量在内皮素中从0.12 ± 0.05降低。0.05在缺血5分钟时降至0.09 ± 0.05。0.04 ml. cntdot. min-1. g-1，心外膜中为0.27 ± 0.25 μ g-1。0.17至0.21. ±. 0.16 ml. cntdot. min-1. g-1，均P <0.05。在粒细胞耗尽的血液灌注心脏中，流量在同一时期从0.18 ± 0.15增加到0.18 ± 0.15。0.15至0.29. ±. 0.18 ml. cntdot. min-1. g-1（P <0.05），心外膜无明显变化（0.36 ± 0.05）。0.22至0.41. ±. 0.24 ml. cntdot. min-1. g-1）。LEU耗尽的血液灌注液含有少于33粒细胞/μ l，而对照灌注液含有4，265粒细胞/μ l。在正常压力下用碳悬浮液再灌注允许无复流现象的组织学评价。全血灌流时，内皮细胞无复流现象发生，毛细血管闭塞率为27%，而LEU耗竭组几乎完全再灌注（毛细血管闭塞率为1%，P <0.05）。此外，LEU耗竭可防止对照组心肌组织含水量的增加，降低室性心律失常的发生率。这些研究表明，粒细胞在心肌缺血第1小时的血流、水肿形成和心律失常的不利反应中有重要作用，并进一步证明了它们在无复流现象中的作用。
Recent evidence indicates that leukocytes (LEU) are large, stiff, viscous cells that naturally adhere to vascular endothelium. Their broad role in the early myocardial microvascular response to acute ischemia was suggested by (1) the role of leukocyte capillary plugging in the no-reflow phenomenon, (2) resistance increases in skeletal muscle with LEU infusions, and (3) salvage of ischemic myocardium by anti-LEU agents. We perfused the coronary circulation under matched, controlled conditions with whole blood or granulocyte-depleted whole blood. During 1 h of ischemia (left anterior descending occlusion) circumflex perfusion pressure was servocontrolled to a constant value. In whole blood-perfused hearts, flow measured by the radiolabeled microsphere method decreased in endocardium from 0.12 .+-. 0.05 at 5 min of ischemia to 0.09 .+-. 0.04 ml .cntdot. min-1 .cntdot. g-1 at 60 min of ischemia and in epicardium from 0.27 .+-. 0.17 to 0.21 .+-. 0.16 ml .cntdot. min-1 .cntdot. g-1, both P < 0.05. In granulocyte-depleted blood-perfused hearts, flow increased over the same period from 0.18 .+-. 0.15 to 0.29 .+-. 0.18 ml .cntdot. min-1 .cntdot. g-1 in endocardium (P < 0.05) and did not change significantly in epicardium (0.36 .+-. 0.22 to 0.41 .+-. 0.24 ml .cntdot. min-1 .cntdot. g-1). The LEU-depleted blood perfusate contained less than 33 granulocytes/.mu.l, whereas control perfusate contained 4,265/.mu.l. Reperfusion at normal pressures with carbon suspension allowed for histologic evaluation of the no-reflow phenomenon. With whole blood perfusion the no-reflow phenomenon in the endocardium was present with 27% of capillaries occluded, compared with nearly complete reperfusion in LEU-depleted animals (1% of capillaries occluded, P < 0.05), Furthermore, LEU depletion prevented the increases in tissue water content seen in control hearts and decreased the incidence of ventricular arrhythmias. These studies demonstrate the significant participation of granulocytes in the unfavorable repsonses of flow, edema formation, and arhythmias to the 1st h of myocardial ischemia and further document their role in the no-reflow phenomenon.