New myocardial motection with cytokine network.

为了阐明中性粒细胞（Np）诱导心肌再灌注损伤的机制，从成年大鼠心脏和血液中分离出Np肌细胞（Mc）和内皮细胞（Ec）。为了阐明Np在再灌注损伤中起作用的假设，我们建立了胶原膜上单层内皮细胞和胶原膜下肌细胞共孵育系统。在该系统中，缺氧2小时后，Np通过Ec迁移、Mc损伤和化学发光计数显著增加。然而，给药抗ICAM-1和IL-6单克隆抗体可降低这些变化。缺氧Mc和Ec中ICAM-1表达显著。低氧心肌细胞上清液中IL-6水平明显高于常氧心肌细胞。这些结果表明，Ec和Mc上的ICAM-1参与通过Ec和Np引起的心肌再灌注损伤的Np迁移，从而延长心肌再灌注损伤。此外，IL-6可能来源于缺氧的肌细胞，促进中性粒细胞诱导的再灌注损伤。

To elucidate the mechanism of neutrophil(Np) induced reperfusion injury in myocardium, Np myocytes(Mc) and endothelial cells(Ec) were isolated from adult rat heart and blood. To elucidate the hypothesis that Np plays a role in reperfusion injury, a coincubation system with a monolayr of endothelial cells on the collagen membrane and myocytes under a collagen membrane was established. In this system, significant increase of Np migration through Ec, Mc damage and count of chemiluminescence were increased by 2 hours of hypoxia.However, these changes were decreased by administration of monoclonal antibody anti ICAM-1 and IL-6. Hypoxic Mc and Ec showed significant expression of ICAM-1. In the supernatant of hypoxic myocyte, significant increase of IL-6 was detected as compared to normoxic myocytes. These results suggested that ICAM-1 on Ec and Mc is implicated in Np migration through Ec and Np induced damage resulting in the extension of reperfusion injury in myocardium. Moreover, IL-6 may be derived from hypoxic myocytes and promote neutrophil induced reperfusion injury.