New myocardial motection with cytokine network.

为探讨中性粒细胞(NP)致心肌再灌注损伤的机制，从成年大鼠心脏和血液中分离出中性粒细胞(NP)心肌细胞(Mc)和内皮细胞(EC)。为阐明NP在再灌注损伤中的作用机制，建立了胶原膜上单层内皮细胞与胶原膜下的肌细胞共孵育体系。在该系统中，NP通过EC的迁移显著增加，Mc损伤和化学发光计数随缺氧时间的延长而增加，但这些变化可被抗ICAM-1和IL-6的单抗抑制。缺氧Mc和EC均有ICAM-1的显著表达。缺氧心肌细胞培养上清液中IL-6水平较常氧心肌细胞明显升高。提示EC和Mc上ICAM-1参与了NP通过EC和NP引起的心肌损伤的迁移，从而导致心肌再灌注损伤的延长。IL-6可能来源于缺氧性心肌细胞，促进中性粒细胞再灌注损伤。

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.