Mukundan C, Gurish M F, Austen K F, Hechtman H B, Friend D S
Department of Surgery, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
J Histochem Cytochem. 2001 Aug;49(8):1055-6. doi: 10.1177/002215540104900813.
We have observed extensive mast cell degranulation in the reperfused hindlimb muscle of the mouse, accompanied by pathological changes within the muscle. As quantitated by the tissue:blood (125)I permeability ratio, both the hindlimbs and lungs exhibited a significant increment in permeability during hindlimb reperfusion. In lungs of the same mice, mast cell-derived chymase mMCP-1 coats alveolar macrophages, an event noted by us in acid-induced direct lung injury. Mast cells in the lung contain mMCP-1, whereas those in the muscle do not. Neither extensive muscle injury nor an increased pulmonary permeability index occurs in the mast cell-deficient W/W(v) mice. We conclude that the mast cell is a key mediator in both local ischemia-reperfusion injury (I-R) of muscle and consequent remote lung injury.
我们观察到小鼠再灌注后肢肌肉中有广泛的肥大细胞脱颗粒现象，同时肌肉内伴有病理变化。通过组织：血液（125）I通透性比值定量分析，后肢再灌注期间后肢和肺部的通透性均显著增加。在同一小鼠的肺部，肥大细胞衍生的糜酶mMCP-1覆盖肺泡巨噬细胞，这是我们在酸诱导的直接肺损伤中注意到的现象。肺中的肥大细胞含有mMCP-1，而肌肉中的肥大细胞则不含。肥大细胞缺陷型W/W（v）小鼠既未出现广泛的肌肉损伤，也未出现肺通透性指数增加的情况。我们得出结论，肥大细胞是肌肉局部缺血再灌注损伤（I-R）及随之而来的远程肺损伤的关键介质。
