Cap Andrew P
US ARMY INSTITUTE OF SURGICAL RESEARCH.
Blood. 2016 Nov 17;128(20):2375-2376. doi: 10.1182/blood-2016-09-735720.
In this issue of , Marcos-Contreras and colleagues present convincing evidence that mechanistically links hyperfibrinolysis, typically seen as a bleeding risk, with increased brain endothelial permeability through plasmin-mediated cleavage of high-molecular-weight kininogen (HMWK) to bradykinin (BK). This study establishes plasmin as a key effector of what might be termed “hemovascular dysfunction”: a pathological state of blood enzymatic activity resulting in vascular structural and functional disruption. Their findings point the way toward improved treatment of patients with pharmacologically (stroke and myocardial infarction) or pathologically activated fibrinolysis (trauma and surgery) through selective blockade of bradykinin activity. Combined blockade of bradykinin and plasmin activation may provide additional therapeutic benefits in hemorrhagic shock by reducing tissue edema in resuscitation while enhancing hemostasis.
在本期杂志中，马科斯 - 孔特雷拉斯及其同事提供了令人信服的证据，从机制上证明了通常被视为出血风险的高纤溶状态与脑内皮通透性增加之间的联系，这种联系是通过纤溶酶介导的高分子量激肽原（HMWK）裂解为缓激肽（BK）实现的。这项研究确立了纤溶酶作为所谓“血管功能障碍”的关键效应因子，“血管功能障碍”是一种血液酶活性的病理状态，会导致血管结构和功能破坏。他们的研究结果为通过选择性阻断缓激肽活性来改善药物性（中风和心肌梗死）或病理性激活纤溶状态（创伤和手术）患者的治疗指明了方向。联合阻断缓激肽和纤溶酶激活可能通过在复苏过程中减轻组织水肿同时增强止血作用，为失血性休克提供额外的治疗益处。
