Lou H C
John F. Kennedy Institute, Glostrup, Denmark.
APMIS Suppl. 1993;40:97-102.
The paper describes the sequence of events typical in the pathogenesis of germinal layer hemorrhage (GLH): An initial, often prenatal, severe asphyxic event, leading to abolishment of autoregulation of cerebral perfusion, and, most likely, to hypoxic-ischemic lesions in the endothelium of the large capillaries of the germinal matrix. The hypoxia is accompanied by exhaustion of myocardial energy reserves with circulatory failure, hypotension and aggravation of cerebral ischemia. In the period immediately after birth, circulation failure proceeds with cardiac insufficiency, hypotension, cerebral ischemia, and possibly venous hypertension. Following resuscitation, arterial blood pressure gradually increases (type 3) with increased strain on the damaged germinal matrix capillary walls in the absence of autoregulation. This effect is further aggravated by arterial blood pressure increments of type 1 and 2 leading to GLH, possibly with increments of venous pressure as a contributing factor.
本文描述了生发层出血（GLH）发病机制中典型的一系列事件：最初往往是产前发生的严重窒息事件，导致脑灌注自动调节功能丧失，极有可能使生发基质大毛细血管内皮发生缺氧缺血性损伤。缺氧伴随着心肌能量储备耗竭，进而出现循环衰竭、低血压以及脑缺血加重。在出生后的即刻，循环衰竭会伴有心功能不全、低血压、脑缺血，还可能出现静脉高压。复苏后，动脉血压逐渐升高（3型），在缺乏自动调节的情况下，受损的生发基质毛细血管壁所承受的压力增加。1型和2型动脉血压升高导致GLH，静脉压升高可能也是一个促成因素，这进一步加剧了上述影响。
