Bland Richard D
Stanford University School of Medicine, Stanford, CA 94305-5162, USA.
Biol Neonate. 2005;88(3):181-91. doi: 10.1159/000087581.
This is a brief review of neonatal chronic lung disease, sometimes called the 'new bronchopulmonary dysplasia (BPD)'. The clinical, radiographic and pathological features of this condition have changed considerably in recent years because of major advances in perinatal care, including widespread use of antenatal glucocorticoid therapy, postnatal surfactant replacement and improved respiratory and nutritional support. Authentic animal models, featuring lengthy mechanical ventilation of surfactant-treated, premature neonatal baboons and lambs, have provided important insights on the pathophysiology and treatment of this disease. Lung histopathology after 2-4 weeks of positive-pressure ventilation with oxygen-rich gas results in failed formation of alveoli and lung capillaries, excess disordered elastin accumulation, smooth muscle overgrowth in small pulmonary arteries and airways, chronic inflammation and interstitial edema. Treatment interventions that have been tested in these animal models include nasal application of continuous positive airway pressure, high-frequency mechanical ventilation, inhaled nitric oxide and retinol. The challenge now is to improve understanding of the molecular mechanisms that regulate normal lung growth and development, and to clarify the dysregulation of lung structure and function that occurs with injury and subsequent repair so that effective treatment or prevention strategies can be devised and implemented.
这是一篇关于新生儿慢性肺疾病的简要综述，该疾病有时被称为“新型支气管肺发育不良（BPD）”。近年来，由于围产期护理取得了重大进展，包括广泛使用产前糖皮质激素治疗、产后表面活性剂替代以及改善呼吸和营养支持，这种疾病的临床、影像学和病理学特征发生了很大变化。真实的动物模型，以对接受表面活性剂治疗的早产狒狒和羔羊进行长时间机械通气为特点，为该疾病的病理生理学和治疗提供了重要见解。用富氧气体进行2至4周正压通气后的肺组织病理学结果显示，肺泡和肺毛细血管形成失败、弹性蛋白过度无序积累、小肺动脉和气道平滑肌过度生长、慢性炎症和间质水肿。在这些动物模型中测试过的治疗干预措施包括经鼻持续气道正压通气、高频机械通气、吸入一氧化氮和视黄醇。现在的挑战是增进对调节正常肺生长和发育的分子机制的理解，并阐明损伤及后续修复过程中发生的肺结构和功能失调，以便能够设计并实施有效的治疗或预防策略。
