Neonatal chronic lung disease in the post-surfactant era.

Richard D Bland
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引用次数: 126

Abstract

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.

后表面活性剂时代的新生儿慢性肺病。
本文对新生儿慢性肺病(有时称为“新型支气管肺发育不良”)作一简要综述。近年来,由于围产期护理的重大进展,包括产前糖皮质激素治疗的广泛使用、产后表面活性剂替代以及呼吸和营养支持的改善,这种疾病的临床、放射学和病理特征发生了很大变化。真实的动物模型,具有长时间机械通气的表面活性剂处理,早产儿狒狒和羔羊,提供了重要的见解,病理生理和治疗的疾病。富氧正压通气2-4周后肺组织病理学表现为肺泡和肺毛细血管形成失败,弹性蛋白堆积过多,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的治疗干预措施包括鼻腔持续气道正压通气、高频机械通气、吸入一氧化氮和视黄醇。现在的挑战是提高对调节正常肺生长和发育的分子机制的理解,并澄清肺结构和功能的失调发生在损伤和随后的修复中,以便有效的治疗或预防策略可以设计和实施。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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