Doerschuk C M, Allard M F, Oyarzun M J
University of British Columbia, Pulmonary Research Laboratory, Vancouver, Canada.
Exp Lung Res. 1990 Jul-Aug;16(4):355-67. doi: 10.3109/01902149009108850.
We investigated the lung injury that occurs following reexpansion of a unilateral pneumothorax and determined the effect of superoxide dismutase (SOD) infused immediately prior to reexpansion on this injury. After 7 days of at least 80% right pneumothorax, rabbits received intravenous infusions of either SOD (n = 7), heat-inactivated SOD (n = 1), or vehicle (n = 7) immediately before lung reexpansion. Lung injury was assessed by measuring the systemic white cell counts, pulmonary blood volumes, extravascular albumin, extravascular lung water, wet/dry weight ratios, and histology 2 h after reexpansion. The reexpanded lung showed increased extravascular albumin, extravascular lung water and wet/dry weight ratios with decreased blood volumes compared to the uninjured lung. SOD delayed the onset of leukopenia and neutropenia at 3 and 7 min after reexpansion, but the white cell counts had decreased to the same level in both groups by 30 min. SOD had no effect on the degree of injury after 2 h. While a single bolus of SOD given immediately before reexpansion delayed the onset of this injury, it did not affect the injury that subsequently developed in the lung.
我们研究了单侧气胸再扩张后发生的肺损伤，并确定了在再扩张前立即注入超氧化物歧化酶（SOD）对该损伤的影响。在至少80%右侧气胸持续7天后，兔子在肺再扩张前立即接受静脉输注SOD（n = 7）、热灭活SOD（n = 1）或赋形剂（n = 7）。在再扩张后2小时，通过测量全身白细胞计数、肺血容量、血管外白蛋白、血管外肺水、湿/干重比和组织学来评估肺损伤。与未损伤的肺相比，再扩张的肺显示血管外白蛋白、血管外肺水和湿/干重比增加，血容量减少。SOD在再扩张后3分钟和7分钟延迟了白细胞减少和中性粒细胞减少的发生，但两组白细胞计数在30分钟时均降至相同水平。SOD对2小时后的损伤程度没有影响。虽然在再扩张前立即给予单次推注SOD延迟了这种损伤的发生，但它并未影响随后在肺中发生的损伤。
