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强心苷地高辛通过损害中性粒细胞动员,破坏实验性肺炎球菌肺炎中的宿主防御。

The cardiac glycoside digoxin disrupts host defense in experimental pneumococcal pneumonia by impairing neutrophil mobilization.

作者信息

Esposito A L, Poirier W J, Clark C A

机构信息

Department of Medicine, Boston University Medical Center, MA.

出版信息

Am Rev Respir Dis. 1989 Dec;140(6):1590-4. doi: 10.1164/ajrccm/140.6.1590.

DOI:10.1164/ajrccm/140.6.1590
PMID:2604288
Abstract

Normal CD-1 mice were administered digoxin (4 micrograms/kg/24 h) and infected with type 3 Streptococcus pneumoniae in order to assess the effects of the cardiac glycoside on the chemotactic responsiveness of peripheral blood neutrophils and the mobilization of granulocytes from storage pools. The chemotactic responses to autologous zymosan-activated serum (C5a) by neutrophils obtained from uninfected digoxin-treated and control animals were similar; comparable observations were made with circulating granulocytes isolated from animals at 24 or 48 h after intratracheal challenge with 5 x 10(5) colony-forming units (cfu) of bacteria. However, at 4 and 6 h after intratracheal pneumococcal challenge, the number of immature neutrophils in the peripheral blood was significantly lower in the glycoside-treated animals versus controls; at 24 and 48 h, these differences were not apparent. Following the intravenous inoculation of pneumococci, the number of circulating immature neutrophils was also found to be significantly lower at 4 and 24 h in animals given the cardiac glycoside versus controls. We conclude that digoxin disrupts host defense in experimental pneumococcal pneumonia and bacteremia by impairing the mobilization of neutrophils.

摘要

对正常的CD - 1小鼠给予地高辛(4微克/千克/24小时),并感染3型肺炎链球菌,以评估强心苷对外周血中性粒细胞趋化反应性以及粒细胞从储存池动员的影响。未感染的地高辛处理动物和对照动物的中性粒细胞对自体酵母聚糖激活血清(C5a)的趋化反应相似;在用5×10⁵菌落形成单位(cfu)细菌进行气管内攻击后24或48小时,从动物分离的循环粒细胞也得到了类似的观察结果。然而,在气管内肺炎球菌攻击后4和6小时,与对照组相比,糖苷处理动物外周血中未成熟中性粒细胞的数量显著降低;在24和48小时,这些差异不明显。静脉接种肺炎球菌后,在给予强心苷的动物中,4小时和24小时循环未成熟中性粒细胞的数量也显著低于对照组。我们得出结论,地高辛通过损害中性粒细胞的动员而破坏实验性肺炎球菌肺炎和菌血症中的宿主防御。

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The cardiac glycoside digoxin disrupts host defense in experimental pneumococcal pneumonia by impairing neutrophil mobilization.强心苷地高辛通过损害中性粒细胞动员,破坏实验性肺炎球菌肺炎中的宿主防御。
Am Rev Respir Dis. 1989 Dec;140(6):1590-4. doi: 10.1164/ajrccm/140.6.1590.
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