心源性休克对氨苄青霉素-舒巴坦药代动力学和组织分布的影响。

Circulatory shock Pub Date : 1994-11-01
W A Arden, D E Barker, W E Strodel, K Record, G Leader, M Derbin, G Gellin, R W Schwartz
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引用次数: 0

摘要

一个可逆的猪心源性休克模型研究了休克诱导的氨苄青霉素-舒巴坦的药代动力学和组织分布的变化,以及这种抗生素方案消除肠道细菌易位的效果。将16头猪随机分为3组:第一组(休克,氨苄西林-舒巴坦,n = 6)、第二组(无休克,氨苄西林-舒巴坦,n = 6)和第三组(休克,无氨苄西林-舒巴坦,n = 4)。将耐萘啶酸大肠杆菌(60 × 10(6) CFU)灌注到每头猪的空肠袢中,并从胸管淋巴结、门静脉周围和肠系膜淋巴结中提取细菌培养物。氨苄西林-舒巴坦以标准剂量3g静脉注射。结果表明:1)心源性休克时氨苄西林、舒巴坦浓度普遍升高;2)心源性休克不增加空肠和肝脏氨苄西林浓度;3)复苏期间胸管淋巴氨苄西林浓度降低;4)在心源性休克期间和之后,标准剂量的氨苄西林-舒巴坦对清除易位细菌有效。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of cardiogenic shock on pharmacokinetics and tissue distribution of ampicillin-sulbactam.

A reversible cardiogenic shock model in pigs investigated shock-induced changes in the pharmacokinetics and tissue distribution of ampicillin-sulbactam and the efficacy of this antibiotic regimen in eliminating enteric bacterial translocation. Sixteen pigs were randomly allocated to 3 groups: group I (shock, ampicillin-sulbactam, n = 6), group II (no shock, ampicillin-sulbactam, n = 6), and group III (shock, no ampicillin-sulbactam, n = 4). Nalidixic acid-resistant E. coli (60 x 10(6) CFU) were instilled into a jejunal loop created in each pig, and bacterial cultures were taken from thoracic duct lymph, periportal, and mesenteric lymph nodes. Ampicillin-sulbactam was administered intravenously at a standard dose of 3 g. Results showed that 1) ampicillin and sulbactam concentrations generally increase during cardiogenic shock; 2) cardiogenic shock does not increase ampicillin concentrations in jejunum and liver; 3) during resuscitation, thoracic duct lymph ampicillin concentrations decrease; and 4) during and immediately after cardiogenic shock, standard doses of ampicillin-sulbactam appear efficacious in eliminating translocated bacteria.

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