THE EFFETS OF LIDOCAINE ON ENDOTOXIN-INDUCED MULTIPLE ORGAN FAILURE.

利多卡因对内毒素引起的多器官衰竭的影响。

基本信息

批准号：
07671660
负责人：
MAEKAWA Nobuhiro
金额：
$ 1.47万
依托单位：
KOBE UNIVERSITY SCHOOL OF MEDICINE
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

项目摘要

We conducted the current study to assss the effects of lidocaine on endotoxin-induced multiple organ failure (MOF). Seventeen male Japanese white rabbits were divided into two groups : Group S (control, n=8) received iv endotoxin (E.Coli) and saline and Group L (n=9) did endotoxin and lidocaine infusion. Arterial blood samples for measurement of PaO2, GOT,GPT,BUN,and creatinine were drawn 0 hr, 6 hr, 12 hr, and 24 hr after endotoxin. Lung mechanics were measured by the passive expiratory flow-volume technique before endotoxin and 24 hr after endotoxin. The animals were killed 24 hr after endotoxin. Then, the lung, kidney, and liver were removed to determine wet to dry weight ratios (W/D) and myeloperoxidase activities. Cytokine and albumin concentrations in bronchoalveolar lavage (BAL) fluid were measured. The lung, kidney, and liver were also fixed by 4% glutaraldehyde solution. The specimens were stained with hematoxylin and eosin and examined under a light microscope. Endotoxin decreased PaO_2 and lung compliance. Lindocaine successfully attenuated deterioration of oxygenation and compliance. Endotoxin also increased the W/D weight ratio of the three organs, and albumin and interleukin (IL) -6, IL-8 in BAL fluid. Lidocaine attenuated the increases. The myeloperoxidase activities of the lung, kidney, and liver were greater in rabbits which did not receive lidocaine. Endotoxin caused extensive morphologic organ damages, which were lessened by lidocaine treatment. These results indicate that lidocaine pre-treatment attenuates endotoxin-induced MOF in rabbits. Because lidocaine markedly reduced the myeloperoxidase of the organs prepared from rabbits with endotoxin, the drug may attenuate the MOF in part by inhibiting activation of neutrophils.

我们进行当前的研究是为了评估利多卡因对内毒素诱导的多器官衰竭（MOF）的影响。将十七只雄性日本白兔分为两组：S组（对照，n=8）接受静脉注射内毒素（大肠杆菌）和盐水，L组（n=9）接受内毒素和利多卡因输注。内毒素后0小时、6小时、12小时和24小时抽取动脉血样用于测量PaO2、GOT、GPT、BUN和肌酐。内毒素处理前和内毒素处理后24小时通过被动呼气流量技术测量肺力学。内毒素后24小时处死动物。然后，取出肺、肾和肝以确定湿重与干重比（W/D）和髓过氧化物酶活性。测量支气管肺泡灌洗（BAL）液中的细胞因子和白蛋白浓度。肺、肾、肝也用4%戊二醛溶液固定。将标本用苏木精和曙红染色并在光学显微镜下检查。内毒素降低 PaO_2 和肺顺应性。林多卡因成功地减轻了氧合和依从性的恶化。内毒素还增加了三个器官的W/D重量比，以及BAL液中的白蛋白和白细胞介素(IL)-6、IL-8。利多卡因减弱了这种增加。未接受利多卡因的兔子的肺、肾和肝的髓过氧化物酶活性较高。内毒素造成广泛的器官形态损伤，利多卡因治疗可减轻这种损伤。这些结果表明利多卡因预处理可减弱兔子内毒素诱导的 MOF。由于利多卡因显着降低了含有内毒素的家兔器官中的髓过氧化物酶，因此该药物可能通过抑制中性粒细胞的活化来部分减弱 MOF。