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:
  • 金额:
    $ 1.47万
  • 依托单位:
  • 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.
我们进行了当前的研究,以评估利多卡因对内毒素诱导的多器官衰竭(MOF)的影响。选取雄性日本大白兔17只,分为两组:S组(对照组,n=8)静脉注射内毒素(大肠杆菌)和生理盐水,L组(n=9)内毒素和利多卡因输注。内毒素作用后0小时、6小时、12小时和24小时,分别取动脉血测定PaO2、GOT、GPT、BUN和肌酐。内毒素前和内毒素后24小时采用被动呼气流量-容积法测定肺力学。内毒素处理后24小时处死。然后,取肺、肾和肝,测定干、湿重比(W/D)和髓过氧化物酶活性。测定支气管肺泡灌洗液中细胞因子和白蛋白的浓度。肺、肾、肝也用4%戊二醛溶液固定。用苏木精和伊红染色,光镜下观察。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。未给予利多卡因的兔肺、肾和肝的髓过氧化物酶活性更大。内毒素引起广泛的器官形态学损害,利多卡因治疗减轻了这种损害。说明利多卡因预处理能减轻内毒素诱导的MOF。由于利多卡因显著降低了兔内毒素器官的髓过氧化物酶,该药物可能部分通过抑制中性粒细胞的激活来减弱MOF。

项目成果

期刊论文数量(18)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Nishina K, et al.: "Inhaled nitric oxide does not prevent endotoxin-indueed lung injury" Acta Anaesthesiol Scand. 41(in press). (1997)
Nishina K 等人:“吸入一氧化氮并不能预防内毒素引起的肺损伤”Acta Anaesthesiol Scand。
  • DOI:
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    0
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  • 通讯作者:
三川,仁科,志賀,他: "NO研究の基礎と臨床 vol.2" 医学図書出版, (1996)
Mikawa、Nishina、Shiga 等:“基础和临床 NO 研究 vol.2” Igaku Tosho Publishing,(1996)
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    0
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  • 通讯作者:
Mikawa K,Nishina K,Maekawa N,Obara H.: "Attenuation of hyperoxic lung injury in rabbit with superoxide dismutase : effects on inflammatory mediators" Acta Anaesthesiol Scand. 39. 317-322 (1995)
Mikawa K、Nishina K、Maekawa N、Obara H.:“超氧化物歧化酶减轻兔子高氧性肺损伤:对炎症介质的影响”Acta Anaesthesiol Scand。
  • DOI:
  • 发表时间:
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  • 影响因子:
    0
  • 作者:
  • 通讯作者:
前川 信博: "呼吸管理の基礎知識" JCHNS. 11. 1711-1717 (1995)
Nobuhiro Maekawa:“呼吸管理基础知识”JCHNS 11. 1711-1717 (1995)。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Mikawa K, et al.: "Attenuation of hyperoxic lurg injury in rabbits with SOD." Acta Anaesthesiol Scand. 39. 317-322 (1995)
Mikawa K 等人:“SOD 可减轻兔子的高氧性损伤。”
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    0
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MAEKAWA Nobuhiro其他文献

MAEKAWA Nobuhiro的其他文献

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{{ truncateString('MAEKAWA Nobuhiro', 18)}}的其他基金

Cosmology in the natural GUT
自然 GUT 中的宇宙学
  • 批准号:
    23540299
  • 财政年份:
    2011
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Natural grand unified theory, cosmology, derivation from superstring, and predictions
自然大统一理论、宇宙学、超弦推导和预测
  • 批准号:
    19340059
  • 财政年份:
    2007
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)

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