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通过因子 XII f 预处理激活激肽释放酶 - 激肽系统对实验性失血性休克的影响。

Effect of kallikrein-kinin system activation by factor XII f pretreatment on experimental hemorrhagic shock.

作者信息

Taucher M, Grässler J, Kühne H, Scheuch D W

机构信息

Institute of Pathological Biochemistry, Medical Academy Carl Gustav Carus Dresden, GDR.

出版信息

Z Med Lab Diagn. 1990;31(1):13-7.

PMID:2330739
Abstract

Effects of Hageman factor fragment (factor XIIf) administration on shock induction were studied in anesthetized male Wistar rats with hemorrhagic shock. Administration of factor XIIf in non-hemorrhaged rats resulted in an immediate decrease of mean arterial pressure (MAP) for 5 min and in significant increases of blood glucose, lactate and hematocrit (Hct) as well as in a strong tendency for plasma kallikreinogen (KKN) to decrease. At the beginning of bleeding (15 min after factor XIIf administration) MAP has been normalized again. During subsequent hemorrhage pretreated rats showed a sharper decrease in MAP which remained significantly lower up to 25% of estimated blood volume (EBV) and recovered more slowly to normal level after hemorrhage. Blood glucose, lactate and Hct were significantly higher in pretreated animals after hemorrhage of 30% EBV. KKN depicted significant lower values during hemorrhage and in the posthemorrhagic period. Mortality within the observation time increased from 20% (control group) to 60% (pretreated animals). The results demonstrate that prehemorrhagic kallikrein-kinin system (KKS) activation induced an increased severity of shock state with higher mortality.

摘要

在麻醉的雄性Wistar大鼠失血性休克模型中,研究了给予Hageman因子片段(因子XIIf)对休克诱导的影响。在未出血的大鼠中给予因子XIIf会导致平均动脉压(MAP)立即下降5分钟,并使血糖、乳酸和血细胞比容(Hct)显著升高,同时血浆激肽释放酶原(KKN)有明显下降趋势。在出血开始时(给予因子XIIf后15分钟),MAP再次恢复正常。在随后的出血过程中,预处理的大鼠MAP下降更剧烈,在估计失血量(EBV)达到25%之前一直显著低于正常水平,且出血后恢复到正常水平的速度更慢。在失血量为30% EBV的出血后,预处理动物的血糖、乳酸和Hct显著更高。KKN在出血期间和出血后阶段的值显著更低。观察期内的死亡率从20%(对照组)增加到60%(预处理动物)。结果表明,出血前激肽释放酶-激肽系统(KKS)激活会导致休克状态严重程度增加,死亡率更高。

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