Taucher M, Grässler J, Kühne H, Scheuch D W
Institute of Pathological Biochemistry, Medical Academy Carl Gustav Carus Dresden, GDR.
Z Med Lab Diagn. 1990;31(1):13-7.
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.
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。
