Haubro Andersen P, Jarløv N
Department of Clinical Studies, Royal Veterinary and Agricultural University, Frederiksberg, Denmark.
Acta Vet Scand. 1990;31(1):27-38. doi: 10.1186/BF03547574.
Rumen acidosis was induced experimentally with 70 g barley/kg b.w. in 2 rumen fistulated cows. The cows were followed for 80 h after the grain engorgement. Endotoxin was monitored in cell-free ruminal fluid and peripheral plasma together with inflammation mediators TXA2, PGI2 and PGE2 and several clinical and clinical-chemical parameters. The results do not support the theory of systemical endotoxemia due to a large increase in rumen endotoxin concentration in cattle suffering from rumen acidosis. However, both clinical and clinical-chemical data suggest that an endotoxicosis developed, but the levels of inflammation mediators TXB2, FGI2 and PGE2 were not significantly elevated in the peripheral circulation. An absorbtion of endotoxins and synthesis of inflammation mediators are therefore suggested to take place prehepatically.
在2头装有瘤胃瘘管的奶牛中,通过按每千克体重70克大麦的剂量进行实验性诱发瘤胃酸中毒。谷物灌服后对奶牛进行80小时的跟踪观察。对无细胞瘤胃液和外周血浆中的内毒素以及炎症介质血栓素A2(TXA2)、前列环素(PGI2)和前列腺素E2(PGE2)以及若干临床和临床化学参数进行监测。结果不支持瘤胃酸中毒的牛因瘤胃内毒素浓度大幅升高而导致全身性内毒素血症的理论。然而,临床和临床化学数据均表明发生了内毒素中毒,但外周循环中炎症介质血栓素B2(TXB2)、前列环素(FGI2)和前列腺素E2(PGE2)的水平并未显著升高。因此,提示内毒素的吸收和炎症介质的合成发生在肝脏之前。