BRAIN CHOLECYSTOKININ LEVEL IN HEPATIC ENCEPHALOPATHY

本文报道了肝性脑病（HE）实验动物模型EcK瘘犬和二甲基亚硝胺（DMN）诱导的急性肝衰竭犬脑内CCK样免疫反应性（CCK-LI）的变化。结果表明，Eck瘘管犬大脑皮质各区域CCK-LI均显著降低，尤其是顶叶和枕叶皮质，其水平约为对照值的40%。在急性肝功能衰竭的狗中，在颞叶和顶叶皮质中观察到CCK-Li减少（分别为对照值的65%和47%）。这些数据进行了比较，与浓度的苯丙氨酸，假神经递质的前体建议引起HE。苯丙氨酸显着增加，在所有领域的EcK瘘狗的皮质和枕叶皮质的狗急性肝衰竭。酪氨酸也显着增加额，顶叶和枕叶皮质的EcK瘘狗，并在颞叶和枕叶皮质的狗急性肝功能衰竭。但HE模型大鼠皮层CCK-LI水平的降低与芳香族氨基酸含量的增加无明显相关性。结果提示，兴奋性神经肽CCK水平的降低可能是通过与诱导假神经递质增加不同的机制引起的。

Cholecystokinin-like immunoreactivity(CCK-LI) was measured in the brain of EcK fistula dogs and dogs with dimethylnitrosamine-induced (DMN) acute hepatic failure which were prepared as experimental models of hepatic encephalopathy (HE). The results showed a significant reduction of CCK-LI in all cortical regions of Eck fistula dogs, especially in parietal and occipital cortex in which the levels were approximatily 40% of control values. In dogs with acute hepatic failure, CCK-Li reduction was observed in the temporal and parietal cortex (65% and 47% of control values, respectively). These data were compared with the concentrations of typrosine and phenylalanine, precursors of false neurotransmitters suggested as causing HE. Phenylalanine was significantly increased in all areas of cortex of EcK fistula dogs and in occipital cortex of dogs with acute hepatic failure. Tyrosine was also significantly increased in frontal, parietal and occipital cortex of the EcK fistula dogs, and in temporal and occipital cortex of dogs with acute hepatic failure. However, amounts of reduction of CCK-LI level did not cbrrelate with those of increment of the aromatic amino acids in cortex of these HE models. Hte results imply that reduced levels of the excitatory neuropeptide CCK may be elicited by the mechanism distinct from that inducing increase of false neurotransmitters.