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1目的 探讨大鼠血浆唾液酸 (SA)水平变化的调节机制。 2方法 采用紫外分光光度法 ,测定乌拉坦麻醉、侧脑室注射多巴胺 (DA)及弓状核 (ARC)区注射谷氨酸钠 (Glu)等后大鼠血浆 SA水平的变化。3结果 乌拉坦麻醉组血浆 SA水平较对照组明显降低 (t=3.2 0 ,P<0 .0 5 ) ;侧脑室注射 DA后 ,血浆 SA水平较注射前明显降低 (F=3.2 9,q=4.2 6 ,P<0 .0 5 ) ,与同一时间对照组相比 ,亦明显降低 (t=2 .5 7,P<0 .0 5 ) ;ARC区注射胞体兴奋剂 Glu溶液 15 ,2 5 m in后 ,血浆 SA水平较注射前明显降低 (F=8.45 ,q=4.90 ,6 .31,P<0 .0 5 ) ,与同一时间对照组相比 ,亦明显降低 (t=2 .35 ,2 .41,P<0 .0 5 ) ,且此效应可被侧脑室注射 DA受体阻断剂 (螺哌啶酮 )阻断。 4结论血浆 SA水平变化受神经和体液因素调节 ,此调节机制与中枢神经递质 DA有关 ,且 ARC可能是此效应的主要调节中枢部位。
1 Objective To investigate the regulatory mechanism of plasma sialic acid (SA) level in rats. 2 Methods UV spectrophotometry was used to determine the changes of plasma SA levels after urethane anesthesia, intracerebroventricular injection of dopamine (DA) and arginine (Glu) in the arcuate nucleus (ARC). 3 Results Compared with the control group, plasma SA level in the urethane anesthesia group was significantly lower than that in the control group (t = 3.2 0, P <0.05). The level of plasma SA was significantly decreased after intracerebroventricular injection of DA (F = 3.2 9, q = 4.2 6, P <0.05), which was significantly lower than that of the control group at the same time point (t = 2.57, P <0.05) Plasma levels of SA were significantly lower than those before injection (F = 8.45, q = 4.90, 6.31, P <0.05) and were significantly lower than those of the control group at the same time point (t = 2.35 , 2.41, P <0.05), and this effect could be blocked by intracerebroventricular injection of DA receptor antagonist (spiperone). 4 Conclusions Changes in plasma SA level are regulated by neurological and humoral factors. The regulatory mechanism is related to central nervous transmitter DA, and ARC may be the main regulatory site of this effect.