Perevozchikov P N, Cheganov V F
Biull Eksp Biol Med. 1988 Oct;106(10):417-9.
Experimental vagus-bacterium pneumonia was modeled on 53 rabbits. Influence of nervous vagus on kallikrein-kinin system (KKS) was studied on 23 rats. It is obvious that disturbance of parasympathetic regulation may be an additional factor of KKS activation. Lowering of kinase II under experimental pneumonia was discovered both in the blood and in the lung. Activation of kinase II in the blood was after vagotomy. So parasympathetic regulation of kinase activity is of no significance in experimental pneumonia, and lowering of kinase activity is connected with bacterial factors.
对53只家兔建立了实验性迷走神经-细菌肺炎模型。在23只大鼠上研究了迷走神经对激肽释放酶-激肽系统(KKS)的影响。很明显,副交感神经调节紊乱可能是KKS激活的一个额外因素。在实验性肺炎中发现血液和肺中的激肽释放酶II均降低。迷走神经切断术后血液中的激肽释放酶II被激活。因此,在实验性肺炎中,副交感神经对激肽释放酶活性的调节无显著意义,激肽释放酶活性降低与细菌因素有关。