Ye Ting-mei, Xu Ce, Gao Qin, Zhou Xin-mei, Shan Qi-xian, Xia Qiang
Zhejianglishui University, Lishui 323000, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 May;23(2):194-8.
To observe the differences of hemodynamics and nitric oxide synthase(NOS) activity of ventricular cardiac muscle in two septic shock models and explore the possible mechanism.
Two rat models of septic shock[lipopolysaccharide(LPS)-induced and cecal ligation and puncture (CLP)-induced septic shock] were used. The hemodynamic parameters and nitric oxide synthase activity of ventricular cardiac muscle were measured.
The hemodynamic parameters in CLP-induced model were increased in the early stage and decreased in the late stage while in LPS-induced model the parameters showed the same change of the CLP late stage. Both LPS model and CLP model (late stage) showed significant increase in NOS activity, but there was no difference between the two models. After treatment of the NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME), the parameters of CLP-late stage and LPS model increased significantly. The NOS activity reached the highest level in the CLP-middle stage. The production of nitrite/nitrate decreased significantly in LPS model and CLP model(late stage) after treatment of L-NAME, but the nitrite/nitrate produced by constitutive NOS in LPS model was higher than CLP model(late stage).
The increase of the NOS activity may be the main reason to lead to the depression of the hemodynamic parameters. Inducible NOS may play the leading role in the LPS model while cNOS and iNOS have the same effect in the CLP model.
观察两种脓毒性休克模型中心室心肌血流动力学及一氧化氮合酶(NOS)活性的差异,并探讨其可能机制。
采用两种大鼠脓毒性休克模型[脂多糖(LPS)诱导和盲肠结扎穿刺(CLP)诱导的脓毒性休克]。测量心室心肌的血流动力学参数及一氧化氮合酶活性。
CLP诱导模型的血流动力学参数在早期升高,晚期降低,而LPS诱导模型的参数变化与CLP晚期相同。LPS模型和CLP模型(晚期)的NOS活性均显著升高,但两种模型之间无差异。用NOS抑制剂N-硝基-L-精氨酸甲酯(L-NAME)处理后,CLP晚期和LPS模型的参数显著升高。NOS活性在CLP中期达到最高水平。L-NAME处理后,LPS模型和CLP模型(晚期)中亚硝酸盐/硝酸盐的产生显著降低,但LPS模型中组成型NOS产生的亚硝酸盐/硝酸盐高于CLP模型(晚期)。
NOS活性增加可能是导致血流动力学参数降低的主要原因。诱导型NOS可能在LPS模型中起主导作用,而在CLP模型中,组成型NOS和诱导型NOS起相同作用。