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探讨在内毒素血症和内毒素休克时肿瘤坏死因子（ＴＮＦ）影响血流动力学的效应是否与降钙素基因相关肽（ＣＧＲＰ）的释放和作用有关。将５６只ＳＤ大白鼠随机分成４组，每组１４只。各组分别经中心静脉注射生理盐水（对照组）、内毒素（实验１组），重组ＴＮＦ（实验２组）和抗ＴＮＦ单抗（ＣＢ０００６）＋内毒素（实验３组）。１小时后测定各组动物的血浆ＣＧＲＰ含量，并测量血流动力学指标。结果：与对照组相比较，各实验组动物的血浆ＣＧＲＰ含量分别增加约７．１倍、６．７倍和５．５倍（Ｐ值均＜０．０１），与此同时各实验组动物平均动脉压（ＭＡＰ）分别显著降低４０．０％、３０．８％和２５．９％，心输出量（ＣＯ）亦分别减少约２０．０％、２８．３％和１５．１％（Ｐ值均＜０．０１）。与对照组动物的总末梢血管阻力（ＴＰＲ）相比，实验１组和３组的动物分别显著降低约２５．９％和１６．３％（Ｐ值均＜０．０１）。结论：内毒素血症时ＣＧＲＰ在ＴＮＦ所致血流动力学改变过程中具有一定的作用
To investigate whether the effect of tumor necrosis factor (TNF) on hemodynamics in endotoxemia and endotoxic shock is related to the release and action of calcitonin gene-related peptide (CGRP). 56 SD rats were randomly divided into 4 groups of 14 rats each. Each group received normal saline (control), endotoxin (experiment 1), recombinant TNF (experiment 2), and anti-TNF monoclonal antibody (CB0006) + endotoxin (experiment 3). One hour later, plasma CGRP levels were measured in each group and hemodynamic parameters were measured. RESULTS: Compared with the control group, the plasma CGRP levels in the experimental groups increased by approximately 7.1-fold, 6.7-fold and 5.5-fold, respectively (all P<0.01). Mean arterial pressure (MAP) decreased significantly by 40.0%, 30.8%, and 25.9%, respectively, and cardiac output (CO) also decreased by approximately 20.0%, 28.3%, and 15.1%, respectively. Values <0.01). Compared with the total peripheral vascular resistance (TPR) of the control animals, the animals of the experimental group 1 and 3 groups were significantly reduced by approximately 25.9% and 16.3%, respectively (P<0.01 for each). Conclusion: CGRP has a certain role in the hemodynamic changes induced by TNF in endotoxemia