WEN-YU YANG*,**, JIN ZHANG*,#, BING-JUN ZHANG*
*Department of Anesthesiology, Affiliated Shengjing Hospital, China Medical University, Shenyang 110004, China - **Department of Anesthesiology, Sanbo Brain Hospital Capital Medical University, Beijing 100080, China
Introduction: To observe the effect of the serotonin 2A (5-HT2A) receptor antagonist ketanserin on hemodynamics in rats with endotoxic shock, in order to provide reference for the treatment of endotoxic shock.
Materials and methods: Thirty Sprague Dawley (SD) rats were randomly divided into three groups: group N, rats received normal saline + 5-HT2A receptor antagonist; group L, lipopolysaccharide (LPS) control group; group K, rats received LPS+5-HT2A receptor antagonist. The body pressure and pulmonary circulation pressure of rats in each group were monitored for six hours. The serum TNF-???? and IL-1???? levels in each group were detected using ELISA at the beginning of the experiment, and at 15 minutes, two hours and six hours after the injection of saline or LPS. Lung tissue hematoxylin and eosin (H&E) staining were observed under a light microscope to value the degree of inflammatory lesions in group K and in group L.
Results: In group L, rats presented with decreased femoral artery pressure and increased pulmonary artery pressure after receiving LPS. In group K, the femoral artery pressure of rats returned to normal levels at one hour after receiving LPS. At six hours after receiving LPS, the blood pressure was completely restored. Pulmonary artery pressure did not significantly increase at 15 minutes after receiving LPS. Thereafter up to six hours after LPS was given, pulmonary artery pressure decreased and then maintained at 28 mmHg. Furthermore, TNF-???? and IL-1???? levels were significantly lower in group K than in group L. Moreover, lung tissue H&E staining results revealed that the degree of inflammatory lesions in lung tissues was significantly lower in group K than in group L.
Conclusion: Ketanserin can improve the hemodynamic disorder caused by endotoxin, playing an anti-shock role.
endotoxic shock, pulmonary hypertension, 5-HT; Ketanserin, endothelium, glycocalyx.
10.19193/0393-6384_2019_5_451