Abstract

Objective The present work was designed to investigate the potential role and mechanism of sulfur dioxide (SO2) in regulating Arterial baroreflex (ABR) in septic rats. Methods The rat model of cecal ligation and puncture (CLP) induced sepsis was established. Sixty six male Spargue-Dawley rats were randomly divided into 11 groups, involved three parts, with random table method. Part1: (1) Sham operation (SO)+ Saline+ intravenous injection (iv) group; (2) CLP+ Saline+ iv group; (3) SO+ SO2+ iv group; (4) CLP+ SO2+ iv group; Part2; (5) SO+ artificial cerebrospinal fluid (aCSF)+ nucleus tractus solitarii (NTS) group; (6) CLP+ aCSF+ NTS group; (7) SO+ SO2+ NTS group; (8) CLP+ SO2+ NTS group; Part3: (9) CLP+ kynurenic acid (KYN)+ NTS group; (10) SO+ aCSF+ SO2+ NTS group; (11) SO+ KYN+ SO2+ NTS group. The ABR value was measured 5 min and 30 min after treatment, which unit denoted by ms/mmHg. Statisticalanalysis of data using the statistical product and service solutions 24.0 software. Results In the same groups: The ABR value in CLP+ SO2+ iv group (5 min: 0.230±0.058, 30 min: 0.171±0.045 vs. baseline: 0.406±0.070, F=132.373, P<0.05) and CLP+ SO2+ NTS group (5 min: 0.180±0.049, 30 min: 0.259±0.089 vs. baseline: 0.413±0.097, F=84.101, P<0.05) were significantly decreased, but the CLP+ kynurenic acid (KYN)+ NTS group (5 min: 0.639±0.071, 30 min: 0.630±0.054 vs. baseline: 0.407±0.058, F=84.101, P<0.05) was Increased. Comparison between the two groups: SO+ KYN+ SO2+ NTS group was significantly higher than that in the SO+ aCSF+ SO2+ NTS group (5 min: 0.831±0.108 vs. 0.351±0.026, F=73.318, P<0.05; 30 min: (0.854±0.122 vs. 0.471±0.040, F=35.184, P<0.05). Conclusion Sulfur dioxide plays an adverse role in septic ABR value, and activating glutamate inotropic non-selective receptor at the pathway of ABR, may be the mechanism involved in the down-regulation of ABR function in septic rat. Key words: Sulfur dioxide; Sepsis; Arterial baroreflex

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