气态甲醛染毒致小鼠气道神经源性炎症的神经受体机制

The Neuro-Receptor Mechanism of Gaseous Formaldehyde Induced Airway Neurogenic Inflammation in Mice

目的探讨不同处理组小鼠呼吸器官(气管、支气管、肺)中P物质substancePSP含量变化和气道神经源性的神经受体机制。方法用不同浓度的气态甲醛对小鼠进行灌流染毒,然后测量呼吸器官中P物质含量变化;预注射不同受体的拮抗剂的小鼠,再用不同浓度的气态甲醛进行灌流染毒,然后测量呼吸器官中P物质含量变化,进行对比分析。结果吸入2.42mg/m3甲醛的小鼠呼吸器官中P物质含量较空气灌流组显著上升(P<0.05),吸入4.81mg/m3甲醛的小鼠呼吸器官中P物质含量较空气灌流组极显著上升(P<0.01)。腹部皮下预注射N-甲基-D-天(门)冬氨酸(NMDA)受体拮抗剂0.2mol/LMgSO40.5ml,再空气灌流的小鼠呼吸器官中P物质的含量,与空气灌流组差异无显著性(P>0.05)。腹部皮下预注射0.2mol/LMgSO40.5ml,再用2.42mg/m3甲醛灌流的小鼠呼吸器官中P物质含量,较2.42mg/m3甲醛灌流组显著下降(P<0.01)。尾静脉预注射类香草素受体(VR1)特异性拮抗剂5×10-5mol/L的Capsazepine0.5ml,再用空气灌流的小鼠呼吸器官中P物质的含量,与空气灌流组差异无显著性(P>0.05)。尾静脉预注射5×10-5mol/LCapsazepine0.5ml,再经2.42mg/m3甲醛灌流的小鼠呼吸器官中P物质的含量较2.42mg/m3甲醛灌流组显著下降(P<0.01)。结论甲醛诱发的气道神经源性炎症的受体机制可能是通?

Objective To explore the contents of substance P (SP) in respiratory organs and the neuro-receptor mechanism of airway neurogenic inflammation induced by gaseous formaldehyde. Methods SP contents in respiratory organs of mice exposed to different concentrations of gaseous formaldehyde and SP contents in respiratory organs of mice pre-injected different receptor antagonist, then exposed to different concentrations of gaseous formaldehyde were determined by radioimmunoassay. Results SP content in respiratory organs of mice inhaled 2.42 mg/m3 formaldehyde (30.89±3.59) pg/0.3 ml was significantly higher than that of the fresh air inhalation group (24.34±3.18) pg/0.3 ml(P<0.05). SP content in respiratory organs of mice inhaled 4.81 mg/m3 formaldehyde (34.71±5.73) pg/0.3 ml was very significantly higher than that of the fresh air inhalation group (24.34±3.18) pg/0.3 ml(P<0.01). The SP content in respiratory organs of 2.42 mg/m3 formaldehyde exposed group with subcutaneous pre-injection of N-methyl-D-aspartate receptor (NMDA-receptor) antagonist MgSO4 0.2 mol/L 0.5 ml in abdominal side (16.51±5.80) pg/0.3 ml was significantly lower than the 2.42 mg/m3 formaldehyde exposed group without pre-injected NMDA-receptor antagonist MgSO4 (30.89±3.59) pg/0.3 ml (P<0.01). The SP concentration in respiratory organs of 2.42 mg/m3 formaldehyde exposed group with intravenous pre-injection of Vanilloid receptor type 1(VR1)antagonist Capsazepine 5×10-5 mol/L 0.5 ml in the tails of mice (16.51±5.80) pg/0.3 ml was significantly lower than the 2.42 mg/m3 formaldehyde exposed group without pre-injected VR1 antagonist Capsazepine (30.89±3.59) pg/0.3 ml (P<0.01). Conclusion It was suggested that the mechanism of airway neurogenic inflammation induced by gaseous formaldehyde might be that formaldehyde could active the NMDA-receptor or/and VR1 of sensory nerve fibre(C-fibre), which elicited axon reflex of nerve terminal and increased the release of tachykinin, thus airway neurogenic inflammation was brought out.