The Wind Evil Quantitative Simulation Study And The Related Factors Of The Lung

Objective: This study combining experiment research and clinical research, throughanalyzing different levels of the wind and the effect of different stimulus time in micelungs and to the wind evil caused by lung disease in clinical observation, to explore thewind and the related factors and the degree of the department of pulmonary diseases, thequantitative relationship. At the same time, this topic of both the cold dampness evil, byanalyzing the cold evil, the origin of the wind effects, to cause to prevention and treatmentof respiratory diseases and research provide some guidance.Methods: Selection of experimental section64mice, blank group8, single factorphase32only; Stage24composite factors. Single factor phase into W1groups (2nd levelwind, that is, the average wind speed of3m/s,2h); W2group (4th level wind, that is, theaverage wind speed of7m/s,2h); The W3group (4th level wind, that is, the average windspeed of7m/s,1h); W4group (grade2wind, that is, the average wind speed of3m/s,1h)environment.Composite factors phase is divided into cold WT (average wind speed of3m/s, temperature0℃, humidity50%~55%,2h); Rheumatism WH (average wind speedof3m/s, humidity85%, temperature (20+2)℃,2h); WTH the wind cold dampnessgroup (average wind speed of3m/s, temperature0℃, humidity85%,2h); Groups arebased on4days after continuous stimulation. Then observe the airway pathologic change,ELISA method to detect lung tissue homogenate of TNF-α, IL-1β, the content of SOD,MDA, rt-pcr method to detect the mice HSP70mRNA expression level change. Select60patients with bronchial asthma clinical part, based on syndrome differentiation for the windmade20cases, lung cold make20cases, lung cold phlegm (wet) make lung20cases. Using SPSS18.0software for statistical processing experimental data.Results: Compared with the blank group, the experimental group indexes havechange, level4wind group of TNF-α、IL-1β、 SOD、 MDA content and HSP70mRNAexpression of the2nd level wind group increased; When the stimulus for2hours, W2group content of each index in lung tissue homogenate in mice increased in the W1group(P <0.01), and when the time is changed to1hour, W3and W4group mice TNF-α、IL-1β, the content of MDA, no significant difference (P>0.05), SOD activity was increased(P <0.05). Chill, rheumatism, wind cold dampness group of each index in lung tissuehomogenate in mice were increased in the blank group (P <0.01), and a cold wind colddampness group, rheumatism group significantly increased (P <0.01). For12months in ayear on average wind speed and wind evil committed type pulmonary bronchial asthmawere related analysis, the results showed that r=0.778, P=0.003, there was a significantstatistical significance; With the wind made the lungs do contrast type of pulmonaryfunction in patients with bronchial asthma, cold made the indexes of lung type increased (P<0.05); With cold than make a lung type, cold phlegm (wet) make the lungs all indexeswas increased (P <0.05); At the same time, cold phlegm (wet) evil committed the index awind chill of lung in patients with bronchial asthma (make type lung increasedsignificantly (P <0.01).Conclusion: The wind cause lung pathological changes and the increase of thecontent of cytokine levels and with the increase of the degree of the wind and stimulate thegrowth of the time, the more severe lung damage. When the wind make lung time is short,the wind have less effect on the lung injury degree of differences. The wind, the wind coldevil, wind cold dampness evil the damage to the lungs to some extent, and cold evil, colddampness evil to a certain extent, can obviously increase the wind damage to the body’slungs, cold origin most serious damage to the lungs.