| With the continuous development of human society and economy,people are paying more and more attention to their own health problems and quality of life.However,air pollution caused by climate change and industrial development poses a serious threat to human health,especially the fine particles in the air.The harm is particularly obvious.Relevant studies in recent years have shown that the health hazards of PM2.5 are not only related to its chemical composition,but also closely related to the particle surface size,number,and diameter.For example,it is easier to gather viruses in the air on particles with larger surfaces.,Toxic heavy metals,acid-base oxides and organic pollutants.PM2.5 will cause the occurrence and progress of many clinical diseases.Global burden of disease research shows that the number of deaths caused by PM2.5 worldwide is as high as 3.15 million.In particular,it has the greatest impact on the body’s heart and lungs.In recent years,the impact of PM2.5 on the cardiovascular system has been paid more and more attention.Due to the small diameter of PM2.5,it can be directly inhaled into the alveoli through the trachea and bronchi of the body,and then enters the circulatory system of the body through the blood-blood barrier.Some experts have also proposed that PM2.5 enters the body’s respiratory system and induces engulfment of macrophages,And then fall in the blood vessels,causing the immune response of the vascular endothelium,which in turn triggers the immune response of the vascular endothelium,leading to cardiovascular diseases.This study is divided into two parts.The first part is the clinical part to observe the effects of PM2.5 exposure on heart rate variability and cardiac ultrasound indicators in outpatient and hospitalized patients with chronic cardiac insufficiency in Shijiazhuang area.The second part is the animal experiment.The PM2.5 multifunctional aerosol concentrated enrichment system was used to expose PM2.5 to PM2.5 particles to observe the pathological changes of PM2.5 and control groups.Meanwhile,immunohistochemistry and Western-blot tested CRP and ICAM-1 in both groups to prove the involvement of CRP and ICAM-1 in PM2.5.PartⅠ Effect of fine particulate matter on cardiac indexes in patients with chronic heart failureObjective: To observe the effects of fine particulate matter on echocardiography and heart rate variability in patients with chronic cardiac insufficiency.Methods: Prospective analysis of 104 patients with chronic cardiac insufficiency in outpatient or inpatient treatment in our hospital,patient grouping: According to my country’s "Ambient Air Quality Index(AQI)Technical Regulations" and "Ambient Air Quality Standards",where0<AQI≤50 The AQI category is excellent,and the grade is grade 1;when50<AQI≤100,the AQI category is good,and the grade is grade 2;when100<AQI≤150,the AQI category is mildly polluted,and the grade is grade 3;when 150<AQI≤200,the AQI category is grade 3.The category is moderately polluted,and the level is four;when 200<AQI≤300,the AQI category is heavily polluted,and the level is five;when >300,the AQI category is severely polluted,and the level is six.The meteorological data are all from Shijiazhuang City Air Quality Release System.The monitoring contents include CO,daily average temperature,NO2,daily average relative humidity,03,SO2 and PM2.5.The obtained PM2.5 concentration data were converted into ambient air quality index,and the patients were divided into two groups according to the actual PM2.5 concentration status,the low concentration group(60 cases,0<AQI≤100)and the high concentration group(44 cases).For example,AQI>100).The clinical data,including gender,age,complications,NYHA classification of cardiac function,heart rate,blood pressure,daily outdoor activity time,etc.,were recorded;the cardiac ultrasound indexes,including left ventricular short axis shortening rate(FS),LVEF and ventricular septal thickness,were recorded.HRV parameters were recorded: frequency domain index: high frequency power(HF),low frequency power(LF),ultra-low frequency power(VLF),low frequency power / high frequency power(LF/HF);time domain index: root mean square difference of normal continuous sinus RR interval(RMSSD),standard deviation of normal cardiac cycle(SDNN).The levels of oxidative stress factors including malondialdehyde(MDA),glutathione peroxidase(GSH-Px),succinate dehydrogenase(SDH)and catalase(CAT)were recorded.Results: There was no significant difference in the mean age,gender,daily outdoor activity time,obesity ratio,smoking history,diabetes history,hypertension history,dyslipidemia history,cardiac function classification and diastolic blood pressure between the low concentration group and the high concentration group before treatment(P>0.05);the systolic blood pressure of the low-concentration group and the high-concentration group were(134.52±11.86)mm Hg and(145.20±12.67)mm Hg,and the average heart rate was(74.10±2.75)beats/min and(78.65±2.50)beats,respectively /min,the difference was statistically significant(P<0.05).The FS of the lowconcentration group and the high-concentration group were(26.86±3.15)%and(27.33±3.10)%,respectively.The thickness of the interventricular septum was(12.29±2.20)mm and(11.95±2.83)mm,respectively.There was no statistically significant difference in the comparison(P>0.05);The LVEF of the low-concentration group and the high-concentration group were(41.65±3.40)% and(37.10±3.82)%,respectively.There is statistical significance(P<0.05).The frequency domain indexes HF,LF,VLF,LF/HF of the low-concentration group were higher than those of the high-concentration group,and the time domain indexes RMSSD and SDNN were higher than those of the high-concentration group.The difference was statistically significant(P<0.05).Summary:1.PM2.5 exposure can increase the systolic blood pressure and average24 h heart rate in patients with chronic heart function;2.PM2.5 exposure decreases the ejection fraction in patients with chronic cardiac function;3.PM2.5 exposure can reduce the heart rate variability of patients with chronic heart function.PartⅡ Study on the mechanism of fine particles on the damage of rat cardiomyocyteObjective: Use the PM2.5 multifunctional aerosol enrichment system to perform online oral and nasal exposure of PM2.5 to rats.Compared with the instillation of PM2.5 particles into the trachea,it is more in line with natural exposure.Observe the PM2.5 exposure group and control The similarities and differences of the pathological changes of the two groups were also used immunohistochemistry and Western-blot to detect the expression of CRP and ICAM-1 in the two groups to prove that the inflammatory response of the myocardial tissue damage in the rats exposed to PM2.5 includes CRP and ICAM-1 participation.Methods: After 2 weeks of adaptive feeding,30 rats were randomly divided into two groups,control group and experimental group,with 15 rats in each group.The 15 rats in the control group breathed the air in the air purification system,5 times a week,4 hours each time,for a total of 3 months.Fifteen rats in the experimental group were exposed to the PM2.5 online enrichment system device for 4 hours a day and 5 days a week for 3consecutive months.Unless there is heavy rain or sandstorm,it will affect the concentration effect.The PM2.5 enrichment system can enrich the concentration of PM2.5 in the environment,which is about 10 times the actual environmental concentration.The pathological conditions of rat myocardial tissue and electron microscope were observed,the expressions of IL-6,TNF-α,ICAM1 and CRP in rat myocardial tissue were detected by ELISA,the levels of MDA in serum and myocardial tissue were detected by TBA method,and the WST-1 method was detected.Serum and myocardial tissue SOD,GSH-PX levels,immunohistochemical detection of CRP,ICAM-1 expression in rat myocardial tissue,Western-blot method to detect CRP,ICAM-1 protein expression in myocardial tissue.Results: There was no abnormality in the myocardial tissue of the rats in the control group,no inflammatory cell infiltration,and no tissue edema.There was no abnormality in the myocardial tissue structure of the rats in the control group,while the myocardial tissue of the rats in the experimental group had pyknosis,fusion of mitochondrial membranes and ridges,expansion of the rough endoplasmic reticulum,degranulation,and cell swelling.The level of IL-6 in the experimental group was(94.85±26.51)pg/ml,and the control The level of IL-6 in the experimental group was(89.57±8.52)pg/ml,and the difference was not statistically significant(P>0.05).The level of TNF-α in the myocardial tissue of rats in the experimental group was(29.05±3.40)pg/ml,and the control The level of TNF-α in the experimental group was(27.35±2.52)pg/ml,and the difference was not statistically significant(P>0.05);The level of ICAM-1 in the myocardial tissue of the experimental group was(5611.72±3513.20)ng/ml.The ICAM-1 level in the group was(2698.08±872.81)ng/ml,and the difference was statistically significant(P<0.05);the CRP level in the experimental group was(0.087±0.02)ng/ml,and the CRP level in the control group was(0.067±0.05)ng/ml,and the difference was statistically significant(P<0.05);The serum SOD level of the rats in the experimental group was(16.03±0.51)U/mg Pro,and the SOD level of the control group was(17.00±0.16)U/mg Pro,and the difference was not statistically significant(P>0.05).The serum MDA level was(5.78±1.27)nmol/mg Pro,and the MDA level of the control group was(6.70±1.93)nmol/mg Pro,and the difference was not statistically significant(P>0.05);the serum GSH-PX of the experimental group rats The level of GSH-PX in the control group was(2602.00±563.76)vitality units,and the GSH-PX level in the control group was(2376.86±1140.68)vitality units,and the difference was not statistically significant(P>0.05);the myocardial tissue of the observation group was positive for CRP and ICAM-1 The proportions of cells were(42.28±6.05)% and(32.45±6.03)%,respectively,which were higher than those of the control group(15.86±3.72)% and(11.28±2.10)%,and the difference was statistically significant(P<0.05).Summary:1.The expression of inflammatory factors in the myocardial tissue of PM2.5-exposed rats was significantly increased;2.There was no significant difference in oxidative stress between serum and myocardial tissue of PM2.5-exposed rats;3.The expression of ICAM-1 and CRP in myocardial tissue of rats induced by PM2.5 exposure may increase It is one of the mechanisms that induce cardiovascular toxicity. |