| Gaseous air pollutants and particulate matter can cause adverse health effects, but it is more obvious that the health effects are caused by particulate matter. The chemical composition that is contained in particulate matter is up to hundreds. Particulate matter carrying of many pollutants has the impact on air quality, and it is being more and more attention. The toxic effects of particulate matter depend on its particle size and the containing chemical content. The particle diameter determines the residence time in the air, sedimentation rate, the possibility of entering the respiratory tract and deposition in the respiratory tract. The small size of the particulate matter is longer suspension in the air and easy for retention of the terminal bronchioles and alveoli, while some of the smaller components can penetrate the alveoli into the blood. The smaller particulate matter size is, the larger surface area is. The fine particulate matter is more easily absorbed toxic organic compounds and metal elements than the coarse particulate matter, which is a greater threat to public health. In2005the WHO positioned guidance of daily mean value of the fine particulate matter as the value of25μg/m3, and the EPA revised to35μg/m3from daily mean value of65μg/m3in2007.The pollution of PM2.5in China is very serious. A large number of epidemiological studies and animal experiments have shown that acute and chronic exposure of particulate matter is positively associated with the occurrence of cardiovascular events, especially in the elderly, diabetics and people with pre-existing cardiovascular disease.The major mechanism of the cardiovascular toxicity of fine particulate matter is not very clear. Some of mechanisms has been proposed, which is generally believed that oxidative stress caused by reactive oxygen species, blood components and changes in rheology caused by inflammatory response, vascular function changes and cardiac autonomic nerve regulatory function change. The definite of the pathogenic pathophysiology principle can propose more effective measures to protect vulnerable populations, and to provide a scientific basis to better protect the health of the population.This subject collected fine particulate matter in the Shanghai urban area. The first part was designed to examine the changes in blood pressure, heart rate and heart rate variability of the fine particulate matter in the atmosphere by intratracheal injection into the spontaneously hypertensive rats; the second part measured changes of blood coagulation and fibrinolysis using the same acute exposure.The first part designed exposure by intratracheal injection into the spontaneously hypertensive rats. Twenty-four male hypertensive rats were randomly divided into four groups:saline control group, low, medium and high dose group (exposure doses were1.6mg/kg body weight,4.0mg/kg body weight,40.0mg/kg body weight respectively).Once exposure daily, continuous exposure for three days.24hours after the last exposure, the rats were anesthetized to monitor and record of blood pressure, heart rate and ECG changes. Blood pressure, resting heart rate and heart rate variability is regulated by the sympathetic and parasympathetic nerve. Increase of blood pressure and heart rate is risk factor for acute cardiovascular event. Heart rate variability contains a wealth of information on cardiovascular regulation. The detection and analysis of such information can be quantitative assessment of cardiac sympathetic and parasympathetic activities tension, balance and its impact on cardiovascular activities. The result is that low, medium and high dose group of rats has higher blood pressure and increased heart rate relative to the saline control group rats, and there is a certain dose-response relationship. Relative to the saline control group, the heart rate variability of high-dose group decreased. The conclusion is that exposure of fine particulate matter changes cardiac autonomic nervous system function of the SH rat.The second part is the same to the first part of the exposure treatment, abdominal aortic blood is determined for measurement of plasma endothelin-1(ET-1), P-selectin and D-dimer. The test results showed that endothelin-1of low, medium and high dose groups have a significant increase than those in the control group, while P-selectin and D-dimer of medium and high dose groups have a significant increase, and there is a dose-response relationship. Endothelin-1is an important factor in regulating cardiovascular function, a strong the vasoconstrictor biological activity and stimulation of endothelial cells releasing of t-PA. Endothelial cells can been stimulated to synthesize and release of ET-1, which is mainly regulated at the transcriptional level. The increase of plasma ET-1is seen in the pro-thrombotic state, types of angina pectoris, myocardial infarction, and exacerbation of DIC protophase significantly higher. The results suggest that exposure of PM2.5may affect vasoconstriction and blood clotting function. P-selectin, also known as activated to platelet dependent on the particle outer membrane molecules, granule membrane protein, is a typical adhesion molecules involved in inflammation-mediated neutrophil, lymphocyte rolling on platelets or activated endothelial cells, participating in the coagulation, thrombosis and inflammation. The results suggest that the exposure of PM2.5causes inflammation and blood clotting effect. D-dimer is a fibrin monomer after cross linking via activation of factor XIII, and then hydrolysis by plasmin generated by a specific degradation product is a specific marker of the fibrinolytic process. D-dimer from a cross linked fibrin clot is dissolved by plasmin. The result of this study is that the exposure of PM2.5can cause an increase of D-dimer, suggesting that the presence of secondary fibrinolysis, and thrombosis. In summary the exposure of PM2.5can cause endothelial dysfunction, platelet activation in the SH rats, which led to the imbalance of coagulation and fibrinolysis. |
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