PM_2.5affect The Change Of Inflammation And Coagulation In The Cardiovascular System In Mice Sample

Objective：Cardiovascular disease is the main causes in the globalmorbidity and mortality,the traditional risk factors of cardiovascular diseasesuch as:smoking, fat, diabetes, metabolic syndrome, high blood pressure haveattracted wide public concern,and have many proteective measures.However,recently, more and more researches are committed to the association betweenenvironmental pollution and adverse cardiovascular disease,particularlyconcerned about the inhaled particles in air pollution.A lot ofepidemiological,experimental and toxic studies show that:air pollution isassociated with cardiovascular morbidity and mortality.The inhaled particlesin air pollution are closely linked to the events of acute and chroniccardiovascular disease.Under the long-term exposure to air pollution mainimpact the atherosclerosis formation and development,and in the short termacute exposure contribute to plaque instability,affect various traditional riskfactors and trigger acute cardiovascular events (myocardial ischemia andinfarction,stroke,heart failure,arrhythmias,and sudden death).But theassociation between the air pollution and cardiovascular diseases iscontentious,and the mechanism of cardiovascular disease that caused by airpollution is still unclear.A lot of epidemiological,experimental and toxicstudies show that particulate matters in air pollution are one of risk factors forcardiovascular morbidity and mortality,however,the mechanism is unclearnow.Particulate matters conclude large particles,smaller particles and fineparticles.Large particles (aerodynamic diameter>10μm) are mostly derivedfrom soil and crustal elements,smaller particles (aerodynamic diameter2.5-10μm),fine particles(aerodynamic diameter＜2.5μm) are primarilyproduced from the combustion of fossil fuels by motor vehicles and power generators,or from atmospheric chemistry.Only particles less than10μm indiameter can be inhaled deep into the lungs.National air quality standards havebeen based on the mass concentration of such 'inhalable'particles,which aretypically defined as having an aerodynamic diameter below10μm (PM10),2.5μm (PM2.5) or0.1μm (nanoparticles).The main arbiter of these adverse health effects seems to becombustion-derived nanoparticles that incorporate reactive organic andtransition metal components.Inhalation of this particulate matter leads topulmonary inflammation with secondary systemic effects or,after translocationfrom the lung into the circulation,to direct toxic cardiovascular effects.Through the induction of cellular oxidative stress and proinflammatorypathways,particulate matter augments the development and progression ofatherosclerosis via detrimental effects on platelets,vascular tissue,and themyocardium.These effects seem to underpin the atherothromboticconsequences of acute and chronic exposure to air pollution.An increasedunderstanding of the mediators and mechanisms of these processes isnecessary if we are to develop strategies to protect individuals at risk andreduce the effect of air pollution on cardiovascular disease.In this article we observe the change of inflammation and coagulationafter intratracheal instillation different dose PM2.5.In ordered to test thepossible mechanism of particles in air pollution in cardiovascular disease,andprobed into particles in air pollution harm the one which had cardiovascularrisk factor easy than the healthy one;and probed into the affect at differentconcentration particles in the cardiovascular system.Methods：In the study,15male Wistar rats weighed180-250g and15highfat male Wistar rats,and each group were randomly divided into threegroups,including one saline control group and two PM2.5exposed groups,PM2.5was administered to the exposed groups by intratracheal instillation at thedoses of15,30mg/kg,respectively.The rats were sacrificed24hour afterexposure.Anesthetized with an intraperitoneal injection of chloral hydrate10%,bloodletting from femoral and collected the blood,centrifugal,collect the blood and centrifuge it,drew out the supernatant fluid,and detected the levelsof CRP,IL-6,PAI-1in the serum,the contents of blood cellls were measured.Results：The levels of CRP,IL-6,WBC,PLT increased markedly in thePM2.5exposed groups compare to the saline control group,P＜0.05hadstatistical significance.And the high concentration group significantlyincreased than the low concentration group,P＜0.05had statisticalsignificance.Also the high fat group significantly increased than the normalgroup,P＜0.05had statistical significance.But the level of PAI-1did notchange in the normal group,P＞0.05had not statisticalsignificance;however,in the high fat group,the level of PAI-1increasedmarkedly in the high concentration group compare to the low concentrationgroup,P＜0.05had statistical significance.Conclusion：The study showed that PM2.5can cause acute inflammatoryreaction,and the higher concentration of PM2.5,the more harm in eachgroup.The rats which have cardiovascular risk factor are more easily affectedthan the common rats.And cause the changes of coagulation in the high fatgroup,but in the normal group did not have changes of coagulation.