{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T02:51:46Z","timestamp":1761706306080},"reference-count":45,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Part Fibre Toxicol"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Strong associations have been observed between exposure to fine ambient particulate matter (PM<jats:sub>2.5<\/jats:sub>) and adverse cardiovascular outcomes. In particular, exposure to traffic related PM<jats:sub>2.5<\/jats:sub> has been associated with increases in left ventricular hypertrophy, a strong risk factor for cardiovascular mortality. As much of traffic related PM<jats:sub>2.5<\/jats:sub> is derived from diesel exhaust (DE), we investigated the effects of chronic DE exposure on cardiac hypertrophy and heart failure in the adult mouse by exposing mice to DE combined with either of two mouse models of cardiac hypertrophy: angiotensin II infusion or pressure overload induced by transverse aortic banding.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Wild type male C57BL\/6\u00a0J mice were either infused with angiotensin II (800\u00a0ng\/kg\/min) via osmotic minipump implanted subcutaneously for 1\u00a0month, or underwent transverse aortic banding (27 gauge needle 1\u00a0week for observing acute reactions, 26 gauge needle 3\u00a0months or 6\u00a0months for observing chronic reactions). Vehicle (saline) infusion or sham surgery was used as a control. Shortly after surgery, mice were transferred to our exposure facility and randomly assigned to either diesel exhaust (300 or 400\u00a0\u03bcg\/m<jats:sup>3<\/jats:sup>) or filtered air exposures. After reaching the end of designated time points, echocardiography was performed to measure heart structure and function. Gravimetric analysis was used to measure the ventricular weight to body weight ratio. We also measured heart rate by telemetry using implanted ambulatory ECG monitors.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Both angiotensin II and transverse aortic banding promoted cardiac hypertrophy compared to vehicle or sham controls. Transverse aortic banding for six months also promoted heart failure in addition to cardiac hypertrophy. In all cases, DE failed to exacerbate the development of hypertrophy or heart failure when compared to filtered air controls. Prolonged DE exposure also led to a decrease in average heart rate.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Up to 6-months of DE exposure had no effect on cardiac hypertrophy and heart function induced by angiotensin II stimulation or pressure overload in adult C57BL\/6\u00a0J mice. This study highlights the potential importance of particle constituents of ambient PM<jats:sub>2.5<\/jats:sub> to elicit cardiotoxic effects. Further investigations on particle constituents and cardiotoxicity are warranted.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1743-8977-10-49","type":"journal-article","created":{"date-parts":[[2013,10,5]],"date-time":"2013-10-05T19:00:49Z","timestamp":1380999649000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Inhalation of diesel exhaust does not exacerbate cardiac hypertrophy or heart failure in two mouse models of cardiac hypertrophy"],"prefix":"10.1186","volume":"10","author":[{"given":"Yonggang","family":"Liu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei-Ming","family":"Chien","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ivan O","family":"Medvedev","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chad S","family":"Weldy","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel L","family":"Luchtel","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael E","family":"Rosenfeld","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael T","family":"Chin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2013,10,5]]},"reference":[{"issue":"8","key":"273_CR1","doi-asserted-by":"publisher","first-page":"933","DOI":"10.1161\/01.CIR.0000027561.41736.3C","volume":"106","author":"J Pekkanen","year":"2002","unstructured":"Pekkanen J, Peters A, Hoek G, Tiittanen P, Brunekreef B, de Hartog J, Heinrich J, Ibald-Mulli A, Kreyling WG, Lanki T, Timonen KL, Vanninen E: Particulate air pollution and risk of ST-segment depression during repeated submaximal exercise tests among subjects with coronary heart disease: the exposure and risk assessment for fine and ultrafine particles in ambient air (ULTRA) study. 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