Diesel exhaust induced pulmonary and cardiovascular impairment: The role of hypertension intervention

被引:24
|
作者
Kodavanti, Urmila P. [1 ]
Thomas, Ronald F. [1 ]
Ledbetter, Allen D. [1 ]
Schladweiler, Mette C. [1 ]
Bass, Virginia [1 ]
Krantz, Q. Todd [1 ]
King, Charly [1 ]
Nyska, Abraham [2 ]
Richards, Judy E. [1 ]
Andrews, Debora [3 ]
Gilmour, M. Ian [1 ]
机构
[1] US EPA, EPHD, NHEERL, ORD, Res Triangle Pk, NC 27711 USA
[2] Tel Aviv Univ, IL-69978 Tel Aviv, Israel
[3] US EPA, Res Core Unit, NHEERL, ORD, Res Triangle Pk, NC 27711 USA
关键词
Air pollution; Diesel exhaust particles; Hydralazine; Hypertension; Cardiovascular; Aorta; Hypertensive rats; PARTICULATE MATTER; AIR-POLLUTION; NITRIC-OXIDE; OXIDATIVE STRESS; BLOOD-PRESSURE; INHALATION; RATS; RESPONSES; PARTICLE; HEALTHY;
D O I
10.1016/j.taap.2013.02.002
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Exposure to diesel exhaust (DE) and associated gases is linked to cardiovascular impairments; however, the susceptibility of hypertensive individuals is poorly understood. The objectives of this study were (1) to determine cardiopulmonary effects of gas-phase versus whole-DE and (2) to examine the contribution of systemic hypertension in pulmonary and cardiovascular effects. Male Wistar Kyoto (WKY) rats were treated with hydralazine to reduce blood pressure (BP) or L-NAME to increase BP. Spontaneously hypertensive (SH) rats were treated with hydralazine to reduce BP. Control and drug-pretreated rats were exposed to air, particle-filtered exhaust (gas), or whole DE (1500 mu g/m(3)), 4 h/day for 2 days or 5 days/week for 4 weeks. Acute and 4-week gas and DE exposures increased neutrophils and gamma-glutamyl transferase (gamma-GT) activity in lavage fluid of WKY and SH rats. DE (4 weeks) caused pulmonary albumin leakage and inflammation in SH rats. Two-day DE increased serum fatty acid binding protein-3 (FABP-3) in WKY. Marked increases occurred in aortic mRNA after 4-week DE in SH (eNOS, TF, tPA, TNF-alpha, MMP-2, RAGE, and HMGB-1). Hydralazine decreased BP in SH while L-NAME tended to increase BP in WKY; however, neither changed inflammation nor BALF gamma-GT. DE-induced and baseline BALF albumin leakage was reduced by hydralazine in SH rats and increased by L-NAME in WKY rats. Hydralazine pretreatment reversed DE-induced TF, tPA, TNF-alpha, and MMP-2 expression but not eNOS, RAGE, and HMGB-1. ET-1 was decreased by HYD. In conclusion, antihypertensive drug treatment reduces gas and DE-induced pulmonary protein leakage and expression of vascular atherogenic markers. Published by Elsevier Inc.
引用
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页码:232 / 240
页数:9
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