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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >Exacerbation of thrombotic events by diesel exhaust particle in mouse model of hypertension.
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Exacerbation of thrombotic events by diesel exhaust particle in mouse model of hypertension.

机译：在高血压小鼠模型中，柴油机排气颗粒加剧了血栓形成事件。

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Several epidemiological studies have shown that acute exposure to particulate air pollution is associated with increases in cardiovascular morbidity and mortality, and that these effects are especially exacerbated among individuals with pre-existing compromised cardiovascular function such as hypertension. This study was undertaken to determine the cardiovascular effect of diesel exhaust on TO mice made hypertensive by implanting osmotic minipump infusing angiotensin II or vehicle (control). On day 13, the animals were intratracheally instilled with either DEP (15 mug/mouse) or saline. 24 h later, pulmonary exposure to DEP had significantly decreased the systolic blood pressure (SBP) in hypertensive (HT) mice (P<0.01), but not in normotensive (NT) mice. The number of leukocytes and red blood cells, and the plasma interleukin 6 concentration in plasma, however, were not affected in any of the animals. The PaO was decreased, and PaCO increased in DEP-treated HT mice compared to NT mice treated with DEP (P<0.05). The number of circulating platelets was significantly increased in DEP-treated HT versus saline-treated HT and DEP-treated NT mice. Moreover, in NT mice, DEP exposure induced a prothrombotic effect in pial arterioles compared with saline-treated NT mice (P<0.05). Interestingly, in DEP-treated HT mice, the prothrombotic events were significantly aggravated compared with saline-treated HT and DEP-treated NT mice. The direct addition of DEP (0.1-1 mug/ml) to untreated mouse blood significantly induced in vitro platelet aggregation in a dose-dependent fashion, and these effects were more pronounced in blood of HT mice. In vitro exposure to DEP (0.25-1 mug/ml) led to activated intravascular coagulation, an effect that was confirmed by a shortening of both the activated partial thromboplastin time (aPTT) and the prothrombin time (PT). The effect of DEP on aPTT was potentiated in the plasma of HT mice. It can be concluded that the thrombotic events caused by DEP are exacerbated by hypertension in mice. Our findings, therefore, provide a possible plausible explanation for the cardiovascular morbidity and mortality accompanying urban air pollution.
机译：几项流行病学研究表明，急性暴露于颗粒空气污染与心血管疾病的发病率和死亡率的增加有关，尤其是在那些已经患有心血管功能受损（例如高血压）的个体中，这些影响尤其恶化。进行这项研究是为了确定柴油机废气对通过植入渗透性微型泵并注入血管紧张素II或媒介物（对照）而致高血压的TO小鼠的心血管作用。在第13天，向动物气管内滴入DEP（15杯/小鼠）或生理盐水。 24小时后，肺部暴露于DEP可使高血压（HT）小鼠的收缩压（SBP）显着降低（P <0.01），而非血压正常（NT）的小鼠。然而，在任何动物中，白细胞和红细胞的数量以及血浆中血浆白介素6的浓度均未受到影响。与经DEP处理的NT小鼠相比，经DEP处理的HT小鼠的PaO降低，而PaCO升高（P <0.05）。与盐水处理的HT和DEP处理的NT小鼠相比，DEP处理的HT的循环血小板数量显着增加。此外，与盐水处理的NT小鼠相比，在NT小鼠中，DEP暴露诱导了其小动脉的血栓形成前作用（P <0.05）。有趣的是，在DEP治疗的HT小鼠中，与盐水治疗的HT和DEP治疗的NT小鼠相比，血栓前事件明显加重。向未经处理的小鼠血液中直接添加DEP（0.1-1 mug / ml）可以剂量依赖性方式显着诱导体外血小板聚集，并且这些作用在HT小鼠的血液中更为明显。体外暴露于DEP（0.25-1 mug / ml）会导致激活的血管内凝血，这种作用已通过激活的部分凝血活酶时间（aPTT）和凝血酶原时间（PT）缩短而得到证实。 DEP对aPTT的作用在HT小鼠血浆中得到增强。可以得出结论，DEP引起的血栓形成事件会因小鼠高血压而加剧。因此，我们的发现为伴随城市空气污染的心血管疾病的发病率和死亡率提供了可能的合理解释。

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