The Effect of Particulate Matter on Resistance and Conductance Vessels in the Rat

Abstract

Epidemiological and clinical studies suggest that air pollution, in particular ambient particulate matter (PM), increases mortality in patients with cardiovascular disease (CVD). Several in vivo studies have shown an increase of blood pressure by PM, but so far the mechanism or responsible particle-component has not been elucidated. We exposed small mesenteric rat artery (SMRA) and rat aorta to ambient particles (EHC-93) to test the ability of ambient particles to modify the vascular tone of different vessel types. PM suspensions (10-100 microg/ml) and filtrates containing only the water-soluble components failed to modify the resting tension of either the aorta or SMRA. However, PM did elicit a dose-dependent vasorelaxation in phenylephrine precontracted SMRA and aorta. The effect of the PM suspensions was higher than that of PM filtrate (without particles). The relaxation was already visible at 10 microg/ml, and the difference with filtrate became significant at 100 microg/ml for aorta (maximal relaxation E(max) = 18% vs. 12% PM filtrate) and as low as 30 microg/ml for SMRA (E(max) = 13% vs. 5% PM filtrate). Although the effect of PM was biggest in aorta, the concentration to cause half of the maximal effect (EC(50)) of suspension and filtrate was the same in both capacity (aorta) and resistance vessels (SMRA). The main difference seen between SMRA and aorta was that PM did not modify the phenylephrine-induced dose-response vasoconstriction in SMRA, while it did do so in the aorta. In conclusion, the in vitro exposure of precontracted blood vessels to ambient PM results in an acute vasorelaxation, which is in contrast to the observation that PM can cause increased blood pressure. Dose calculations show that the elevation of blood pressure observed in vivo is not likely due to direct effects of particles or constituents. We therefore suggest that the in vivo effect of PM on vasoconstriction acts through other pathways, such as the central nervous system.

Ambient Particulate Matter Affects Cardiac Recovery in a Langendorff Ischemia Model

“…A disturbance of vascular function elicited by PM has been reported by our group (Bagate et al, 2004a(Bagate et al, , 2004bKnaapen et al, 2001) as well as others (Batalha et al, 2002;Brook et al, 2002;Mills et al, 2005;Nurkiewicz et al, 2006). This suggests that if sufficient particles or their soluble constituents are translocated upon inhalation and reach the blood they are capable of inducing direct effects on the cardiovascular system.…”

“…The role of soluble metals in cardiovascular effects of PM has been indicated by several studies (Kodavanti et al, 2002a(Kodavanti et al, , 2002b(Kodavanti et al, , 2003Bagate et al, 2004aBagate et al, , 2004b. However, the mechanism by which PM and its soluble components elicit a disturbance of cardiac function is not well understood.…”

“…To test whether the effects of in vivo pretreatment on cardiac function were due to a direct effect of soluble components on the heart muscle, as noted previously for aorta (Bagate et al, 2004a(Bagate et al, , 2004b, we studied Ca uptake in isolated cardiomyocytes. Isolated cardiomyocytes were loaded with fura-2, and uptake of Ca was studied after stimulation with KCl (receptor independent) or with ATP (receptor dependent).…”

Die EU-Feinstaub-Richtlinie und das Herz: Wo stehen wir heute in Europa?

“…Pathophysiologisch konnte eine Assoziation der Aktivierung des lokalen Renin-Angiotensin-Systems via den Angiotensin-Typ-1-Rezeptor und der durch Feinstaub induzierten kardiovaskulären Effekte gezeigt werden [39]. Im Gegensatz zu den beschriebenen Beobachtungen wurde im Modell sowohl für Leitungs-als auch Widerstandsgefäße eine Gefäßdilatation gezeigt, welche die Vermutung einer indirekten Modulation des Blutdrucks durch Partikel wie beispielsweise einer Beeinträchtigung neuronaler Regelkreise nahelegen [40]. Die potentiellen biologischen Mechanismen der beobachteten Vasokonstriktion über einen reflektorischen Anstieg der Aktivität des sympathischen Nervensystems via die Stimulation pulmonaler vagaler Afferenzen [41] sowie der akute Anstieg der vaskulären Endothelinfreisetzung wurden analog für den Zigarettenrauch diskutiert.…”

Possible Role of Nrf2 in Oxidative and Inflammatory Processes During Menopause

“…The solid matter alters lung, cardiovascular, nervous system functions, resulting in vascular inflammation, vascular dysfunction, and increased oxidative stress [38][39][40][41]. Nrf2 participates in resistance to hyperoxia-induced lung injury, it is also important in the response of epithelial cells particle exposure.…”