RESUMO
Substantial ultrafine zinc particles exist in air pollutions. The level of Zn concentrations in serum and tissue could affect patients with myocardial infarction (MI). The aim of the study is to investigate the change of cardiac functions and peripheral hemodynamics in MI rats after long-term inhalation of ultrafine Zn particles. Coronary artery ligation surgery was performed to induce MI in Wistar rats. The inhalation of ultrafine Zn particles was carried out for 6 weeks after the operation. Physiological and hemodynamic measurements and computational biomechanics analysis were demonstrated in eight groups of rats at postoperative 4 and 6 weeks. There was no statistical significance between shams and shams with inhalation of ultrafine Zn particles. There were significant impairments of cardiac and hemodynamic functions in MI rats. In comparison with MI rats, the inhalation of ultrafine Zn particles for 4 weeks slowed down the progression from MI to heart failure, but the inhalation for 6 weeks accelerated the process. The long-term inhalation of ultrafine zinc particles induced excessive accumulation of zinc in serum and tissue, which deteriorated cardiac and hemodynamic dysfunctions in MI rats. The findings suggested the importance for regulating Zn intake of MI patients as well as looking at ways to lower zinc concentrations in air pollutions.
RESUMO
It is not clear for inhalation of ultrafine metal particles in air pollution to impair human health. In the study, we aimed to investigate whether short-term (4 weeks) inhalation of ultrafine zinc particles could deteriorate the cardiac and hemodynamic functions in rats of myocardial infarction (MI). MI was induced in Wistar rats through coronary artery ligation surgery and given an inhalation of ultrafine zinc particles for 4 weeks (post-MI 4 weeks, 4 days per week, and 4 h per day). Cardiac strain and strain rate were quantified by the speckle tracking echocardiography. The pressure and flow wave were recorded in the carotid artery and analyzed by using the Womersley model. Myocardial infarction resulted in the LV wall thinning, LV cavity dilation, remarkable decrease of ejection fraction, dp/dt Max, -dp/dt Min, myocardial strain and strain rates, and increased LV end-diastolic pressure, as well as impaired hemodynamic environment. The short-term inhalation of ultrafine zinc particles significantly alleviated cardiac and hemodynamic dysfunctions, which could protect from the MI-induced myocardial and hemodynamic impairments albeit it is unknown for the long-term inhalation.
RESUMO
BACKGROUND: The traditional herbal compound Danggui Buxue decoction (DBD), has long been used for the prevention and treatment of cardiovascular diseases, however, the underlying molecular mechanism for its effect remains still unknown. So this study would to investigate the effect of DBD on cardiac damage induced by myocardial infarction (MI) challenge. METHODS: SD Rats with ligation of left anterior descending (LAD) coronary artery were randomly divided into MI, MI plus Betaloc Zok, MI plus DBD high dose, and MI plus DBD low dose group, together with sham-operated group. After corresponding treatment for consecutive 4 weeks, cardiac function was evaluated by hemodynamics with the method of pressure-volume conduit system. Cardiac histological morphology, microvascular density and the expressions of VEGF and VEGFR1/2 mRNA and their relative protein including VEGF, membranous VEGFR1 (VEGFR1), soluble VEGFR1 (sVEGFR1), VEGFR2, and sVEGFR2 were examined by hematoxylin & eosin staining, immunohistochemical staining and quantitative polymerase chain reaction and western blot assay, respectively. RESULTS: It showed that a significant impaired cardiac function and a remarkably inducible increase in fibrotic scar formation, microvascular density and VEGF mRNA expressions in MI rats. While DBD treatment could markedly boost cardiac angiogenesis further, hinder fibrotic scar formation, and improve declined cardiac function. Apart from the up-regulation of VEGF mRNA and VEGF and the down-regulation of sVEGFR1/2, high dose of DBD dedicated to increasing VEGFR1 mRNA and VEGFR1 expression, while low dose to elevating VEGFR2 mRNA and VEGFR2 expression. CONCLUSION: The present study demonstrated that DBD could accelerate cardiac angiogenesis, restrain fibrous scar formation and thus ameliorate cardiac function in post-MI, via the active regulation of VEGF/VEGFRs signaling pathway.