Long-Term Inhalation of Ultrafine Zinc Particles Deteriorated Cardiac and Cardiovascular Functions in Rats of Myocardial Infarction

Abstract

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.

Keywords: Womersley analysis; myocardium infraction; speckle-tracing echocardiography; strain analysis; ultrafine zinc particle.

FIGURE 1

Cardiac functions and zinc levels in eight groups. Panels (A–D) show the change of EF, FS, SV, CO, respectively. Panels (E,F) show the change of serum and myocardium zinc concentrations, respectively. All of the data were shown as Mean ± SEM. ^* p < 0.05, MI vs. Sham; ^◆ p < 0.05, ShamZn vs. MIZn; ^# p < 0.05, MIZn vs. MI.

FIGURE 2

Strain peak values in the longitudinal (A), circumferential (B) and radial (C) directions of myocardial infarction zone and non-infarction zone in eight groups, L: Longitudinal, C: Circumferential, R: Radial. All of the data were shown as Mean ± SEM. ^* p < 0.05, MI vs. Sham; ^◆ p < 0.05, ShamZn vs. MIZn; ^# p < 0.05, MIZn vs. MI.

FIGURE 3

Strain rate peak values in the longitudinal (A), circumferential (B) and radial (C) directions of myocardial infarction zone and non-infarction zone in eight groups, L: Longitudinal, C: Circumferential, R: Radial. All of the data were shown as Mean ± SEM. ^* p < 0.05, MI vs. Sham; ^◆ p < 0.05, ShamZn vs. MIZn; ^# p < 0.05, MIZn vs. MI.

FIGURE 4

Representative diagrams of WGA + DAPI redyeing (A) and statistical results of myocyte number per unit area (image magnification: $\times$ 200 and scales: 50 µm) (B); Representative diagrams of Sirius red staining (C) and statistical results of type I collagen (yellow) (D) and type III collagen (green) (E). Schematic panoramas of Masson staining (F) and statistical results of myocardium fibrosis (scales: 2.5 mm) (G). All of the data were shown as Mean ± SEM. ^* p < 0.05, MI vs. Sham; ^◆ p < 0.05, ShamZn vs. MIZn; ^# p < 0.05, MIZn vs. MI.