濃縮大氣微粒對心肌損傷大鼠之心血管毒性研究

Abstract

流行病學研究指出，大氣微粒會造成心臟衰竭住院率及死亡率的上升，然而機轉還不清楚。本研究目的在探討，長期暴露濃縮大氣微粒，對心肌損傷大鼠心血管系統的亞慢性效應。 將SD大鼠注射 isoproterenol (150mg/kg)後造成心肌損傷，作為心肌受損疾病動物模式，再以細粒徑微粒濃縮器 (濃縮倍率約6.4倍)，進行長期微粒全身性呼吸暴露 (每天五小時，每週四天，共三個月)，並以呼吸過濾空氣之大鼠作為對照組。結果發現，大氣濃縮微粒暴露會使凝血功能指標 Fibrinogen上升 (190.7 ± 15.0 vs 160.5 ± 24.2 mg/dL, p < .05)，心跳變異性指標HF顯著上升(0.77 ± 0.15 vs 0.31 ± 0.05ms2, p < .05)，而心臟衰竭指標BNP及發炎指標CRP則無顯著變化。 本研究發現以心肌受損大鼠暴露大氣微粒，對左心室功能並無顯著的急性與慢性效應，但有明顯凝血功能指標fibrinogen上升及心臟自律調節功能改變，顯示在目前大氣微粒濃度下，經慢性暴露後心血管危險因子仍可能上升，微粒空氣污染對心血管的效應值得進一步研究。

Epidemiologic studies have shown that ambient particulate matter (PM) is associated with the mortality and hospital admissions of congestive heart failure. However, the mechanism is still unclear. The goal of this study is to investigate the subchronic effects of concentrated ambient particles (CAPs) on cardiovascular toxicity in rats with myocardial injury. Male SD rats received 150 mg/kg isoproterenol by subcutaneous injection to induce myocardial injury. Ultrafine particle concentrator (UFPC) was used for subchronic CAPs exposure (Whole body inhalation exposure, 5hours/day, 4days/week for 13 weeks). Compared to filter air inhalation controls, CAPs exposure group had significantly higher fibrinogen level (190.7 ±15.0 vs 160.5 ±24.2 mg/dL, p < .05); heart rate variability parameters, HF level, was higher in CAPs exposure group than controls (0.77 ± 0.15 vs 0.31 ± 0.05ms2, p < .05). CAPs group also had higher BNP and CRP level but not significant. Our results showed that PM exposure in rats with myocardial injury had no obvious acute or chronic effect in left ventricle, but increased fibrinogen level and altered cardiac autonomic function. Our results suggest cardiovascular risk factors may increase after chronic exposure to ambient particle under present PM concentration.