Paraquat (PQT) herbicide is widely used in agricultural practices despite is highly toxic to humans. It has been proposed that PQT exposure may promote cardiorespiratory impairment. However, the physiological mechanisms involved in cardiorespiratory dysfunction following PQT exposure are poorly known. We aimed to determine the effects of PQT on ventilatory chemoreflex control, cardiac autonomic control and cardiac function in rats. Male Sprague-Dawley rats received 2 injections/week of PQT (5mg·Kg^-1 i.p.) for 4 weeks. Cardiac function was assessed through echocardiography and pressure-volume loops. Ventilatory function was evaluated using whole-body plethysmography. Autonomic control was indirectly evaluated by heart rate variability (HRV). Cardiac electrophysiology (EKG) and exercise capacity were also measured. Four-weeks of PQT administration markedly enlarged the heart as evidenced by increases in ventricular volumes and induced cardiac diastolic dysfunction. Indeed, end-diastolic pressure was significantly higher in PQT rats compared to control (2.42 ± 0.90 vs. 4.01 ± 0.92 mmHg, PQT vs. Control, p<0.05). In addition, PQT significantly reduced both the hypercapnic and hypoxic ventilatory chemoreflex response and induced irregular breathing. Also, PQT induced autonomic imbalance and reductions in the amplitude of EKG waves. Finally, PQT administration impaired exercise capacity in rats as evidenced by a ~2-fold decrease in times-to-fatigue compared to Control rats. Our results showed that 4 weeks of PQT treatment induces cardiorespiratory dysfunction in rats and suggests that repetitive exposure to PQT may induce harmful mid/long term cardiovascular, respiratory and cardiac consequences.

中文翻译：

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百草枯除草剂降低了化学反射敏感性，导致大鼠自律性失调并损害了大鼠的心脏功能

尽管百草枯（PQT）除草剂对人类有剧毒，但仍广泛用于农业实践中。已经提出，PQT暴露可能促进心肺功能损害。然而，PQT暴露后参与心肺功能障碍的生理机制知之甚少。我们旨在确定PQT对大鼠通气化学反射控制，心脏自主神经控制和心脏功能的影响。Sprague-Dawley雄性大鼠每周接受2次PQT注射（5mg·Kg ^-1ip）4周。通过超声心动图和压力容量环评估心脏功能。使用全身体积描记法评估通气功能。自主控制通过心率变异性（HRV）间接评估。还测量了心脏电生理学（EKG）和运动能力。PQT给药四周显着扩大了心脏，如心室容积增加和诱发的心脏舒张功能障碍所证明。实际上，与对照组相比，PQT大鼠的舒张末期压力明显更高（2.42±0.90 vs. 4.01±0.92 mmHg，PQT vs.对照，p <0.05）。此外，PQT显着降低了高碳酸血症和低氧性通气化学反射反应，并引起呼吸不规则。同样，PQT引起自主神经失衡并降低EKG波的振幅。最后，PQT给药会损害大鼠的运动能力，与对照组相比，疲劳时间降低了约2倍，证明了这一点。我们的结果表明，PQT治疗4周可诱发大鼠心肺功能不全，并表明重复暴露于PQT可能会导致有害的中长期心血管，呼吸和心脏疾病。