Arterial baroreflex dysfunction fails to mimic Parkinson's disease in rats.

Arterial baroreflex dysfunction fails to mimic Parkinson's disease in rats.
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DOI:
10.1254/jphs.08144fp
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发表时间:
2008
影响因子:
3.5
通讯作者:
Jian-guang Yu;Jian Wu;F. Shen;G. Cai;Jian-guo Liu;D. Su
Jian-guang Yu;Jian Wu;F. Shen;G. Cai;Jian-guo Liu;D. Su
中科院分区:
医学3区
文献类型:
--
作者:
Jian-guang Yu;Jian Wu;F. Shen;G. Cai;Jian-guo Liu;D. Su

文献摘要

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帕金森病(PD)患者的压力反射功能通常减弱,这可能发生在PD相关运动障碍发作之前。本研究的目的是测试是否受损的动脉压力反射(ABR)功能可能有助于PD的发病机制。6-大鼠左侧黑质微量注射羟基多巴胺(8 μ g/4穆尔)建立单侧PD模型,通过渗透微泵给予鱼藤酮(2.5 mg/kg)4周建立双侧PD模型。kg(-1)。天(-1)。采用去窦弓神经(SAD)法建立ABR功能障碍模型。在清醒大鼠中测定血流动力学变量。PD样症状和纹状体(CS)中的多巴胺含量也进行了评估。6-羟基多巴胺和鱼藤酮治疗和SAD与血压变异性(BPV)增强和压力反射敏感性(BRS)减弱相关。鱼藤酮,但不SAD,显着降低多巴胺含量的CS,诱导僵住症,抑制饲养和探索行为。在给予鱼藤酮之前SAD并不加重鱼藤酮诱导的多巴胺能损伤。我们的研究结果不支持假设,ABR功能障碍有助于PD大鼠的发病机制。
Patients with Parkinson's disease (PD) often have attenuated baroreflex function, which may occur before the onset of PD-associated movement disorders. The aim of the present study was to test whether impaired arterial baroreflex (ABR) function could contribute to the pathogenesis of PD. 6-Hydroxydopamine (8 mug in 4 mul) was microinjected into the left substantia nigra of rats to establish unilateral PD models, and bilateral PD models were established in rats by administration of rotenone by osmotic minipump for four weeks, at a dose of 2.5 mg . kg(-1) . day(-1). An ABR dysfunction model was obtained by performing sinoaortic denervation (SAD). Hemodynamic variables were determined in conscious rats. PD-like symptoms and dopamine content in corpus striatum (CS) were also assessed. 6-Hydroxydopamine and rotenone treatment and SAD were associated with enhanced blood pressure variability (BPV) and blunted baroreflex sensitivity (BRS). Rotenone, but not SAD, significantly reduced dopamine content in the CS, induced catalepsy, and inhibited rearing and exploratory behavior. SAD before the administration of rotenone did not aggravate the rotenone-induced dopaminergic lesion. Our findings do not support the presumption that ABR dysfunction contributes to the pathogenesis of PD in rats.