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Animal models of psychogenic cardiovascular disorders: What we can learn from them and what we cannot

机译:心理心血管疾病的动物模型:我们可以从他们那里学到什么以及我们不能

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摘要

Epidemiological and clinical studies from the past 50years provide unequivocal evidence for a close association and causative links between psychological stresses and cardiovascular dysfunction in humans. Not surprisingly, numerous animal experiments have been undertaken in an attempt to clarify underlying pathophysiological mechanisms. The present review focuses on animal models that provide insight into the mechanisms of stress-induced cardiovascular dysfunction. Great success was achieved in elucidating the neural pathways and neurotransmitters responsible for the cardiac consequences of acute stressors, such as stress-induced ventricular arrhythmias and stress cardiomyopathy. These disturbances were reproduced successfully in canine and rodent models. The most important finding from these animal models is that these disturbances are mediated by elevated sympathetic outflow to the ventricular myocardium. In contrast, attempts to induce psychogenic hypertension in rodents produced inconsistent and contentious results. More recent studies using biotelemetry raised serious doubts regarding the validity of earlier results obtained with the tail-cuff method and it remains unclear whether chronic stress can lead to sustained hypertension in animal models.
机译:过去50年的流行病学和临床研究为人类心理应激和心血管功能障碍之间的密切关联和致病联系提供了明确的证据。毫不奇怪,已经进行了许多动物实验,试图阐明潜在的病理生理机制。本综述侧重于动物模型,提供对应力诱导的心血管功能障碍机制的洞察力。取得了巨大的成功,阐明了负责急性压力源的心脏后果的神经途径和神经递质,例如应激诱导的心律失常和压力心肌病。这些干扰成功地在犬和啮齿动物模型中复制。这些动物模型中最重要的发现是这些扰动是通过对心室心肌的升高而介导的。相比之下,试图诱导啮齿动物心理高血压产生不一致和令人争议的结果。使用BioteLeMetry的最近研究提出了关于使用尾巴纤维法获得的早期结果的有效性的严重怀疑,并且仍然尚不清楚慢性胁迫是否会导致动物模型中持续的高血压。

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