逼尿肌活动不足,一种情况,其中膀胱肌肉没有强烈或足够长的收缩,以完全排空膀胱或在正常的时间范围内,是男女老年人下尿路症状的常见原因。尽管衰老是逼尿肌活动不足的已知危险因素,其病理生理机制尚不完全清楚。因此,建立紧密模拟人类逼尿肌活动不足的病理生理学的动物模型对于阐明这些机制是必要的。代谢综合征是几个危险因素的集合,包括肥胖,高脂血症,高血糖症,和高血压,与糖尿病的发展有关,心血管疾病,男女下尿路功能障碍。值得注意的是,在患有糖尿病的动物模型中,与没有糖尿病的动物模型相比,在更早的年龄观察到由于逼尿肌活动不足而导致的膀胱功能障碍。最近,在代谢综合征的动物模型中,在相对较早的年龄观察到逼尿肌活动不足样表型,涉及肥胖,高脂血症,和高血压,与没有的相比。因此,这篇综述介绍了逼尿肌活动不足与衰老和代谢综合征的关系,以及从各种动物模型的报道中发现逼尿肌活动不足的可能病理生理机制。值得注意的是,代谢综合征可能会加速年龄相关性逼尿肌活动不足的发作,进一步分析代谢综合征的老动物模型可能有助于阐明人类逼尿肌活动不足的发病机理。
Detrusor underactivity, a condition in which the
bladder muscle does not contract strongly or long enough to empty the
bladder completely or within the normal time frame, is a common cause of lower urinary tract symptoms in older individuals of both sexes. Although aging is a known risk factor for detrusor underactivity, its pathophysiological mechanisms are not fully understood. Therefore, establishing animal models that closely mimic the pathophysiology of detrusor underactivity in humans is necessary to elucidate these mechanisms. Metabolic syndrome is a cluster of several risk factors, including obesity, hyperlipidemia, hyperglycemia, and hypertension, which are associated with the development of diabetes, cardiovascular disease, and lower urinary tract dysfunction in both sexes. Notably,
bladder dysfunction resulting from detrusor underactivity is observed at an earlier age in animal models with diabetes mellitus than in those without. Recently, detrusor underactivity-like phenotypes have been observed at a relatively early age in animal models with metabolic syndrome, involving obesity, hyperlipidemia, and hypertension, compared with those without. Therefore, this review introduces the association of detrusor underactivity with aging and metabolic syndrome, as well as possible pathophysiological mechanisms for detrusor underactivity from reports of various animal models. Notably, metabolic syndrome may accelerate the onset of age-related detrusor underactivity, and further analysis of old animal models with metabolic syndrome may help elucidate the pathogenesis of detrusor underactivity in humans.