Kirpatovskii V I, Mudraya I S, Mkrtchyan K G, Revenko S V, Efremov G D, Nadtochii O N, Kabanova I V
Department of Experimental Modeling of Urological Diseases, Research Institute of Urology, Russian Ministry of Health, Moscow, Russia,
Bull Exp Biol Med. 2015 Apr;158(6):718-22. doi: 10.1007/s10517-015-2845-5. Epub 2015 Apr 22.
Blood supply to the pelvic organs of outbred male rats was diminished by graduated constriction of the distal part of the inferior vena cava. Deficiency of intramural blood supply in prostate and urinary bladder was revealed by bioimpedance harmonic analysis according to the magnitude of first cardiac peak in the bioimpedance spectrogram. In 1-1.5 months, the histological examination revealed the glandular-stromal form of progressive benign prostatic hyperplasia in all ischemic rats. The development of hyperplasia was not accompanied by the changes in testosterone, dihydrotestosterone, or estradiol in blood and prostatic tissue. Assessment of vesical functional status by recording the intravesical pressure during infusion cystometry revealed an increase in the amplitude of spontaneous fluctuations of detrusor tone and intravesical pressure during bladder filling, which can be considered as indicator of detrusor hyperactivity. The data conclude that chronic ischemia of pelvic organs is an individual pathogenic factor in the development of benign prostatic hyperplasia and associated urinary disorders.
通过逐步缩窄下腔静脉远端,减少杂种雄性大鼠盆腔器官的血液供应。根据生物电阻抗频谱图中第一个心脏峰值的大小,通过生物电阻抗谐波分析揭示前列腺和膀胱壁内血液供应不足。在1至1.5个月时,组织学检查显示所有缺血大鼠均出现进行性良性前列腺增生的腺-基质形式。增生的发展并未伴随血液和前列腺组织中睾酮、双氢睾酮或雌二醇的变化。通过在充盈性膀胱测压期间记录膀胱内压来评估膀胱功能状态,结果显示在膀胱充盈期间逼尿肌张力和膀胱内压的自发波动幅度增加,这可被视为逼尿肌活动亢进的指标。数据表明,盆腔器官的慢性缺血是良性前列腺增生及相关泌尿系统疾病发生发展的一个独立致病因素。