Murray B M, Paller M S
Clin Nephrol. 1986;25 Suppl 1:S37-9.
We have previously shown that both acute infusion of cyclosporine and chronic intraperitoneal cyclosporine result in decreased renal blood flow in rats. This effect of cyclosporine infusion was mediated via the sympathetic nervous system. In this study, renal denervation was found to also prevent the decrease in glomerular filtration rate after cyclosporine infusion. Male Sprague-Dawley rats underwent unilateral renal denervation and three days later inulin clearance was measured following infusion of cyclosporine (20 mg/kg). GFR fell by 43% in innervated kidneys, but remained normal in denervated kidneys. In addition, administration of the alpha-adrenergic antagonist prazosin prevented the rise in serum creatinine and the fall in renal blood flow associated with chronic cyclosporine administration (20 mg/kg intraperitoneally for 7 days). These findings further support the hypothesis that sympathetic nervous system-mediated vasoconstriction is responsible for renal dysfunction in rats after acute and chronic cyclosporine administration.
我们之前已经表明，急性输注环孢素和慢性腹腔注射环孢素都会导致大鼠肾血流量减少。环孢素输注的这种作用是通过交感神经系统介导的。在本研究中，发现肾去神经支配也能预防环孢素输注后肾小球滤过率的降低。雄性Sprague-Dawley大鼠接受单侧肾去神经支配，三天后在输注环孢素（20mg/kg）后测量菊粉清除率。神经支配完整的肾脏中肾小球滤过率下降了43%，但去神经支配的肾脏中肾小球滤过率保持正常。此外，给予α-肾上腺素能拮抗剂哌唑嗪可预防与慢性环孢素给药（腹腔注射20mg/kg，持续7天）相关的血清肌酐升高和肾血流量下降。这些发现进一步支持了以下假设，即交感神经系统介导的血管收缩是急性和慢性环孢素给药后大鼠肾功能障碍的原因。
