Khraibi A A, Haas J A, Knox F G
Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905.
Am J Physiol. 1989 Jan;256(1 Pt 2):F165-70. doi: 10.1152/ajprenal.1989.256.1.F165.
The purpose of this study was to investigate the hypothesis that changes in renal perfusion pressure may be transmitted to the renal interstitium and cause alterations in renal interstitial hydrostatic pressure and sodium excretion. A method that utilizes a chronically implanted polyethylene matrix that allows for direct continuous measurement of renal interstitial hydrostatic pressure, and agrees well with subcapsular measurement in rats, was developed. Renal interstitial hydrostatic pressure, fractional excretion of sodium, and urine flow rate were 3.0 +/- 0.3 mmHg, 0.35 +/- 0.13%, and 19.44 +/- 3.00 microliter/min, respectively, when renal perfusion pressure was 101 +/- 0.8 mmHg. When renal perfusion pressure was increased to 123 +/- 0.9 mmHg renal interstitial hydrostatic pressure, fractional excretion of sodium, and urine flow rate increased significantly to 5.8 +/- 0.6 mmHg, 1.29 +/- 0.29%, and 50.76 +/- 8.83 microliter/min, respectively, in anesthetized male Sprague-Dawley rats. These changes occur despite a well-autoregulated glomerular filtration rate and renal blood flow. In conclusion, increasing renal perfusion pressure caused a significant increase in renal interstitial hydrostatic pressure as measured directly by the implanted polyethylene matrix method and was associated with a significant increase in sodium excretion.
本研究的目的是探讨肾灌注压的变化可能会传递至肾间质并导致肾间质静水压和钠排泄改变这一假说。我们开发了一种方法，该方法利用长期植入的聚乙烯基质，可直接连续测量肾间质静水压，且与大鼠肾被膜下测量结果高度吻合。当肾灌注压为101±0.8 mmHg时，肾间质静水压、钠排泄分数和尿流率分别为3.0±0.3 mmHg、0.35±0.13%和19.44±3.00微升/分钟。在麻醉的雄性Sprague-Dawley大鼠中，当肾灌注压升高至123±0.9 mmHg时，肾间质静水压、钠排泄分数和尿流率显著增加，分别增至5.8±0.6 mmHg、1.29±0.29%和50.76±8.83微升/分钟。尽管肾小球滤过率和肾血流量得到了良好的自身调节，但这些变化仍然发生。总之，通过植入聚乙烯基质方法直接测量发现，增加肾灌注压会导致肾间质静水压显著升高，并伴有钠排泄显著增加。
