DETERMINANTS OF INTRARENAL OXYGENATION .2. HEMODYNAMIC-EFFECTS
DETERMINANTS OF INTRARENAL OXYGENATION .2. HEMODYNAMIC-EFFECTS
复制标题
DOI：
10.1152/ajprenal.1994.267.6.f1063
复制
发表时间：
1994-12-01
影响因子：
4.2
通讯作者：
EPSTEIN, FH
中科院分区：
文献类型：
--
作者：
BREZIS, M;HEYMAN, SN;EPSTEIN, FH
为了研究血流动力学对肾内氧合的影响，将 O-2 微电极插入大鼠肾脏。在之前的一项研究中[M. Brezis、Y. Agmon 和 F. H. Epstein。是。 J.生理学。 267（肾液电解质生理学。36）：F1059-F1062，1994]，我们表明肾小管代谢是肾内氧合的主要决定因素，部分原因是在基础条件下观察到的髓质缺氧。急性低血压（通过控制出血、主动脉结扎或硝普钠输注）反而会增加髓质 PO2（从 21 +/- 2 至 39 +/- 2 mmHg，P < 0.001），同时降低皮质 PO2（从 46 +/- 2 至 32 +/- 3 mmHg，P < 0.001），消除皮质髓质梯度氧气。激光多普勒研究表明，虽然低血压期间皮质血流量减少，但髓质血流量没有变化或增加。低血压引起的髓质 Pot 增加被预先给予呋塞米所消除，这表明在低血压期间，肾小球滤过率 (GFR) 降低、远端输送和重吸收导致氧利用率降低。急性输注atriopeptin III（0.1-1 mu g kg(-1) min(-1)）可降低皮质PO2（从61 +/- 2至55 +/- 2 mmHg，P < 0.001）和髓质PO2（从15 +/- 1至7 +/- 1 mmHg，P < 0.001），这与atriopeptin诱导的GFR增加一致和管状重吸收功。这些数据表明，髓质氧利用率在肾灌注不足期间增加，而在肾血管舒张期间可能减少。
To study hemodynamic effects on intrarenal oxygenation, O-2 microelectrodes were inserted into rat kidneys. In a previous study [M. Brezis, Y. Agmon, and F. H. Epstein. Am. J. Physiol. 267 (Renal Fluid Electrolyte Physiol. 36): F1059-F1062, 1994], we showed that tubular metabolism is a major determinant of intrarenal oxygenation, in part responsible for medullary hypoxia observed under basal conditions. Acute hypotension (by controlled hemorrhage, aortic ligation, or nitroprusside infusion) paradoxically increased medullary PO2 (from 21 +/- 2 to 39 +/- 2 mmHg, P < 0.001) while decreasing cortical PO2 (from 46 +/- 2 to 32 +/- 3 mmHg, P < 0.001), abolishing corticomedullary gradients of oxygen. Laser-Doppler studies indicated that, while cortical blood flow was reduced during hypotension, medullary blood flow was unchanged or increased. The increase in medullary Pot induced by hypotension was abolished by prior administration of furosemide, suggesting that during hypotension, reduced glomerular filtration rate (GFR), distal delivery, and reabsorption result in decreased oxygen utilization. Acute infusions of atriopeptin III (0.1-1 mu g kg(-1) min(-1)) decreased both cortical PO2 (from 61 +/- 2 to 55 +/- 2 mmHg, P < 0.001) and medullary PO2 (from 15 +/- 1 to 7 +/- 1 mmHg, P < 0.001), consistent with atriopeptin-induced increases in GFR and tubular reabsorptive work. These data suggest that medullary oxygen availability increases during renal hypoperfusion and may decrease during renal vasodilation.