Thron C D, Chen J, Leiter J C, Ou L C
Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire, USA.
Kidney Int. 1998 Dec;54(6):2014-20. doi: 10.1046/j.1523-1755.1998.00186.x.
Chronic hypoxia in rats produces polycythemia, and the plasma fraction falls, reducing renal plasma flow (RPF) relative to renal blood flow (RBF). Polycythemia also causes increased blood viscosity, which tends to reduce RBF and renal oxygen delivery. We studied how renal regulation of electrolyte balance and renal tissue oxygenation (which is crucial for erythropoietin regulation) are maintained in rats during hypoxic exposure.
Rats of two strains with differing polycythemic responses, with surgically implanted catheters in the urinary bladder, femoral artery, and left renal and right external jugular veins, were exposed to a simulated high altitude (0.5 atm) for 0, 1, 3, 14, and 30 days, after which RPF (para-aminohippurate clearance), glomerular filtration rate (GFR, polyfructosan clearance), hematocrit and blood gases were measured, and RBF, renal vascular resistance and hindrance (resistance/viscosity), renal oxygen delivery, and renal oxygen consumption were calculated.
During chronic hypoxia RBF increased, but RPF decreased because of the polycythemia. GFR remained normal because the filtration fraction (FF) increased. Renal vascular resistance decreased, and renal vascular hindrance decreased more markedly. Renal oxygen delivery and consumption both increased.
During chronic hypoxia GFR homeostasis apparently took precedence over RBF autoregulation. The large decrease in renal vascular hindrance suggested that renal vascular remodeling contributes to GFR regulation. The reduced hindrance also prevented a vicious cycle of increasing polycythemia and blood viscosity, decreasing RBF, and increasing renal hypoxia and erythropoietin release.
大鼠慢性缺氧会导致红细胞增多症，血浆成分减少，相对于肾血流量（RBF），肾血浆流量（RPF）降低。红细胞增多症还会导致血液粘度增加，这往往会降低肾血流量和肾脏氧输送。我们研究了在低氧暴露期间，大鼠如何维持电解质平衡的肾脏调节和肾组织氧合作用（这对促红细胞生成素调节至关重要）。
将具有不同红细胞增多症反应的两个品系的大鼠，通过手术在膀胱、股动脉、左肾静脉和右颈外静脉植入导管，使其暴露于模拟高海拔（0.5个大气压）环境中0、1、3、14和30天，之后测量肾血浆流量（对氨基马尿酸盐清除率）、肾小球滤过率（GFR，聚果糖清除率）、血细胞比容和血气，并计算肾血流量、肾血管阻力和阻碍（阻力/粘度）、肾脏氧输送和肾脏氧消耗。
在慢性缺氧期间，肾血流量增加，但由于红细胞增多症，肾血浆流量降低。肾小球滤过率保持正常，因为滤过分数（FF）增加。肾血管阻力降低，肾血管阻碍更明显降低。肾脏氧输送和消耗均增加。
在慢性缺氧期间，肾小球滤过率的稳态显然优先于肾血流量的自身调节。肾血管阻碍的大幅降低表明肾血管重塑有助于肾小球滤过率的调节。阻碍的降低还防止了红细胞增多症和血液粘度增加、肾血流量降低、肾脏缺氧和促红细胞生成素释放增加的恶性循环。
