W Lieberthal, G W Stephens, E F Wolf, H G Rennke, M L Vasilevsky, C R Valeri, N G Levinsky
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引用次数: 21
摘要
我们研究了红细胞对离体大鼠肾脏功能和形态的影响,这些肾脏灌注了生理浓度的牛白蛋白(45 g/l)。(1)无红细胞灌注的肾脏,肾血管阻力(RVR)低(4.2 +/- 0.3 mm Hg/ml/min/g),分数钠排泄(FeNa)高(14.5 +/- 1.8%),浓缩能力受损(最大尿渗透压343 +/- 4 mmol/kg)。无红细胞肾也发生髓质厚升肢(mTAL)细胞坏死。(2)红细胞比容为4-6%时,RVR未发生改变,但可阻止mTAL的缺血性改变,并使FeNa降至9.4 +/- 0.03%。尽管存在形态正常的tal,但红细胞压积为4-6%并不能提高集中能力。(3)红细胞压积40-45%时,RVR升高(至11.2 +/- 0.4 mm Hg/ml/min/g), FeNa进一步降低至3.5 +/- 0.6%。尿浓缩能力显著提高(最大尿渗透压640 +/- 35 mmol/kg)。(4)造血比容40 ~ 45%的离体灌注肾(IPK)能够自动调节GFR肾灌注流量,但不完全自动调节。灌注压从100 ~ 150 mm Hg增加50%,肾灌注液流速和GFR分别增加27%和29%。因此,IPK在体内不能像肾脏那样有效地自动调节,即使在正常红细胞压积下存在红细胞时也是如此。
Effect of erythrocytes on the function and morphology of the isolated perfused rat kidney.
We have examined the effects of erythrocytes on the function and morphology of isolated rat kidneys perfused with a physiological concentration of bovine albumin (45 g/l). (1) In kidneys perfused without red cells, renal vascular resistance (RVR) was low (4.2 +/- 0.3 mm Hg/ml/min/g), fractional sodium excretion (FeNa) was high (14.5 +/- 1.8%) and concentrating ability impaired (maximum urine osmolality 343 +/- 4 mmol/kg). The erythrocyte-free kidney also developed necrosis of the cells of the medullary thick ascending limb (mTAL). (2) Erythrocytes at a hematocrit of 4-6% did not alter RVR but prevented ischemic changes in the mTAL and reduced FeNa to 9.4 +/- 0.03%. Concentrating ability was not improved by a hematocrit of 4-6% despite the presence of a morphologically normal mTAL. (3) At a hematocrit of 40-45%, RVR was increased (to 11.2 +/- 0.4 mm Hg/ml/min/g) and FeNa was further lowered to 3.5 +/- 0.6%. Also, urinary concentrating ability was markedly improved (maximum urine osmolality 640 +/- 35 mmol/kg). (4) The isolated perfused kidney (IPK) at a hematocrit of 40-45% was able to autoregulate renal perfusate flow rate of GFR but autoregulation was incomplete. A 50% increase in perfusion pressure from 100 to 150 mm Hg increased renal perfusate flow rate and GFR 27 and 29%, respectively. Thus the IPK is not able to autoregulate as efficiently as the kidney in vivo, even in the presence of red cells at a normal hematocrit.