Stone A M, Stein T, LaFortune J, Wise L
Surg Gynecol Obstet. 1979 May;148(5):731-4.
The intrarenal hemodynamics of nine dogs were studied using 15 micron diameter plastic radioactive microspheres labeled with either 85Sr or 141Ce injected before and with the alternative isotope injected 30 minutes after the induction of sepsis. Total renal microsphere trapping increased by 30.6 per cent, p less than 0.01, after the induction of sepsis. The glomerular filtration rate was unchanged. Microsphere trapping in the outer and inner cortex increased by 36.9 per cent, p less than 0.005, and by 20.3 per cent, p less than 0.05, respectively, reflecting increased renal blood flow. Fractional renal microsphere distribution in the outer cortex increased from 70.0 to 73.4 per cent, p less than 0.01, following the induction of sepsis. These data confirm that sepsis results in renal vasodilatation. In addition, a shift in intrarenal blood flow to the outer cortex was demonstrated. Since the outer cortex is perfused with blood which first passes through the inner cortex, it can be hypothesized that renal blood flow in septic states may be passing through dilated glomerular vessels unable to trap microspheres in the inner cortex or passing through precapillary open arteriovenous shunts, or both, thereby bypassing inner cortical functioning glomeruli. This may partly explain the decreased renal function associated with increased renal blood flow in septic states.
利用直径为15微米、分别标记有85Sr或141Ce的塑料放射性微球，对9只狗的肾内血流动力学进行了研究。在诱导脓毒症之前注射一种同位素，30分钟后注射另一种同位素。诱导脓毒症后，总的肾微球捕获量增加了30.6%，p<0.01。肾小球滤过率未发生变化。外皮质和内皮质的微球捕获量分别增加了36.9%，p<0.005，以及20.3%，p<0.05，这反映了肾血流量的增加。诱导脓毒症后，外皮质中肾微球分布分数从70.0%增加到73.4%，p<0.01。这些数据证实脓毒症会导致肾血管舒张。此外，还证明了肾内血流向外皮质转移。由于外皮质由首先流经内皮质的血液灌注，因此可以推测，脓毒症状态下的肾血流可能通过扩张的肾小球血管，这些血管无法在内皮质捕获微球，或者通过毛细血管前开放的动静脉分流，或两者兼而有之，从而绕过内皮质有功能的肾小球。这可能部分解释了脓毒症状态下肾功能下降与肾血流量增加相关的原因。
