Glomerular haemodynamics during renal artery clamping and haemorrhage in the dog

Abstract

SUMMARYThe influence of a gradual decline in renal perfusion pressure (RPP) due either to renal artery clamping (C) or to haemorrhagic hypotension (HH) was studied using micropuncture techniques in anaesthetized dogs. The decrease in renal blood flow (RBF) was more profound and set in earlier during HH than during C, where perfect autoregulation was observed down to a mean arterial blood pressure of 85 mmHg. Glomerular filtration rate (GFR) was also only slightly decreased during C with no change in filtration fraction (FF); again, a much greater decrease in GFR with an increase in FF was seen in HH. The excretion of water, electrolytes and urea were also more decreased during HHAan during C.-Simlar--hanges were seen at the single nephron (SN) level. Opposite changes were observed in arteriolar resistances: during C a decrease in total arteriolar resistance (RT) amounting to -22 % at a RPP of 84 mmHg and -13 % at 60 mmHg was seen, due exclusively to a drop in afferent resistance (RA), but during HH there was a significant increase in RT by +36 % at a RPP of 110 mmHg, +39 % at 85 mmHg and +68 % at 60 mmHg. This increase was mainly due to an increase in efferent resistance (RE) rather than in RA: +42 vs. +31 %, respectively, at 1 10 mmHg and +67 vs. +19 %, respectively, at 85 mmHg. It was not until a RPP of 60 mmHg was reached that this difference between RE and RA disappeared, being +67 % for RE and +69 % for RA. The ultrafiltration coefficient, Kf, did not change during C and only decreased slightly with the biggest drop in RPP during HH (2-84 /sl mmHg-1 min-1 during HH vs.4.19 #1 mmHg-' min-' before HH). The SNGFR/GFR ratio remained unchanged during C but declined with decreasing RPP during HH, which probably indicates a 'redistribution' of RBF to the deeper regions of the renal cortex. In conclusion, major differences in renal function were observed between C and HH whose cause is unknown.

Extremity trauma exacerbates acute kidney injury following prolonged hemorrhagic hypotension

“…We also found that in the 70-H group, circulating Cr levels were maintained within a normal range during the 3 hours of renal hypoperfusion 23 along with a continuous increase in CCr. These results are consistent with previous findings 24,25 that the glomerular filtration fraction can be elevated in response to hemorrhage to compensate for the decreased RBF. 24,25 Notably, such a "self-protecting" response of the kidney appears to be absent or overridden following a severe hemorrhage, as we found in the 55-H group that CCr was diminished along with a rapid accumulation of circulating Cr.…”

Effects of a Single Dose of Parecoxib on Inflammatory Response and Ischemic Tubular Injury Caused by Hemorrhagic Shock in Rats

“…Hypovolemia causes an increase in renal vascular resistance and decreases RBF and GFR, according to the tubuloglomerular feedback mechanism, observed in hemorrhage group pretreated with placebo. Heller and Horáček [ 38 ] observed earlier and more pronounced decrease in RBF and GFR after hypotension by hemorrhage than after clamping of the renal artery. They also observed that the sharp decline in RBF during hemorrhage was accompanied by a significant increase in RVR, from both the afferent and efferent arterioles.…”

Comparison of acute kidney injury of different etiology reveals in-common mechanisms of tissue damage

“…In addition, reduced energetic efficiency of sodium transport in AKI means that even the reduced total reabsorption in AKI with reduced GFR may cause hypoxia (146). This may be further aggravated in hypovolemic states where predominant efferent arteriolar contraction means that filtration fraction is increased, leading to both relatively increased tubular load for reabsorption and reduced peritubular blood flow, thereby potentially worsening hypoxia (61). We have previously argued that blocking neurohormonal signaling like angiotensin II might reduce active reabsorption and protect the kidney from hypoxia during AKI (71); however, recent data show that the effect may be short lived as we cannot detect improved oxygenation after 1 wk of losartan treatment (115).…”