CHANGES IN RENAL MICROCIRCULATION INDUCED BY INFUSION OF (FE3-MYOGLOBIN AND (FE2+)-MYOGLOBIN DURING HEMORRHAGIC HYPOTENSION IN THE ANESTHETIZED RAT - INFLUENCE OF L-NAME AND 8-BR-CYCLIC GMP())
F. Vetterlein et al., CHANGES IN RENAL MICROCIRCULATION INDUCED BY INFUSION OF (FE3-MYOGLOBIN AND (FE2+)-MYOGLOBIN DURING HEMORRHAGIC HYPOTENSION IN THE ANESTHETIZED RAT - INFLUENCE OF L-NAME AND 8-BR-CYCLIC GMP()), Nephron, 73(2), 1996, pp. 243-250
The effects of myoglobin on renal microcirculation were studied in ane
sthetized rats subjected to hemorrhagic hypotension. Capillary flow di
stribution was determined by allowing two dyes to circulate for 3 and
I min, respectively, freezing the left kidney and quantifying the dye
distribution in histological sections by analyzing the distances of re
gularly spaced test points to the next dye-labeled capillary. Control
experiments showed 88% of distances to be <12 mu m in the cortex [medu
llary outer stripe (OS): 77%, inner stripe (IS): 93%] and no distance
to be >60 mu m. Myoglobin induced disturbances in intrarenal perfusion
with a significantly higher potency of (Fe2+)- as compared to (Fe3+)-
myoglobin. With the reduced species, the fraction of distances >60 mu
m increased to 54% in the cortex (OS: 69%; IS: 67%). L-NAME, an inhibi
tor of nitric oxide synthesis, induced similar defects of perfusion. T
he cGMP analogue 8-Br-cGMP was able to nearly completely prevent these
effects. The results support the view that myoglobin when released du
ring hemorrhagic hypotension impairs renal microcirculation supposedly
by scavenging the endogenous relaxing factor nitric oxide.