Key result
Higher hematocrit inversely lowers single-nephron GFR while directly increasing filtration fraction in rat models.
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This study was undertaken in an effort to examine the effects of selective variations in systemic hematocrit on the preglomerular, glomerular, and postglomerular micocirculation in the rat. By isovolemic exchange transfusions, systemic hematocrit (control 51 ml/100 ml) was either reduced (21 ml/100 ml, N equal 7 rats) or elevated (62 ml/100 ml, N equal 7). Single nephron glomerular filtration rate varied inversely and filtration fraction varied directly with the changes in hematocrit. The fall in filtration fraction with decreased hematocrit was due to a decline in the measured glomerular transcapillary hydraulic pressure difference and to a marked increased in the initial glomerular plasma flow rate. Afferent (RA)and efferent (RE) arteriolar resistance declined with the fall in hematocrit; RA fell proportionately more than did RE. The rise in filtration fraction with the elevation in hematocrit was due to a marked increase in in part due to a relatively greater rise in RE than in RA. These findings provide an attractive explanation for the general tendency for filtration fraction to vary directly with hematocrit in anemic and polycythemic states in man.
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Myers et al. (1975) studied Anemic and polycythemic states (experimental variations in systemic hematocrit in rats) (n=14). Isovolemic exchange transfusion altering systemic hematocrit vs. Control systemic hematocrit (51 ml/100 ml) was evaluated on Single nephron glomerular filtration rate and filtration fraction. Selective variations in systemic hematocrit (21 vs 51 vs 62 ml/100 ml) caused single nephron GFR to vary inversely and filtration fraction to vary directly with hematocrit in rats.
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