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The decreased hematocrit that occurs with hemodilution leads to a decrease in peripheral resistance while venous return and cardiac output increase. We determined systemic and renal responses to hemodilution with a solution of albumin or a crosslinked hemoglobin-based oxygen carrier (XLHb) and the effect of inhibition of NO synthesis on the responses to albumin. Clearance experiments were done on anesthetized rats to determine mean arterial pressure (MAP), glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and sodium excretion before and after isovolemic exchange transfusion (2 ml per 100 gm body weight) with either (1) 5% albumin (n = 5), (2) 5% albumin plus Nω-nitro-L-arginine methyl ester (L-NAME, 3.5 mg/kg; n = 6), or (3) 6% XLHb (n = 7) and after administration of L-NAME alone (n = 4). Hematocrit decreased similarly in all exchange groups (from 42 ± 1.0 to 29 ± 1.3). MAP decreased with albumin exchange, increased with LNAME, and remained unchanged with albumin+L-NAME or XLHb. GFR, ERPF, and renal blood flow increased while filtration fraction and renal resistance decreased with albumin exchange; responses were the opposite with L-NAME, and with albumin+L-NAME and XLHb these parameters remained approximately the same as control values. Red cell delivery decreased with L-NAME, albumin+L-NAME, and XLHb but remained at control levels with albumin. In conclusion, renal effects of decreased hematocrit can be offset by decreased NO availability. The similarity of results with XLHb and albumin+L-NAME is consistent with NO scavenging by hemoglobin. Increased renal vascular tone with XLHb limits oxygen delivery.
Abbreviations:ERPF (Effective renal plasma flow), %FENa (fractional sodium excretion), FF (filtration fraction), GFR (glomerular filtration rate), L-NAME (Nω-nitro-Larginine methyl ester), MAP (mean arterial pressure), PAH (para-amino hippuric acid), RCD (red cell delivery), RBF (renal blood flow), RR (renal vascular resistance), UNaV (urinary sodium excretion), XLHb (crosslinked hemoglobin)
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Accepted: March 17, 1998
Received in revised form: March 9, 1998
Received: September 10, 1997
☆Supported by funds from the Frank C. Bressler Research Foundation of the University of Maryland Medical School and by National Institutes of Health Grant POI-HL-48517.
© 1998 Published by Elsevier Inc.