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Abstract
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)To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
March 17,
1998
Received in revised form:
March 9,
1998
Received:
September 10,
1997
Footnotes
☆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.
Identification
Copyright
© 1998 Published by Elsevier Inc.
