Lb. Johansen et al., HEMODILUTION, CENTRAL BLOOD-VOLUME, AND RENAL RESPONSES AFTER AN ISOTONIC SALINE INFUSION IN HUMANS, American journal of physiology. Regulatory, integrative and comparative physiology, 41(2), 1997, pp. 549-556
To test the hypothesis that hemodilution is a mediator of the renal re
sponses to an isotonic saline infusion in the supine position, eight m
ales underwent 1) intravenous infusion of 1.5 liter of saline over 21
min (Saline), 2) infusion of 1.5 liter of saline in combination with l
ower body negative pressure for 3 h (LBNP+Saline) to maintain central
blood volume unchanged, and 3) a control study without infusion or LBN
P During the Saline series, central venous pressure (CVP) and left. at
rial diameter (LAD) increased by 4.4 +/- 0.6 mmHg and 2.6 +/- 0.4 mm (
P < 0.05), respectively, whereafter they declined toward preinfusion l
evels. During LBNP+Saline, CVP and LAD were unchanged. Plasma colloid
osmotic pressure remained unchanged during control and showed identica
l decreases by 5 mmHg (P < 0.05) in the Saline and LBNP+Saline series.
During the 3rd h of LBNP, renal sodium excretion (UNaV) peaked at 296
+/- 55 mu mol/min vs. a higher value of 383 +/- 54 mu mol/min (P < 0.
05) during Saline. The increase in UNaV above that of control during t
he 3rd h of LBNP+Saline constituted 48% of that during Saline. Plasma
renin activity and plasma aldosterone concentration showed similar pat
terns of decrease after saline infusion irrespective of LBNP, whereas
plasma norepinephrine was elevated late in the LBNP period compared wi
th during Saline and control (P < 0.05). It is concluded that the main
tenance of a constant CVP and LAD reduces the natriuresis of acute sal
ine loading by about one-half. Thus hemodilution in conjunction with s
uppression of renin and aldosterone release (independent of change in
CVP and LAD) might account for the remaining natriuresis of infusion.