Although a great deal is known concerning the pathophysiology of sepsi
s, it is not clear whether circulating blood volume (CBV) is altered u
nder such conditions. To study this, rats were subjected to sepsis by
cecal ligation and puncture (CLP). Immediately after CLP or sham opera
tion, the animals received 3 ml/100 g body weight normal saline subcut
aneously. CBV was determined by using in vivo indocyanine green (ICG)
clearance at 2, 5, 10, or 20 hr after CLP or sham operation. This tech
nique does not require any blood sampling. Serum glutamic pyruvic tran
saminase (SGPT) and glutamic oxaloacetic transaminase (SGOT) were assa
yed enzymatically as indicators of hepatocyte damage. Hepatic microcir
culation was assessed at a selected time point (10 hr post-CLP) by usi
ng laser Doppler flowmetry and colloidal carbon infusion techniques. T
he results indicate that CBV, as determined by ICG clearance, remained
unchanged up to 10 hr following the onset of sepsis (i.e., early seps
is) but decreased significantly at 20 hr after CLP (late sepsis). Howe
ver, systemic hematocrit increased significantly at 5, 10, and 20 hr a
fter CLP, indicating that plasma volume decreased at those time points
. This suggests that there may be limitations in accurately assessing
CBV at 5 and 10 hr after CLP, i.e., during the hyperdynamic circulator
y state of sepsis, using the ICG clearance method. Moreover, SGPT and
SGOT levels increased significantly at 10 hr, and the levels increased
further at 20 hr post-CLP. In contrast, microvascular blood flow and
carbon-perfused areas in the liver were significantly increased at 10
hr post-CLP. Thus, the hepatocyte damage, which occurs in early sepsis
at 1 0 hr after CLP (as demonstrated by elevated SGPT and SGOT levels
), is not due to any reduction in hepatic microcirculation, but may be
due to elevated inflammatory cytokines.