Differential response of the microvasculature in the liver during bacteremia

To determine the initial hepatic microvascular responses to bacteremia, male Sprague-Dawley rats (n = 19) were decerebrated and the left liver lobe from each animal exteriorized and suffused with environmentally controlled Krebs solution. Direct in vivo videomicroscopy was used to measure diameter changes in at least four portal venules (PV) and four proximal periportal sinusoids (PS) at the inlet of hepatic lobules in each of seven livers or four terminal centrilobular sinusoids (CS) and four collecting central venules (CV) at the outlet in each of 12 livers during a baseline period and for 2 hr after intravenous (i.v.) infusion of 1 X 10(9) live Escherichia coli or saline (control). Cardiac output, systemic arterial blood pressure, and body temperature were monitored continuously during the experiments. These data indicate that E. coli bacteremia causes a redistribution of hepatic microvascular blood flow within the liver lobule at both the inlet and outlet regions with increased perfusion of certain microvascular segments and decreased perfusion of others. In the areas observed, a 2:1 dilated/constricted microvessel ratio suggests an initial increased overall liver blood flow within the first 2 hr of experimentally induced bacteremia.