Hypoperfusion of the gut mucosa is thought to be a factor in the development of gut barrier failure during sepsis and septic shock. Dopamine stimulates DA-1 receptors which mediate regional vasodilatation in the gut. Therefore, we have investigated the effect low-dose dopamine of (3 mu g kg(-1) min(-1)) on the intestinal villus microcirculation during endotoxaemia in a rat model of normotensive endotoxaemia, using in vivo videomicroscopy. Blood flow in and the diameters of central villus arterioles were measured before, immediately after and 60 min after a 1 - h continuous infusion of endotoxin 1.5 mg/kg body weight. After baseline measurements were obtained, rats received either an infusion of 0.9% saline (group A; n = 7) or a volume-equivalent infusion of dopamine 3 mu g kg(-1) min(-1) (group B; n = 7) throughout the study. Control animals (group C; n = 7) received no endotoxin or dopamine. In group A, villus blood flow (mean baseline 8.4 (SEM 0.9) nl min(-1)) decreased by 29.7 (8.9) % to 5.9 (0.9) nl min(-1) immediately after endotoxin challenge and by a total of 43.1 (7.3) % to 4.7 (0.7) nl min(-1) after another 60 min. Simultaneously, villus arteriolar diameters decreased from 7.8 (0.2) to 6.9 (0.3) mu m and to 6.5 (0.3) mu m, respectively. In group B, villus blood flow (baseline 8.7 (0.4) nl min(-1)) was unchanged immediately after the 1 - h infusion of endotoxin (8.3 (0.4) nl min(-1)). However, another 60 min later blood flow decreased by 28.8 (8.0) % to 6.1 (0.7) nl min(-1). In contrast with group A, the diameters of the central villus arterioles were unchanged despite administration of endotoxin (7.9 (0.2) mu m; 8.1 (0.4) mu m; 8.2 (0.5) mu m). In group C, there were no changes in villus blood flow or arteriolar diameters throughout the study. Our results indicated that low-dose dopamine did not prevent, but delayed and attenuated, the decrease in intestinal villus blood during normotensive endotoxaemia.