Somatostatin and its analogue, octreotide acetate, are thought to decrease mesenteric blood flow; however, it is unknown whether the decrease occurs at the central, regional, or microvascular level. We hypothesized that the circulatory effects of octreotide are regulated at the microvascular level. Changes in superior mesentery artery (SMA) flow in response to octreotide were measured with a perivascular ultrasonic flow probe. In separate experiments, the jejunal microcirculatory effects of octreotide were studied using in vivo videomicroscopy. After accrual of baseline hemodynamic and microcirculatory data, animals were randomized to control or treatment (10 micrograms/kg octreotide) iv groups. Measurements were made every 15 min during the infusion and for 90 min after the completion of the infusion. Results are expressed as means +/- SEM. Intravenous infusion of octreotide caused no significant change in arterial pressure, cardiac index, or systemic vascular resistance index in either group in either set of experiments. A statistically significant decrease in heart rate (9%) occurred in the control group of animals undergoing SMA flow measurement. SMA flow did not change significantly with infusion of octreotide. In contrast, jejunal first-order arteriole flow increased to 117.9 +/- 9.7% of baseline (P < 0.05) in the absence of significant changes in microvessel diameters. This was due to an increase in centerline red cell velocity (116 +/- 5% of baseline, P < 0.05). We conclude that octreotide increases jejunal first order arteriole flow by mechanisms that are regulated at the microcirculatory level.