Somatostatin and its analogue, octreotide acetate, are thought to decr
ease mesenteric blood flow; however, it is unknown whether the decreas
e occurs at the central, regional, or microvascular level. We hypothes
ized that the circulatory effects of octreotide are regulated at the m
icrovascular level. Changes in superior mesentery artery (SMA) flow in
response to octreotide were measured with a perivascular ultrasonic f
low probe. In separate experiments, the jejunal microcirculatory effec
ts of octreotide were studied using in vivo videomicroscopy. After acc
rual of baseline hemodynamic and microcirculatory data, animals were r
andomized to control or treatment (10 mu g/kg octreotide) iv groups. M
easurements 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 chang
e in arterial pressure, cardiac index, or systemic vascular resistance
index in either group in either set of experiments. A statistically s
ignificant decrease in heart rate (9%) occurred in the control group o
f animals undergoing SMA flow measurement. SMA flow did not change sig
nificantly with infusion of octreotide. In contrast, jejunal first-ord
er arteriole flow increased to 117.9 +/- 9.7% of baseline (P < 0.05) i
n the absence of significant changes in microvessel diameters. This wa
s due to an increase in centerline red cell velocity (116 +/- 5% of ba
seline, P < 0.05). We conclude that octreotide increases jejunal first
order arteriole flow by mechanisms that are regulated at the microcir
culatory level. (C) 1994 Academic Press, Inc.