BACKGROUND: Intravenous somatostatin decreases acid secretion, splanchnic blood flow, and portal pressure, but the evidence for its efficacy in the treatment of non-variceal upper gastrointestinal bleeding has been mixed. We aimed to evaluate the vasoactive effect and possible mechanisms of somatostatin infusion in the cessation of non-variceal upper gastrointestinal bleeding. MATERIAL/ METHODS: Patients with non-variceal upper gastrointestinal bleeding without portal hypertension were enrolled in the study. They were given somatostatin infusion in a dose of 250 microgr/hour for 72 hours. Superior mesenteric arterial average flow velocity (SMA-V), SMA pulsatility index (SMA-PI), portal venous volume flow (PV-F), and renal artery resistance index (RA-RI) were measured two times for each patient by Doppler ultrasound; once on the first day of infusion therapy and again 6 hours or more after stopping the infusion. RESULTS: 21 patients (12 male, mean age 44.1 +/- 9.9) with bleeding peptic ulcer were enrolled. During somatostatin infusion, PV-F was 33.7 +/- 12.7 cm3/sec. After stopping infusion, it increased to 56.3 +/- 16.0 cm3/sec (p=0.001). SMA-V was 39.7 +/- 13.1 cm/sec and 64.4 +/- 15.1 cm/sec during somatostatin infusion and after cessation of somatostatin respectively (p=0.01). SMA-PI was 2.0 +/- 0.8 during somatostatin infusion but 2.8 +/- 0.8 without somatostatin infusion (p=0.02). However, RA-RI showed no difference between states with or without somatostatin infusion (p>0.05). CONCLUSIONS: Somatostatin infusion causes a decrease in arterial blood flow to the stomach and duodenum in patients with non-variceal upper gastrointestinal bleeding without portal hypertension. Somatostatin therapy also decreases portal blood flow while not altering renal blood.
BACKGROUND: Intravenous somatostatin decreases acid secretion, splanchnic blood flow, and portal pressure, but the evidence for its efficacy in the treatment of non-variceal upper gastrointestinal bleeding has been mixed. We aimed to evaluate the vasoactive effect and possible mechanisms of somatostatin infusion in the cessation of non-variceal upper gastrointestinal bleeding. MATERIAL/ METHODS:Patients with non-variceal upper gastrointestinal bleeding without portal hypertension were enrolled in the study. They were given somatostatin infusion in a dose of 250 microgr/hour for 72 hours. Superior mesenteric arterial average flow velocity (SMA-V), SMA pulsatility index (SMA-PI), portal venous volume flow (PV-F), and renal artery resistance index (RA-RI) were measured two times for each patient by Doppler ultrasound; once on the first day of infusion therapy and again 6 hours or more after stopping the infusion. RESULTS: 21 patients (12 male, mean age 44.1 +/- 9.9) with bleeding peptic ulcer were enrolled. During somatostatin infusion, PV-F was 33.7 +/- 12.7 cm3/sec. After stopping infusion, it increased to 56.3 +/- 16.0 cm3/sec (p=0.001). SMA-V was 39.7 +/- 13.1 cm/sec and 64.4 +/- 15.1 cm/sec during somatostatin infusion and after cessation of somatostatin respectively (p=0.01). SMA-PI was 2.0 +/- 0.8 during somatostatin infusion but 2.8 +/- 0.8 without somatostatin infusion (p=0.02). However, RA-RI showed no difference between states with or without somatostatin infusion (p>0.05). CONCLUSIONS:Somatostatin infusion causes a decrease in arterial blood flow to the stomach and duodenum in patients with non-variceal upper gastrointestinal bleeding without portal hypertension. Somatostatin therapy also decreases portal blood flow while not altering renal blood.