Postprandial flow measurements in the superior mesenteric artery are closely related to clinical but not endoscopic disease activity in patients with Crohn's disease. The repeated measurement of the postprandial pulsatility index allows estimation of the risk of recurrence.

(Gut 1999;45:546-552)

No abstract

Postprandial flow measurements in the superior mesenteric artery are closely related to clinical but not endoscopic disease activity in patients with Crohn's disease. The repeated measurement of the postprandial pulsatility index allows estimation of the risk of recurrence.

Background : Octreotide is a potent splanchnic hypotensive somatostatin analogue effective in the treatment of acute variceal bleeding. Aim : To study the effects of octreotide on basal and postprandial splanchnic and systemic haemodynamics, and hormonal changes in humans. Methods : Twenty‐four healthy volunteers were randomized to receive a liquid meal and either octreotide (OCT, 100 μg bolus) or placebo repeatedly every 4 h for 48 h. Splanchnic (Doppler ultrasound) and systemic haemodynamics (non‐invasive cardiac monitoring) were assessed for 2 h on four consecutive days: one control day and after doses 1 (0 h), 7 (24 h) and 13 (48 h). Results : The maximum postprandial increases in mean blood velocity of the superior mesenteric artery (SMA–Vmean + 72%), portal (PBF + 52%) and total hepatic blood flow (HBF + 50%) observed in the placebo group, were abolished after the first dose of octreotide (SMA–Vmean – 23%, P < 0.01; PBF – 22%, P < 0.01; HBF – 21%, P < 0.01). Postprandial hyperemia was restored at the end of the 48‐h study period, but baseline SMA–Vmean (placebo 40 ± 12, OCT 29 ± 11 cm/s, P < 0.05) and PBF (placebo 1200 ± 971, OCT 743 ± 449 mL/min, P < 0.05) remained significantly lower in the octreotide group. The postprandial decrease of systemic vascular resistance and increase of cardiac index were prevented by octreotide for 48 h. Conclusions : Repeated 4‐hourly bolus injections of octreotide reduce splanchnic blood flow for at least 48 h, but the prevention of food‐induced splanchnic hyperemia is short‐lasting.