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Effect of meal on portal hemodynamics in healthy humans and in patients with chronic liver disease

✍ Scribed by Stefano Gaiani; Luigi Bolondi; Silvia Li Bassi; Vittorio Santi; Gianni Zironi; Luigi Barbara


Publisher
John Wiley and Sons
Year
1989
Tongue
English
Weight
616 KB
Volume
9
Category
Article
ISSN
0270-9139

No coin nor oath required. For personal study only.

✦ Synopsis


The effect of a standard Italian meal on portal hemodynamics was evaluated in 12 normal subjects, in 11 patients with chronic active hepatitis and in 11 patients with liver cirrhosis using duplex Doppler ultrasound, which allows a noninvasive assessment of portal blood flow. In the fasting state, the portal vein caliber was significantly higher in patients with liver cirrhosis than in normal subjects and patients with chronic active hepatitis, whereas the mean flow velocity in the portal vein was significantly lower in this group. Basal flow volume of the portal vein was greater in patients with liver cirrhosis than in normal subjects and patients with chronic active hepatitis. Sixty minutes after the standard meal, we observed both in normal subjects and in patients with chronic active hepatitis a significant increase of mean caliber, mean velocity and flow volume in the portal vein, whereas in patients with liver cirrhosis, these parameters remained almost unchanged. In addition, the examination of individual patterns showed that flow velocity and flow volume in the portal vein decreased in some cirrhotic patients after the meal. This behavior is probably related to the hypertensive state in the splanchnic venous bed and diversion of splanchnic blood flow into spontaneous portosystemic collaterals. Splanchnic vasodilation and hyperemia occur following intake of food in animals (1) and healthy humans ( 2 ) , owing to the interaction of intrinsic (change in arteriolar transmural pressure and/or increase in vasodilator tissue metabolites) or extrinsic mechanisms (autonomic nervous system) (3-5) and the effect of gastrointestinal hormones, namely gastrin, cholecystokinin and glucagon, as demonstrated by experimental studies (6, 7). Our knowledge of the mechanisms involved in splanchnic postprandial hemodynamics is derived mainly from experimental investigations in animals, whereas measurement of splanchnic venous flow in humans has been limited by the fact that it required, until few years ago, complex and invasive techniques such as electromagnetic flowmetry (8, 9) or cineangiography (lo), and noninvasive methods were not feasible. The development of ultrasound pulsed Doppler technology allows measurement of flow velocity in deep abdominal vessels and, by simultaneously measuring cross-sectional


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