Duodenal Blood Flow in Acute Portal Hypertension
Eisuke Iwasaki
1, Tetsuo Morishita
1, Eiichi Sekizuka
2, Kouji Miyazaki
2, Takashi Osada
1, Hiroshi Kishikawa
1,
Masaru Nakano
1, Hidekazu Suzuki
4, Tadashi Ohara
1,3, Jiro Nishida
1, Hiroshi Nagata
4, and Hiromasa Ishii
4Key words.
Microcirculation, Duodenum, Portal hypertension, In vivo micro- scopy, Blood vessels
Introduction
We have already reported gastric microcirculatory changes in portal hyper- tension [1]. Duodenal mucosal lesions such as erosions are often seen in patients with portal hypertension. The purpose of this study was to examine the changes of the mucosal and submucosal vessels in the rat duodenum during the stepwise increase of the portal vein pressure.
Materials and Methods
Male Wister rats fasted overnight were anesthetized with 50 mg/kg sodium pentobarbital i.p. A fine vinyl tube and polyethylene tube were utilized to make a small circle around the portal vein at the porta hepatis for partial ligation of the portal vein. The pressure was increased in a stepwise manner from the control up to +5 cmH
2O, +10 cmH
2O, +15 cmH
2O, and +20 cmH
2O.
The aimed pressure (±10%) was maintained for 2 min at each level. Duodenal blood flow, 1–3 cm anal to the pyloric ring, was measured from the mucosal side with a laser-Doppler flowmeter (ALF 2100, Advance, Japan). An in vivo
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1Departments of Internal Medicine and Gastroenterology, Tokyo Dental College, Ichikawa General Hospital, 5-1-13 Sugano, Ichikawa, Chiba 272-8513, Japan
2Saitama National Hospital, 2 Suwa, Wako, Saitama 351-0102, Japan
3Tokyo Dental College, Chiba Hospital, 1-1-2 Masago, Mihama-ku, Chiba 261-8502, Japan
4Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
microscopy technique was used to study the mucosal and submucosal microvasculature changes. Blood cell velocity in the duodenal mucosal capil- lary was measured with the CapiFlow (Stockholm, Sweden) system. Diameter of the submucosal arterioles and venules was measured with an image analy- sis system (Avionix TVIP-2000; NEC PC-9801, Japan). Mean duodenal blood flow and blood cell velocity in the capillaries were taken during the last 1 min at each level of the portal pressure.
Results
Duodenal blood flow decreased as the portal pressure increased from the control (49.0 ± 4.6 ml/min per 100 g, Mean ± SD) up to +20 cmH
2O (18.6 ± 1 .8 ml/min per 100 g) with significant (P < 0.05) differences between the control and at +5 cmH
2O (40.0 ± 4.6 ml/min per 100 g), +5 cmH
2O and +10 cmH
2O (33.4 ± 4.0 ml/min per 100 mg), and +20 cmH
2O (Fig. 1). Blood cell velocity in the mucosal capillaries decreased from the control (0.12 ± 0 .02 mm/s) with significant differences as the portal pressure increased.
124 E. Iwasaki et al.
Fig. 1. Duodenal blood flow during the increase in portal vein pressure. Duodenal blood flow decreased from the control (49.0 ± 4.6 ml/min per 100 g, mean ± SD, seven rats) with significant (*P < 0.05) differences as the portal pressure increased
Diameter of the submucosal arterioles decreased from the control (26.7 ± 2 .0 mm) with significant differences as the portal pressure increased.
Diameter of the submucosal venules (53.3 ± 3.1 mm) showed no significant differences among the levels.
Discussion
Acute portal hypertension, which is induced by inflammation, tumor, or thrombosis, is often accompanied with abdominal pain and fatal hemorrhagic necrosis of the intestine. Our study showed that stepwise increase of the portal vein pressure decreased the blood flow, the blood cell velocity of the mucosal capillaries, and the diameter of submucosal arterioles in the duodenum. This phenomenon seems to be similar to gastric and ileal microcirculatory changes [1,2]. The mechanism of the duodenal microcirculatory change is still un- known. In the stomach, both endothelin and nitric oxide are involved in the diameter changes of submucosal arterioles, and the arterioles are constricted through the predominant function of endothelin over nitric oxide [2,3].
Further studies on the mechanism of duodenal microcirculatory changes are needed. In conclusion, duodenal blood flow decreases with the constriction of submucosal arterioles in acute portal hypertension.
References
1. Morisita T, Iwasaki E, Ishii H, et al (1990) Microcirculatory changes of the stomach in the portal hypertension. Microcirc Annu 5:99–100
2. Nagata H, Sekizuka E, Morisita T, et al (1993) Regional differences in microvascular response in rat intestine during acute elevation of portal pressure. J Gastroenterol Hepatol 8:315–321
3. Morisita T, Iwasaki E, Ishii H, et al (1993) Role of endothelin and nitric oxide in gastric submucosal arteriolar changes in acute portal hypertension. Microcirc Annu 9:109–110 Duodenal Microcirculation in Portal Hypertension 125
