A310 AGA ABSTRACTS GASTROENTEROLOGY, Vol. 108, No. 4

• MAGNETIC RESONANCE ANGIOGRAPHY OF THE SPLANCHNIC VASCULATURE. A.F. MUlleL S. Whittaker. The Kent & Canterbury Hospital and the University Hospital, Nettingham~ England.

Magnetic resonance angiogmphy (MRA) can be a useful nen-invasive means of assessing the vascular tree. It overcomes the problems of other non-invasive techniques such as the non visualisation of vessels due to obesity and bowel gas with Doppler ultrasound. For patients (pts) with chronic abdominal pain, whose symptoms may be due to intestinal ischaemia, it may allow the selection of patients for therapeutic vascular angiography. Little has been published on the value of MRA in studying the splanchnic vasculature. We have examined the superior mesenteric and coeliac arteries (SMA & CA) by MRA in 6 patients (5 male aged 47 - 79 years, 1 female aged 73 yrs; mean 66 yrs) with postprandial abdominal pain, in whom other investigations, including endoscopy had been unhelpful. In each, mesenteric ischaemia was considered. Two pts had a past history of myocardial infarction, another 2, transient ischaemic attacks, with carotid atheroma demonstrated on ultrasound and a fifth pt was in renal failure and on dialysis. Each pt underwent 2D and 3D time of flight studies Of the splanchnic vasculature using a Siemens Magneton SP4000 machine. The proximal splanchnic vascular tree was clearly demonstrated in 5 of 6 pts. The 6th pt had occlusion of the aorta high in the abdomen, with no filling of the SMA or CA. Occlusion of the splanchnic vessels was confirmed in this pt at post mortem, 2 months after the study. Two pts had mild to moderate atheroma of either the SMA or CA without significant stenosis (pts l&2). One pt (3) had atheroma at the origin of the coeliae axis causing a 50% stenosis. The 4th pt had a normal SMA and CA, but a tight right renal artery stenosis. The study was normal in pt 5. In pts 1-5, these findings were not thought to be consistent with a diagnosis of mesenterie ischaemia. Magnetic resonance angiography is a useful non-invasive method of assessing the splanctmic vascUlature. It can demonstrate clearly atherema and stenoses and may be of use in patients thought to have chronic mesenteric ischaemia. Traditional angiography remains the current gold standard for examining the splanehnic vasculature and a formal comparison with MRA should be recommended.

Q ETHANOL DILATES RAT GASTRIC ARTERIOLES VIA ADENOSINE A2 RECEPTORS. I-i Na~ata, E. Seldzuka, IV[ Morishita, M~ Tatemichi, A. Mizuld, H. Ishii: Dept. of Medidne, Saiseikai Central Hospital, Institute of Clinical Research, Nat/anal Saitama Hospital and Keio School of Medidne, Japan.

Topical ethanol induced gastric vasodilation by release of adenosine in dogs (Am J Physio1264: G664, 1993). We studied the specific adenosine receptor involved in ethanol-induced vasodila~on in arterioles of the rat gastric submucos~ the vessels that control the mucosal blood flow. A rat was anesthetized, and the stomach exteriolized. Serosa and muscle were removed from a small area. Using in vivo mic~escopy, changes in arteriolar diameters were measured after topical application of ethanol. Agents tested: anAl antagonist 8-phenyltheophylline (8-PT, 10-~M),.an A2 antagonist 3,7-dimethyl-l,prepargylxanthine (DMPX, 10~M), anAl agonist N6-cyclopentyladenosine (CPA), an A2 agonist 51-(N- cyclopropyl)carbo~Amidoadenosine (CPCA), an H1 antagonist pyrilamine 10-51Vi atropine 10~M, an CGRP antagonist CGRPs.37 1 ~ L-NAME 300/AVI and indomethadn 10mg/Kg iv. Results: Mean + SE of% of basal diameter, n=6 1. Effect ofvasodilator antagonists on 5% ethanol-induced arteriolar dila- tion. ~No difference from control (ethanol alone). control p ~ e atropine CGRP847 indomethacin L-NAME 128-+ 6 137+1(F llSe10 ~ 131+12 ¢ 124! 9 ~ 130-+13 *

2. Effect of adenosine receptor antagonists ( p<0.05, t-test) ethanol concentration 1% 5% 10% 20% control (ethanolalone) 116-+ 7 134~ 9 153+16 166+-21 ethanol+8-PT 122~13 149i-_14 126~11 152.%16 ethanol+DMPX 102_+2" 103-+3" 121+ 7* 115!-_7" 3. Adenosine receptor agonists study.

10~M 10-7M I0-6M 10-SM 104M CPA 100!-_ 3 101~ 3 103-+ 8 116-+ 5 CPCA 91_+2 115-+7 117±5 125_+5 120±4 Cenclusions: In the rat stomach, an A2 antagonist, but not an A1 antago- nist, prevents ethanol- induced arteriolar dilation. An A2 agonist, but not an ,%1 agonist, dilates arterioles in a dose-dependent manner. Other vasodila- tors, such as histamine, aestylcholine, CGRP, prestaglandin or nitric oxide, are not involved in ethanol-induced vasodilation. Ethanol increases the gastric mucosal blood flow via A2 receptors in submucosal arterioles.

CRYPT CELL MORPHOMETRY IN COELIAC DISEASE: CORRELATION WITH FOLIC ACID AND VITAMIN BI2 STATUS AND COMPARISON WITH PROTEIN AND DNA MUCOSAL CELLULAR CONTENT. I M Nakshabendi, F D Lee*, S Downie + , M J Rennie + , R I Russell, Department of Gastroenterology & Pathology*, Royal Infirmary, Glasgow and Department of Anatomy & Physiology + , University of Dundee, Scotland.

We have applied the method of histomorphometry to assess the nuclear, cellular and cytoplasmic surface areas (SA) in 8 patients with untreated coeliac disease and 4 normal subjects. METHODS: Standard histology was performed and SA of the nuclei, cytoplasm and cells were calculated. DNA content was measured using UV absorbance and the protein content was measured using standard methods. Serum BI2, fo!ic acid and red cell (RC) folate levels assessed. RESULTS: Results are expressed in means ± SD. Nuclear SA in coeliac disease was greater than in control subjects (258 ± 46.82 2u v 110.48 ± 10.88 2u, P<0.008; ). Protein / DNA ratios and cytoplasmic / nuclear SA ratios were reduced in patients with coeliac disease compared with normal subjects (9.2 ± 1.6 mg/ug v 13;0 ± 2.2 mg/ug, p<0.05; 1.35 ± 0.29 2u/2u v 4.08 ± 0.38 2u/2u, p<0.008 respectively). Although the folate levels tend to decrease with the increase in the nuclear SA, no consistent correlation between the folate, RC folate levels and serum B12 was found with the crypt cell morphometric characteristics. CONCLUSION: These results suggest that in coeliac disease the nuclear SA is greater than 'normal, probably a reflection of increased mitotic activity, the mucosal cell protein content and cytoplasmic SA is reduced, 'but no correlation was found between the folate, RC folate levels and El2 , and the morphometry of crypt cells.

MEASUREMENT OF DUODENAL MUCOSAL PROTEIN SYNTHESIS IN PATIENTS WITH COELIAC DISEASE. I M Nakshabendi, S Downie*, M J Rennie*, R I Russell. Department of Gastroenterology, Royal Infirmaryz Glasgow and Department of Anatomy & Physiology ~ , University of Dundee, Dundee, Scotland.

We have applied a stable-isotope tracer amxno acid method to measure the rate of protein synthesis in distal duodenal mucosa in patients with untreated coeliac disease (CD). 8 patients (4 males, 4 females, 39-65 yr, 40-67 kg) were studied and the results compared to those from a group of normal control subjects (C). METHODS: Primed intravenous (IV) and intragastric (IG) infusion of [I-13C] leucine and [I- 13C] valine were administered ~o the patients after an overnight fast. Blood samples were taken over 4 hours then distal duodenal mucosa was biopsied endoscopically. Incorporatxon of tracers into protein was determined by isotope ratio mass spectrometry. Protein synthesis was calculated relative to intracellular free amino acid labelling. Protein and nucleic acids were measured by standard methods. RESULTS: Protein/DNA ratios were reduced in CD (9.2 ± 1.6 mg/micgm vs 13.0 • 2.2 mg/micgm, respectively) suggesting reduced mucosal cell slze in CD. RNA/DNA ratios were identical in each group. Duodenal mucosal protein synthesis was markedly (P < 0.01) elevated in CD compared with the C subjecss whether determined by incorporation of the IV or IG infused tracers (IV tracer, CD vs C 3.58 ± 0.45 vs 2.26 ± 0.22%/h; IG tracer 6.25 z 0.97 vs 2.34 ± 0.52 %/h, respectLvely). Labelling of mucosal intracellular amino acids was threefold higher when tracer was given IG than IV but there were no differences between the groups, suggesting that the higher rate of protein synthesis measured with IG tracer in the CD patients is not the result of differential precursor labelling or luminal tracer malabsorption. CONCLUSIONS: Despite villous atrophy and reduced mucosal cell size observed in CD, mucosal protein synthesis was elevated by between 50 and 200 % suggesting a concomitantly increased cell metabolism and high rate of protein breakdown or cell loss in the coeliac patients.