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Gut 1996; 39 (Suppl3) Gut 1996; 39 (Suppl3) A121 type 3 wave form (continuous flow pattem with a minimal fluttering) indicating Baseline portal (BPF) and splenic (BSF) flow were equal in the control group decreased compliance of the vein was registered in 2 of 4 patients with portal (BPF 13.8 ± 4.2 cmJs, BSF 13.8 + 3.4 m/s). The postprandial increase of portal hypertension. Duplex Doppler can be a non-invasive method to estimate flow (PIPF) exceeded the increase of splenic flow (PISF) significantly (PIPF Gut: first published as 10.1136/gut.39.Suppl_3.A121 on 1 January 1996. Downloaded from hepatic hemodynamics in the follow-up of postoperative patients with BA. 1.65 ± 0.29, PISF 1.15 ± 0.2; p < 0.05). BPF was lower in cirrhotic patients but not significantly different compared to the control group. In most patients with esophageal varices (82.5% with 1-11, 100% with 111) BSF exceeded BPF Expression and Distribution of Nitric Oxide Synthase in whereas in 90% of controls BSF was lower than BPF. PIPF was inversely Patients with Portal Hypertensive Gastropathy (PHG) related to the severity of liver disease (Child's score, p < 0.002) and portal K.B. Hahm, K.J. Lee, Y.S. Moon, Y.S. Kim, H.K. Kang, J.H. Kim, S.W. Cho. hypertension (esophageal vances, p < 0.02; bleeding vs. non-bleeding, p < Department of Gastroenterology, Ajou University School of Medicine, Suwon, 0.0005; PHG, p < 0.002). In contrast to the controls, postprandial splenic flow Korea decreased in most cirrhotic patients. The maximal reduction of splenic flow was observed in severe cirrhosis (Child C, p < 0.005; EV 1110, p < 0.005; Nitric oxide (NO) is associated with hyperdynamic circulation and development severe PHG, p < 0.001). of collaterals in portal hypertension. However, still controversies exist in Patients with disease and a the involvement of NOS in the pathogenesis of PHG The distribution and chronic liver splenic flow exceeding portal flow have a high prevalence (> 80%) of esophageal varices. The postprandial expression of NO synthase (NOS) have not been explored in detail in patients increase in portal flow is related negatively, the decrease in splenic flow with portal hypertension. The aim of this study was to investigate whether NOS positively to the severity of liver cirrhosis and ia activated in the PHG. The subjects composed of 19 patients, admitted due to portal hypertension. complications of PHG; hematmesis or melena, and 19 normal controls showing normal looking gastric mucosa at endoscopy (H. pyloni (-)). Obtaining 4-5 Hemodynamic Alterations in Decompensation of Liver pieces of mucosal biopsied tissues, cNOS and iNOS activities were measured Cirrhosis and Portal by measuring the conversion of 14C-arginine to 14C-citrulline, respectively. Hypertension Westem blotting and immunohistochemical staining were performed using K. Boulanov. Institute of Clinical and Experimental Surgery, Kiev, Ukraine antibody, eNOS and iNOS from Affinity Bioreagent Co. (1:250, 1:500 dilutions). Alterations in splanchnic hemodynamics play key role in the natural course of MPO activities were measured according to the method by Bradley. The cNOS liver cirrhosis and portal hypertension. The aim of the study was to evaluate re- activities were significantly elevated as compared to those of normal controls sults of serial determination of hemodynamics in 90 cirrhotic patients subjected (0.98 + 0.14 vs. 0.12 ± 0.02, P < 0.01). However, iNOS activities were to surgical treatment. Measurements were performed using duplex system, not differed each other between PHG and normal controls. MPO activities dynamic scintigraphy, venous phase of superior arteriomesentericography and were significantly elevated in PHG than normal + vs. controls (0.06 0.03 direct portomanometry and included the following parameters: splenic arterial 0.018 + 0.009, P < 0.001). The cNOS activities were correlated with Child flow (SAF), splenic venous flow (SVF), portal venous flow (PVF), hepatic classification grade and total bilirubin levels. In 80% of the PHG, strong cNOS arterial flow (HAF), portal congestive index (PCI), hepatoportal index (HPI), staining was noted in the endothelium of congested, dilated lamina proprial degree of portal perfusion (DPP), portal pressure (PP). Results given in the capillaries and gastric glands, whereas positive iNOS staining was observed table are means. in only 20% of PHG. The results of immunostaining were correlated with the results of western blottings. In conclusion, NOS didn't show causative role Normal Child A Child B Child C in the development of PHG in portal hypertension. Increased cNOS activities N 30 30 30 30 and expressions seemed to be the consequence of shear forces of portal SAF mVmin 189.5 349.8* 283.8*# 232.3# hyperdynamic circulation. SVF mVmin 206.2 949.0* 616.8*# 595.0*# PVF mVmin 916.8 883.3 542.2*# 459.0*# IEvaluation of Haemodynamic Parameters of Portal Vein HAF mVmin 210.0 174.0 100.3*# 69.9*# PCI cm.s 0.04 0.10* 0.16* 0.18*# as Indicators of Portal Hypertension - An Echo Doppler Study HPI % 66.2 45.5 30.5* 18.5*# PP mmHg 8.7 32.8* 25.3*# 21.4*# 0. Chira 1, R. Badea, A. Ban, A.S. Chira. 1 Inst of Hyg&Public Hlth, Hlth Serv DPP 1.0 1.3 2.7*# 3.2*# ad and Management, Medical Clinic, Cluj, Romania *P < 0.05 compared with normal, 0 P < 0.05 compared with group A Over the past few years special attention has been paid to the haemodynamic These results suggest, that major hemodynamic alterations responsible http://gut.bmj.com/ parameters of the portal vein in the assessment of portal hypertension. The for decompensation of liver cirrhosis and deterioration of functional hepatic aim of this study was to evaluate the maximum velocity in the portal vein reserve are the following: change of hyperdynamic state of splenic circulation and the congestion index of the portal vein, recorded by duplex-doppler into congestive, gradual reduce of total and effective hepatic inflow and ultrasonogaphy, in patients with various degrees of liver fibrosis. decrease of portal pressure. In 75 patients with liver disease who underwent liver biopsy, the cross sectional area, mean and maximum velocity in the portal vein were recorded with Toshiba Sal 140. The congestion index of the portal vein was calculated 693 Role of Sensory Neurons and Nitric Oxide in the (Cl = cross sectional area/mean velocity). Based on a semiquantitative evalu- Control of Hepatic Blood Flow ation of hepatic fibrosis according to Knodell's scoring system, we divided the on September 27, 2021 by guest. Protected copyright. patients into two groups: one with mild fibrosis (grade 1) and another with se- K. Czamobilski, R. Sendur, M. Zejc-Bajsarowicz, J. Biernat, W.W. Pawlik. vere fibrosis (grade 3-4). We compared the above mentioned haemodynamic Inst. of Physiol., Jagiellonian Univ. Med. School, Krakow, Poland parameters in these two groups. An evidence exists that sensory nerve terminals (C-fibers) which contain dif- The patients with extensive fibrosis: grade 4 (cirrhosis) had the maximum ferent vasodilator peptides are found in the liver vasculature. In the present velocity in the portal vein which was significantly lower than patients with mild study the acute utilizing of neurotoxin-capsaicin (CAP) was used to explore fibrosis (16.7 + 3.5 cm/s vs 25.7 + 7 cm/s; p = 0.001) and the congestion the role of C-fibers in the maintenance of hepatic blood flow. The mediatory index of the portal vein was significantly higher (0.08 ± 0.02 cm x s vs 0.03 role of endogenous nitric oxide (NO) in the regulation of hepatic vasculature ± 0.01 cm x s; p = 0.001). When we compared patients with grade 1 fibrosis tone was also determined. Experiments were performed on rats under nem- to those with grade 3 (bridging fibrosis) the difference remained statistically butal anesthesia. Hepatic blood flow (HBF) was registered continuously by significant: 25.7 ±7 cm/s vs 18.6 ± 3.7 cm/s; p = 0.001 for maximum velocity Laser Doppler flowmeter (Periflux 4001 Master). Portal blood flow (PBF) was and 0.03 ± 0.01 cm x s vs 0.06 ± 0.02 cm x s; p = 0.001 for congestion measured ultrasonically (Transonic System 206T). Systemic arterial pressure index of the portal vein. (AP) was measured with a strain gauge transducer. Topical application of CAP We think that this haemodynamic parameters of portal vein could be good (0.5 mg) to periarterial nerves located in the hepatic porta evoked an initial predictors for extensive fibrosis. vasodilation (at 8 minute HBF and PBF increased 77 ± 6 and 48 ± 4% respec- tively, while blood pressure decreased (19 + 3%). The apparent vasodilation [ IPostprandial Portal and Splenic Flow is Related to the was succeeded by vasoconstriction (at 30 min, HBF and PBF were decreased Severity of Portal Hypertension in Chronic Liver 31 ± 5 and 55 ± 3% respectively from control). Inhibition of NO synthase by Disease N-nitro-L-arginine (L-NNA) (15 mg/kg i.v.) decreased HBF by 38 + 7 and PBF by 29 + 7% respectively and increased AP by 28 ± 4%. Pretreatment of the D. Ludwig, C.M. Korbel, B. Schiefer, K. Schwarting, EF. Stange. Dept. of animals with L-arginine (L-Arg) (100 mg/kg i.v.) was without any hemodynamic Medicine 1, University of Lubeck, Germany effects. However L-Arg reversed all circulatory effects of L-NNA. We conclude The purpose of this study was to determine if the combined analysis of portal that acute responses to CAP of the hepatic circulation reflect release of pep- and splenic flow in the postprandial state is related to the severity of portal tide neurotransmitters (initial vasodilation) and their subsequent depletion (late hypertension in cirrhotic patients.
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