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Biomedical subjects

M C Hou

Publications and source records attributed to M C Hou.

At least 55 records · Page 3Linked to original sources
PubMed1998

Haemodynamic effects of 8-day octreotide and prazosin administration in portal hypertensive rats.

BACKGROUND: Octreotide and prazosin are both effective portal hypotensive drugs in the control or prevention of variceal bleeding. The present study was undertaken to investigate the haemodynamic effects of octreotide and prazosin, alone or in combination, in portal hypertensive rats. METHODS: Portal hypertension was induced by partial portal vein ligation. Portal hypertensive rats were allocated into one of the four groups-vehicle group (saline, 0.5 mL 12 h-1), octreotide group (30 micrograms kg-1 12 h-1), prazosin group (0.4 mg kg-1 12 h-1), and octreotide (30 micrograms kg-1 12 h-1) plus prazosin (0.4 mg kg-1 12 h-1) group-with eight rats in each group. Prazosin or saline was administered by gavage, whereas octreotide was administered by subcutaneous injection. The drug was given on the day of ligation and continued for 8 consecutive days. Systemic as well as splanchnic haemodynamic parameters were measured thereafter. RESULTS: Portal vein-ligated rats exhibited typical hyperdynamic state compared with sham-operated rats. The portal venous pressure, portal tributary blood flow and cardiac index were significantly reduced by treatment of octreotide, prazosin or octreotide plus prazosin in portal hypertensive rats. Hyperdynamic parameters of systemic, renal and portal territory vascular resistances, and renal as well as hepatic arterial blood flow were ameliorated by treatment of octreotide or octreotide plus prazosin in portal hypertensive rats. Overall, octreotide treatment exerted more beneficial haemodynamic effects than prazosin treatment. The combination of octreotide and prazosin exerted better haemodynamic effects in cardiac index but worse effects in systemic as well as portal territory vascular resistance than octreotide treatment alone.

Animals↗
PubMed1998

Effect of sucralfate granules in suspension on endoscopic variceal sclerotherapy induced ulcer: analysis of the factors determining ulcer healing.

Oesophageal ulcers commonly occur after endoscopic variceal sclerotherapy and usually cause complications and a delay in further sclerotherapy. The aims of this study are to investigate the effect of sucralfate granules in suspension on the treatment of endoscopic variceal sclerotherapy induced ulcer and analyse the factors determining the ulcer healing. Fifty-two patients with oesophageal variceal bleeding received elective endoscopic variceal sclerotherapy. After endoscopically proved oesophageal ulcers, they were randomized to receive either sucralfate granules in suspension (n = 22) or antacid (n = 23). Follow-up endoscopy was performed weekly. Ulcer healing rates were compared between the groups using the log-rank test. Forty-one ulcers receiving sucralfate and 48 ulcers receiving antacid treatment were evaluated. The clinical characteristics of the ulcers were similar in both groups. The ulcers in patients receiving sucralfate healed faster than those receiving antacid (P<0.02). On analysis of factors affecting ulcer healing, ulcers smaller than 1 cm2 (n = 59) appeared to heal faster than those larger than 1 cm2 (n = 30; P= 0.059) and shallow ulcers (n = 46) healed faster than deep ulcers (n = 43; P<0.001). On multifactorial analysis, ulcer depth was the only factor determining ulcer healing. The ulcer healing effects of sucralfate became more prominent when the ulcer was larger than 1.0cm2 (1.7+/-0.6 weeks vs 2.3+/-0.6 weeks, P= 0.011) and deep (1.7+/-0.7 weeks vs 2.5+/-1.0 weeks, P= 0.013) when compared with those receiving antacid. Sucralfate granules in suspension speed the healing of endoscopic variceal sclerotherapy induced ulcer, especially deep and large ulcers.

Adult↗
PubMed1998

Case report: successful obliteration of a bleeding duodenal varix using endoscopic ligation.

The occurrence of duodenal varices is rare and experience in the control of haemorrhage from duodenal varices is limited. A 69-year-old man with hepatocellular carcinoma presenting with upper gastrointestinal bleeding is reported. Emergency upper gastrointestinal endoscopy indicated one varix 1.5 cm in diameter with white nipple sign at the anterior wall of the duodenal bulb. Endosonography confirmed the diagnosis of duodenal varix. The patient was treated with endoscopic ligation and follow-up endoscopy showed complete eradication of duodenal varix 3 weeks later.

Aged↗
PubMed1998

The effect of ciprofloxacin in the prevention of bacterial infection in patients with cirrhosis after upper gastrointestinal bleeding.

OBJECTIVES: Cirrhotic patients with upper gastrointestinal bleeding are prone to bacterial infection. The aim of this study was to investigate the efficacy of prophylactic intestinal decontamination with oral ciprofloxacin for the prevention of bacterial infections in cirrhotic patients with upper gastrointestinal bleeding. METHODS: A total of 120 cirrhotic patients with acute upper gastrointestinal bleeding were enrolled. Sixty patients received ciprofloxacin 500 mg twice daily given orally or through nasogastric tube immediately after upper gastrointestinal endoscopic examination; drug administration continued for 7 days. The remaining 60 patients, who received placebo, served as controls. RESULTS: The incidence of proven bacterial infection in the ciprofloxacin-treated group was significantly lower than that of placebo group (10% vs 45%, p < 0.001). The incidences of bacteremia, spontaneous bacterial peritonitis, and urinary tract infection in the ciprofloxacin-treated group were significantly lower than those in the placebo group (0% vs 23%, 3.3% vs 13%, and 5% vs 18%, respectively; p < 0.05, respectively). Multivariate logistic regression analysis showed that a lack of prophylactic treatment with ciprofloxacin and severity of cirrhosis were the independent significant predictors for cirrhotic patients with acute gastrointestinal bleeding with infection. CONCLUSIONS: Prophylactic intestinal decontamination with oral ciprofloxacin is effective in the prevention of bacterial infections in patients with cirrhosis who were suffering from acute upper gastrointestinal hemorrhage.

Acute Disease↗
PubMed1998

Can advanced hemostatic parameters detect disseminated intravascular coagulation more accurately in patients with cirrhosis of the liver?

BACKGROUND: Laboratory diagnosis of disseminated intravascular coagulation (DIC) is difficult in patients with cirrhosis of the liver due to the complicated hemostatic changes of DIC. More recently, newer molecular hemostatic markers have been used to improve the diagnosis of DIC. This study evaluated the ability of the more advanced hemostatic tests to diagnose DIC in patients with cirrhosis of the liver. METHODS: A series of hemostatic tests and parameters including activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), factor VIII assay, antithrombin (AT) activity, fibrinogen, plasminogen, protamine sulfate test (PST), fibrin (ogen) degradation product (FDP), D-dimer, thrombin-antithrombin complex (TAT) (measured by modified antithrombin, ATM), euglobulin lysis test (ELT) and platelet count were performed in 51 patients with cirrhosis of the liver. A diagnosis of DIC was made according to the following parameters and criteria: a) platelets less than 80 x 10(9)/l; b) PT greater than 1.5, c) APTT greater than 1.3; d) TT greater than 24 sec; e) AT less than 60%; f) ATM greater than 14.7 ng/ml (normal, mean +/- 3 SD); g) fibrinogen less than 1.50 g/l; h) positive PST; i) D-dimer greater than 1.0 microgram/ml; j) FDP greater than 20 micrograms/ml; k) ELT less than 150 min; l) plasminogen less than 50%. DIC was diagnosed if six or more of the above items were present, and at least two of them were item (a) to (h), and at least two were item (g) to (l). RESULTS: Although eight patients had results that fitted the diagnostic criteria of DIC by using the more advanced tests, only two of them were diagnosed with DIC by conventional testing. The concentration of factor VIII in these eight patients did not markedly decrease. CONCLUSIONS: New tests are not necessary to improve the diagnosis of DIC in patients with cirrhosis of the liver.

Adult↗
PubMed1997

Enhanced G-protein-induced relaxation in portal hypertensive rats: role of nitric oxide.

Portal hypertension (PHT) is characterized by splanchnic hyperemia due to a reduction in mesenteric vascular resistance. The reasons for the decreased resistance include an increased responsiveness to a vasodilator substance. Because the activation of an inhibitory guanine nucleotide regulatory (Gi) protein can result in endothelium-dependent relaxation, we tested the hypothesis that exaggerated Gi-protein induced relaxation via a nitric oxide (NO)-dependent pathway partly reflects the enhanced Gi-protein expression in PHT vessels. PHT was created in Sprague-Dawley rats by a partial portal-vein ligation. Control animals were sham operated. Using isolated vascular rings in the absence or presence of an intact endothelium, N(G)-nitro-L-arginine methyl ester (L-NAME), and pertussis toxin, dose response relationships for sodium fluoride (NaF; range, 0.1-4 mmol/L), a Gi protein activator, were determined in a cumulative manner. Gi-protein expression was determined by Western blotting. NaF caused a dose-dependent relaxation in both sham and portal hypertensive pre-contracted vessels, an effect that was significantly inhibited by pertussis toxin, endothelial denudation, and L-NAME. Concentrations of NaF greater than 4 mmol/L caused contractions, an effect that was unaffected by L-NAME. The NaF-induced relaxation response was significantly greater in PHT vessels as compared with sham concomitant with increased Gi-protein expression in PHT vessels. These data suggest that the enhanced endothelial Gi-protein-induced relaxation in PHT vessels may partly reflect enhanced expression of Gi-proteins in PHT vessels and may, thus, represent an important mechanism for exaggerated NO-dependent relaxation in the PHT vasculature.

Animals↗
PubMed1997

Hyperdynamic circulation of cirrhotic rats with ascites: role of endotoxin, tumour necrosis factor-alpha and nitric oxide.

1. Hyperdynamic circulation observed in portal hypertensive states is characterized by generalized vasodilation, increased cardiac index and increased systemic and regional blood flows. Endotoxin, tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) have been reported to be involved in the pathogenesis of hyperdynamic circulation, but the interactions between endotoxin, TNF-alpha and NO in cirrhotic rats with ascites have never been specifically addressed. 2. This study was designed to determine systemic and portal haemodynamics and plasma levels of endotoxin, TNF-alpha and nitrate/nitrite in cirrhotic rats with ascites and investigate the relationships between these substances. 3. Plasma concentrations of endotoxin, TNF-alpha and nitrate/nitrite (an index of NO production) were determined in 25 cirrhotic rats with ascites and 17 control rats using the Limulus assay, ELISA and a colorimetric assay respectively. In addition, haemodynamic studies were performed in another ten cirrhotic rats with ascites and ten control rats. 4. Cirrhotic rats with ascites had hyperdynamic circulation accompanied by increased plasma levels of endotoxin, TNF-alpha and nitrate/nitrite, as compared with control rats. Significant correlation existed between plasma levels of endotoxin and nitrate/ nitrite (r = 0.59, P < 0.0001) and between plasma levels of endotoxin and TNF-alpha (r = 0.63, P < 0.0001). No correlation was detected between plasma levels of TNF-alpha and nitrate/nitrite (r = 0.24, P > 0.05). 5. This study suggests that endotoxaemia developed in cirrhotic rats with ascites may stimulate NO formation directly or indirectly via cytokine cascade, and consequently participate in the development and/or maintenance of hyperdynamic circulation.

Animals↗
PubMed1997

Chronic administration of propranolol improves vascular contractile responsiveness in portal hypertensive rats.

Propranolol is used clinically as a prophylactic drug to prevent oesophageal variceal bleeding in cirrhotic patients with portal hypertension. Vascular hyporesponsiveness is a common characteristic of the portal hypertensive state. The present study aimed to investigate whether chronic administration of propranolol could improve vascular responsiveness in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL). Sham-operated rats served as controls. There were four study groups: PVL-propranolol group (portal hypertensive rats receiving propranolol), PVL-vehicle group (portal hypertensive rats receiving saline), sham-propranolol group (sham-operated rats receiving propranolol) and sham-vehicle group (sham-operated rats receiving saline). Propranolol (30 mg kg-1 day-1) or saline was given for 9 days via gastric gavage starting 1 day before ligation and thereafter. Then, the superior mesenteric artery was removed from each group for contractile study after haemodynamic measurement. In portal hypertensive rats, propranolol significantly alleviated the hyperdynamic state, including portal pressure, cardiac index and total peripheral resistance in the treated group compared with the vehicle group. The maximal contractile responses to KCl and vasopressin in mesenteric artery were significantly greater in the sham-vehicle group than in the PVL-vehicle group. Long-term propranolol treatment enhanced the contractile reactivity of mesenteric artery to KCl and vasopressin in PVL rats, and the contractile profiles were corrected towards those in sham-treated animals. In contrast, propranolol treatment decreased heart rate, mean arterial pressure and cardiac index but did not alter the contractile responsiveness of sham-operated rats. These results showed that, in portal vein stenosed rats, long-term treatment with propranolol improved arterial contractile reactivity together with portal pressure reduction. The propranolol effect on vascular reactivity is probably related to haemodynamic improvement, instead of a direct contractile effect on the vasculature.

Animals↗
PubMed1997

The hemodynamic effects of AT-112, an analog of ketanserin, in portal hypertensive rats.

A serotonin mechanism has been reported to contribute to the hyperdynamic circulation of portal hypertension. Different studies have demonstrated that serotonin antagonists decrease portal pressure in portal hypertensive patients and animals. The present study was undertaken to investigate the effect of AT-112, an analog of ketanserin, on portal hypertension induced by partial portal vein ligation in rats. Since ketanserin is known to possess alpha 1-adrenergic antagonistic activity, the effect of AT-112 was compared to that of prazosin. A single dose (prazosin 4.2 micrograms/kg, AT-112 1 mg/kg) was chosen to produce a similar hypotensive effect (-20 +/- 4% for prazosin and -24 +/- 4% for AT-112). At this dose, prazosin significantly decreased total peripheral resistance whereas AT-112 significantly decreased cardiac index and heart rate. Both agents significantly decreased the portal tributary blood flow and portal pressure. In rats receiving AT-112, a significant correlation was found between the magnitudes of decrease in cardiac index and the decrease in portal tributary blood flow. We also found that the magnitude of reduction in portal pressure was greater following AT-112 administration. This study suggested that AT-112 may have more beneficial hemodynamic effects than prazosin in portal hypertensive rats. Our results provide further support for the serotonergic mechanism in the pathogenesis of hyperdynamic circulation in portal hypertension.

Animals↗
PubMed1997

Hemodynamic studies and esophageal morphometric analyses in portal hypertensive rats with left adrenal vein ligation.

BACKGROUND: Despite many attempts to create esophageal varices in experimental animals, most of them have failed. This study investigated whether rats with partial portal vein ligation (PVL) and left adrenal vein ligation (LAL) develop hyperdynamic circulation and dilated esophageal submucosal veins as compared with sham-operated (Sham) plus LAL rats. METHODS: Two series of experiments were performed to measure (a) systemic and portal hemodynamics and (b) the cross-sectional area of esophageal submucosal veins in Sham, PVL, Sham plus LAL, and PVL plus LAL rats. Hemodynamic studies with a thermodilution technique and esophageal morphometric analyses were performed 14 days after the operation. RESULTS: PVL rats with or without LAL had a significantly lower mean arterial pressure and systemic vascular resistance accompanied by a significantly cardiac index and portal pressure than Sham rats with or without LAL (P < 0.05). LAL did not induce changes in mean arterial pressure, cardiac index, systemic vascular resistance, hear rate, or portal pressure in either Sham or PVL rats (P > 0.05). The mean cross-sectional area of esophageal submucosal veins in PVL rats with LAL (7340 +/- 833 microns2) was significantly larger than that in Sham rats with LAL (4236 +/- 556 microns2; P < 0.05). There was no significant difference in the mean cross-sectional area of esophageal submucosal veins between PVL and Sham rats without LAL. CONCLUSIONS: PVL rats with LAL developed hyperdynamic circulation similar to PVL rats without LAL. In addition, PVL plus LAL rats had larger esophageal submucosal veins than Sham plus LAL rats. This study shows that the esophageal submucosal veins of the 14-day partially portal vein-ligated rats with LAL resemble the structural abnormalities observed in human esophageal varices, suggesting that this model could be useful to investigate this entity.

Adrenal Glands↗
PubMed1997

Hyperdynamic circulation of cirrhotic rats: role of substance P and its relationship to nitric oxide.

BACKGROUND: It has been suggested that excessive formation of nitric oxide (NO) is responsible for the hyperdynamic circulation observed in portal hypertension. Substance P is a neuropeptide partly cleared by the liver and causes vasodilatation through the activation of the endothelial NO pathway. However, there are no previously published data concerning the plasma level of substance P in cirrhotic rats and its relationship to NO. METHODS: Plasma concentrations of substance P and nitrate/nitrite (an index of NO production) were determined in control rats and cirrhotic rats with or without ascites using an enzyme-linked immununosorbent assay and a colorimetric assay, respectively. In addition, systemic and portal hemodynamics were evaluated by a thermodilution technique and catheterization. RESULTS: Cirrhotic rats with and without ascites had a lower systemic vascular resistance (2.6 +/- 0.2 and 3.9 +/- 0.4 mmHg ml(-1) x min x 100 g body weight, respectively) and higher portal pressure (14.6 +/- 0.6 and 11.3 +/- 1.8 mmHg) than control rats (6.5 +/- 0.3 mmHg x ml(-1) x min x 100 g BW and 6.8 +/- 0.2 mmHg, respectively, P < 0.05), and cirrhotic rats with ascites had the lowest systemic vascular resistance. Plasma levels of nitrate/nitrite progressively increased in relation to the severity of liver dysfunction (control rats, 2.7 +/- 0.5 nmol/ml; cirrhotic rats without ascites, 5.6 +/- 1.3 nmol/ml; cirrhotic rats with ascites, 8.3 +/- 2.2 nmol/ml; P < 0.05). Cirrhotic rats with ascites displayed higher plasma values of substance P (57.7 +/- 5.9 pg/ml) than cirrhotic rats without ascites (37.9 +/- 3.1 pg/ml, P < 0.05) and control rats (30.1 +/- 1.0 pg/ml, P < 0.05). There was no significant difference in plasma substance P values between control rats and cirrhotic rats without ascites (P > 0.05). No correlation was found between plasma levels of substance P and nitrate/nitrite (r = 0.318, P > 0.05). CONCLUSIONS: Excessive formation of NO may be responsible, at least partly, for the hemodynamic derangements in cirrhosis. Although substance P may not participate in the initiation of a hyperdynamic circulation in cirrhosis, it may contribute to the maintenance of the hyperdynamic circulation observed in cirrhotic rats with ascites.

Analysis of Variance↗
PubMed1997

Plasma substance P levels in patients with liver cirrhosis: relationship to systemic and portal hemodynamics.

OBJECTIVES: Nitric oxide has been proposed as being responsible for the hyperdynamic circulation observed in portal hypertensive states. Substance P, a neuropeptide partly cleared by liver, induces vasodilation through the activation of the endothelial nitric oxide pathway. This study investigated the plasma levels of substance P in cirrhotic patients and the relationship of these levels to systemic and portal hemodynamics. METHODS: Sixty-four patients with cirrhosis and 53 healthy controls had blood samples taken for determining plasma values of substance P by ELISA. Systemic and portal hemodynamics were measured on the same day of blood sampling using a Swan-Ganz catheterization and thermodilution technique. RESULTS: Plasma levels of substance P were higher in cirrhotic patients than in healthy controls (45.7 +/- 2.0 vs 32.9 +/- 1.0 pg/ml, p < 0.001) and directly correlated with Child-Pugh's score (r = 0.52, p < 0.0001). Compared with compensated cirrhotic patients, decompensated cirrhotic patients had higher plasma levels of substance P accompanied by a lower systemic vascular resistance and higher hepatic venous pressure gradient. There was no significant correlation between plasma levels of substance P and systemic vascular resistance and hepatic venous pressure gradient. In addition, no significant difference in plasma levels of substance P was observed between cirrhotic patients with and cirrhotic patients without a hepatic venous pressure gradient > 12 mm Hg or between patients with and patients without large esophageal varices. CONCLUSIONS: Plasma levels of substance P are increased in patients with cirrhosis and may contribute to the pathogenesis and/or maintenance of hyperdynamic circulation in decompensated patients. The severity of cirrhosis is more important than portal hypertension and the severity of esophageal varices for the development of increased plasma substance P levels.

Female↗
PubMed1997

Sequential changes of esophageal motility after endoscopic injection sclerotherapy or variceal ligation for esophageal variceal bleeding: a scintigraphic study.

OBJECTIVE: Endoscopic injection sclerotherapy and variceal ligation are two popular endoscopic methods used to treat esophageal variceal hemorrhage. These two methods have not been compared with regard to esophageal dysfunction after treatment. This is a prospective investigation of esophageal dysmotility after endoscopic injection sclerotherapy and variceal ligation. METHODS: Sequential changes of esophageal motility after endoscopic injection sclerotherapy (n = 25) and variceal ligation (n = 25) were investigated in 50 cirrhotic patients with recent variceal bleeding. Another 22 cirrhotics without esophageal varices were included as controls. Radionuclide esophageal transit tests were performed before initial endoscopic treatment, and 1 and 3 months after variceal eradication. RESULTS: The baseline esophageal transit time was longer in both the sclerotherapy (n = 25, 7.8 +/- 1.4 s) and ligation groups (n = 25, 8.2 +/- 1.8 s) than in controls (n = 22, 6.7 +/- 0.7 s, p < 0.005). The transit time was longer in patients with large varices than in those with small varices (8.3 +/- 1.7 vs. 7.2 +/- 0.7 s, p < 0.05). In the sclerotherapy group, the transit time was prolonged 1 month after variceal eradication, compared with its pretreatment state (n = 20, 7.6 +/- 1.5 vs. 10.0 +/- 2.2 s, p < 0.0001) but was shortened at 3 months compared with 1 month after variceal eradication (n = 12, 10.7 +/- 1.5 vs. 8.6 +/- 2.2 s, p < 0.05). Multiple regression analysis showed that the number of treatment sessions required to eradicate varices was the only significant factor associated with prolonged transit time (p < 0.05). In the ligation group, the transit time changed little at 1 month or 3 months after variceal eradication. CONCLUSIONS: Impairment of esophageal motility can be significant with endoscopic injection sclerotherapy but is reversible. However, endoscopic variceal ligation exerts no significant impact on esophageal motility.

Esophageal and Gastric Varices↗
PubMed1996

Effects of long-term administration of octreotide in portal vein-stenosed rats.

The hemodynamic effects of long-term administration of octreotide in portal hypertension has not been established. In addition, whether long-term octreotide treatment prevents the development of portosystemic shunts has not yet been evaluated. Hence, the current study was undertaken to evaluate the effects of long-term administration of octreotide in rats with portal vein stenosis. Immediately after portal vein stenosis or sham operation, rats were given either a long-term octreotide administration of 100 micrograms/kg or a placebo every 12 hours by subcutaneous injection for 14 consecutive days. Systemic hemodynamics and regional blood flows, degree of mesenteric-systemic shunts, and plasma glucagon concentrations were measured after the final dose of octreotide or placebo. A fifth group of portal vein-stenosed rats received hemodynamic and plasma glucagon measurements after 1-day octreotide treatment given at 14 days after surgery. Long-term octreotide treatment modified the hyperdynamic circulation without affecting the degree of mesenteric-systemic shunts, and 1-day octreotide treatment decreased portal tributary blood flow without affecting the portal pressure, systemic hemodynamics, and degree of mesenteric-systemic shunts. Plasma glucagon levels were decreased in portal vein-stenosed rats receiving either long-term or 1-day octreodtide compared with rats receiving placebo. In contrast, chronic octreotide treatment did not affect any of the hemodynamic values or plasma glucagon levels in sham-operated rats. In conclusion, long-term administration of octreotide modified in part the development of portal hypertension and hyperdynamic circulation in portal vein-stenosed rats without affecting the degree of mesenteric-systemic shunts.

Analysis of Variance↗
PubMed1996

Effect of octreotide on total effective vascular compliance in patients with posthepatitic cirrhosis.

BACKGROUND/AIMS: This study aimed to evaluate the effect of octreotide on total effective vascular compliance, measured during rapid volume expansion, in patients with posthepatitic cirrhosis. METHODS: Twenty-nine patients with posthepatitic cirrhosis were randomly assigned to receive a 100-micrograms/h infusion of octreotide after a 100-micrograms bolus (n = 15), or a placebo (n = 14). Hemodynamic measurements were recorded before and 30 min after drug administration. Thereafter, rapid volume expansion was performed in each patient and hemodynamic measurements were repeated immediately after volume expansion. RESULTS: Before volume expansion, placebo administration did not affect any of the hemodynamic values, while the hepatic blood flow was significantly decreased following octreotide administration. After volume expansion, the hemodynamic changes were similar between patients receiving octreotide and the placebo. However, the increase in right atrial pressure from the beginning to the end of volume expansion was higher and the total effective vascular compliance was lower in patients receiving octreotide (+3.5 +/- 0.3 mmHg, p = 0.05 and 1.69 +/- 0.16 ml.mmHg-1.kg-1, p < 0.05) compared to patients receiving placebo (+2.5 +/- 0.3 mmHg, 2.60 +/- 0.34 ml.mmHg-1.kg-1). CONCLUSIONS: The present study suggests that octreotide decreased total effective vascular compliance in patients with posthepatitic cirrhosis. It is possible that, in patients with posthepatitic cirrhosis, venoconstriction was induced following octreotide administration.

Aged↗
PubMed1996

Prevalence of gastric ulcer in cirrhotic patients and its relation to portal hypertension.

The prevalence of gastric ulcer and its relationship to the severity of cirrhosis and degree of portal hypertension was evaluated in 245 cirrhotic patients, and compared with 245 age- and sex-matched healthy subjects. Portal and systemic haemodynamic studies were performed in cirrhotic patients. The prevalence of gastric ulcer in cirrhotic patients was 20.8%, which was significantly higher than the 4.0% found in healthy controls. Using a multivariate logistic regression model, the hepatic venous pressure gradient was found to be the only predictor of the prevalence of gastric ulcer in cirrhotic patients to present with gastric ulcer. The hepatic venous pressure gradient was significantly higher in cirrhotic patients with gastric ulcer than in those without (17.3 +/- 4.4 vs 15.5 +/- 5.0 mmHg, P = 0.01). Other variables, including sex, smoking, cardiac output and severity or aetiology of cirrhosis did not show significant differences between the two patient groups. The prevalence of gastric ulcer in cirrhotic patients whose hepatic venous pressure gradient was below 12 mmHg (4.5%) was similar to that observed in the healthy controls (4.0%). However, when the hepatic venous pressure gradient was > 12 mmHg, the prevalence of gastric ulcer (24.4%) was significantly higher than that in control subjects. However, the incidence of gastric ulcer was not related to the degree of portal hypertension. In conclusion, the prevalence of gastric ulcer in cirrhotic patients was found to be significantly higher than in the age- and sex-matched healthy subjects. Portal hypertension with a hepatic venous pressure gradient > 12 mmHg may be an important factor contributing to the increased prevalence of gastric ulcer observed in patients with liver cirrhosis.

Case-Control Studies↗