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Biomedical subjects

F Y Lee

Publications and source records attributed to F Y Lee.

At least 163 records · Page 9Linked to original sources
PubMed1995

YC-1 inhibited human platelet aggregation through NO-independent activation of soluble guanylate cyclase.

1. Our previous study demonstrated that YC-1, a derivative of benzylindazole, is a novel activator of soluble guanylate cyclase (sGC) in rabbit platelets. This work investigated whether the antiplatelet effect of YC-1 was mediated by a nitric oxide (NO)/sGC/cyclic GMP pathway in human platelets. 2. In human washed platelets, YC-1 inhibited platelet aggregation and ATP released induced by U46619 (2 microM), collagen (10 micro ml(-1)) and thrombin (0.1 u ml(-1)) in a concentration-dependent manner with IC50 values of (microM) 2.1 +/- 0.03, 11.7 +/- 2.1 and 59.3 +/- 7.1, respectively. 3. In a 30,000 g supernatant fraction from human platelet homogenate, YC-1 (5-100 microM) increased sGC activity in a concentration-dependent manner. At the same concentration-range, YC-1 elevated cyclic GMP levels markedly, but only slightly elevated cyclic AMP levels in the intact platelets. 4. MY-5445, a selective inhibitor of cyclic GMP phosphodiesterase, potentiated the increases in cyclic GMP caused by YC-1, and shifted the concentration-anti-aggregation curve of YC-1 to the left. In contrast, HL-725, a selective inhibitor of cyclic AMP phosphodiesterase, did not affect either the increases in cyclic nucleotides or the anti-aggregatory effect caused by YC-1. 5. Methylene blue, an inhibitor of sGC, blocked the increases of cyclic GMP caused by YC-1, and attenuated markedly the anti-aggregatory effect of YC-1. The adenylate cyclase inhibitor, 2',5'-dideoxyadenosine (DDA) did not affect YC-1-induced inhibition of platelet aggregation. 6. Haemoglobin, which binds NO, prevented the activation of sGC and anti-aggregatory effect caused by sodium nitroprusside, but did not affect YC-1 response. 7. These results would suggest that YC-1 activates sGC of human platelets by a NO-dependent mechanism, and exerts its antiplatelet effects through the sGC/cyclic GMP pathway.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

The effects of chronic administration of indomethacin and misoprostol on renal function in cirrhotic patients with and without ascites.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) often cause renal dysfunction in cirrhotic patients with ascites through inhibition of prostaglandin synthesis. However, their renal effects in cirrhotic patients without ascites are controversial. In addition, the role of prostaglandins in cirrhotic patients with ascites and in non-ascitic cirrhotic patients receiving NSAIDs also remains elusive. Thus we evaluated the chronic renal effects of indomethacin and misoprostol in 9 cirrhotic patients with ascites (protocol 1) and 21 cirrhotic patients without ascites (protocol 2). METHODS: The patients of protocol 1 received 200 micrograms of misoprostol every 6 h for 7 consecutive days. In protocol 2, 11 patients received 25 mg indomethacin three times a day for 7 consecutive days. The other 10 patients received 25 mg indomethacin three times a day plus 200 micrograms misoprostol every 6 h for 7 consecutive days. Renal function tests, plasma renin activity, and plasma aldosterone concentration were measured before and after treatment. RESULTS: In protocol 1, misoprostol tended to reduce the urinary sodium excretion (p = 0.08). In protocol 2, indomethacin alone greatly impaired renal plasma flow (p < 0.05), creatinine clearance (p < 0.05), blood urea nitrogen (p < 0.05), and serum creatinine (p = 0.06) in 11 patients. Similar magnitudes of renal dysfunction were observed in the other 10 patients despite the concomitant misoprostol treatment. CONCLUSION: Chronic administration of misoprostol may have caused a negative natriuretic effect in cirrhotic patients with ascites. In cirrhotic patients without ascites chronic administration of indomethacin may induce a renal dysfunction that cannot be reversed by misoprostol.

Aged↗
PubMed1995

Comparison of endoscopic variceal injection sclerotherapy and ligation for the treatment of esophageal variceal hemorrhage: a prospective randomized trial.

To determine the efficacy of endoscopic variceal sclerotherapy (EVS) and ligation (EVL) in the management of esophageal variceal bleeding, 134 cirrhotic patients were randomized to receive either treatment. The clinical and endoscopic characteristics were similar in both groups. Active bleeding was controlled with ligation (20 of 20) as efficiently as with sclerotherapy (14 of 16). Elective sclerotherapy consumed less time than ligation (7.9 +/- 1.8 minutes vs. 11.5 +/- 2.7 minutes, P < .001), but there was no difference between emergent sclerotherapy (14.5 +/- 5.8 minutes) and ligation (14.9 +/- 4.1 minutes). Ligation reduced one grade of variceal size more quickly than sclerotherapy (1.1 +/- 0.4 vs. 2.0 +/- 1.7 session, P < .001). The rebleeding rate was lower with ligation (13 of 67 vs. 28 of 67, P < .01). Esophageal ulcer was the most common source of rebleeding. Recurrence of varices appears more probable with ligation (P = .079). The complication rate was higher with sclerotherapy (15 of 67 vs. 3 of 67, P < .01), with esophageal stricture being the most common cause. Survival rate was the same in both groups even after stratifying patients into good and poor hepatic reserve groups. Hepatic failure was the major cause of death, followed by exsanguination. In summary, EVL was superior to EVS regarding rebleeding and complications but not in other aspects such as time consumption in elective treatment and recurrence of varices. Substantial results for long-term follow-up are required before conclusion of the treatment of choice.

Esophageal and Gastric Varices↗
PubMed1995

Prevalence of duodenal ulcer in cirrhotic patients and its relation to Helicobacter pylori and portal hypertension.

BACKGROUND: The prevalence of duodenal ulcer increases in cirrhotic patients. However, the pathogenesis remains unclear. METHODS: The prevalence of duodenal ulcer and their relationship to cirrhosis and portal hypertension were evaluated in 325 cirrhotic patients, and compared with 325 age- and sex-matched healthy subjects. Portal and systemic hemodynamic studies were performed in all cirrhotic patients. Histological examination of gastric antral mucosa for Helicobacter pylori (H. pylori) was performed in 16 cirrhotic patients with duodenal ulcer and in 34 cirrhotic patients without duodenal lesions. RESULTS: The prevalence of duodenal ulcer in cirrhotic patients was 9.5% (31 out of 325), significantly higher than 4.0% (13 out of 325) in the healthy controls (p = 0.007), but was not related to the severity of liver cirrhosis. The positive rate of H. pylori was not different between cirrhotic patients with duodenal ulcer and those without duodenal lesions (9/16 vs. 18/34, p > 0.05). The hepatic venous pressure gradient was also not different between these groups (17.2 +/- 5.1 vs. 16.1 +/- 4.9 mmHg, p > 0.05). Other variables including sex, smoking, and etiology of cirrhosis did not show significant differences. CONCLUSIONS: The prevalence of duodenal ulcer is significantly higher in cirrhotic patients than in the age- and sex-matched healthy subjects. The severity of cirrhosis, the presence of H. pylori or portal hypertension per se does not play an important role in the increased prevalence of duodenal ulcer in cirrhotic patients.

Duodenal Ulcer↗
PubMed1995

Comparative effects of strophanthidin in tilapia and human heart tissues.

It is well documented that the cardiotonic steroid strophanthidin increases myocardial contractile force through an inhibition of the sarcolemmal Na(+)-K+ pump in mammalian heart cells. The aim of the present study was to determine the effect of this digitalis substance on action potential and contraction in cardiac tissues obtained from a cultured freshwater fish tilapia (Oreochromis sp.) and compare with those observed in human heart tissues obtained at cardiac surgery. In tilapia atria superfused at 25 degrees C 1-2 microM strophanthidin shortened the spontaneous cycle length while increased progressively the twitch force. In tilapia ventricular tissues, strophanthidin also increased the force but shortened the APD50. When temperature of the superfusate was elevated from 25 to 37 degrees C, strophanthidin induced a smaller positive or even negative inotropic effect but increased significantly the diastolic tension through an inhibition of the relaxation process. High temperature also facilitated the occurrence of delayed afterdepolarizations, repetitive slow response action potentials and episodes of contracture. The same concentration of stroph induced rather sustained positive inotropic effects without deteriorating actions in human ventricular trabeculae driven at 37 degrees C. In human atrial trabeculae, however, 2 microM strophanthidin readily induced abnormal automatic and triggered rhythms along with the positive inotropy. The present findings provide the functional evidence for the presence of sarcolemmal Na+, K(+)-pump in fish myocardial fibers. The major differences in the electro-mechanical actions of strophanthidin in tilapia versus human heart tissues are the smaller positive inotropy and the proneness to contracture in tilapia heart at 37 degrees C.

Action Potentials↗
PubMed1995

Interaction of phosphodiesterase inhibitor and isoproterenol in human and guinea-pig ventricular tissues and myocytes.

We studied the interaction of phosphodiesterase inhibitor and isoproterenol in human and guinea-pig ventricular muscle fibers and guinea-pig ventricular myocytes. In ventricular trabeculae obtained from the explanted hearts of 5 patients with dilated cardiomyopathy, isoproterenol (Iso, 10(-8)-10(-6)M) increased twitch force in a concentration-dependent manner. Isobutylmethyl-xanthine (IBMX, 3 x 10(-6)M) alone did not change significantly the twitch force but potentiated the effect of Iso and reduced the concentration for half maximal effect (EC50) of Iso from 140 to 18 x 10(-9)M. As compared to the diseased human heart tissues, papillary muscles obtained from 6 healthy guinea-pigs were much more sensitive to the positive inotropic action of Iso but less reactive to the potentiative effect of IBMX on Iso. The EC50 for the inotropic action of Iso (10(-9) approximately 10(-7)M) in the absence and presence of 3 x 10(-6)M IBMX were 28 and 15 x 10(-9)M, respectively. In 16 guinea-pig ventricular myocytes isolated enzymatically, L-type Ca currents (ICa,L) were recorded in K-free superfusate with whole-cell voltage-clamp technique. The increase in ICa,L induced by the lowest concentration (10(-9)M) of Iso was not significant. Those induced by 10(-8)M and 10(-7)M Iso were about the same (+108 +/- 29% and +75 +/- 20%, respectively). IBMX potentiated the effect of Iso. It is concluded that indeed the ventricular muscles obtained from the failing hearts are poorly responsive to the beta-adrenoceptor agonist. This defect could be corrected at least partially by the PDE inhibitor IBMX. However, the concentration-dependent inotropic and arrhythmogenic effects in guinea-pig ventricular muscle were not accompanied by a parallel increase in iCaL at high concentration of Iso(10(-7)M), suggesting involvement of other mechanisms such as actions on intracellular Ca2+ regulation induced by Iso.

1-Methyl-3-isobutylxanthine↗
PubMed1995

A model of experimental acute necrotizing pancreatitis.

BACKGROUND: A model of moderate acute necrotizing pancreatitis is essential for the study of the pathophysiology of the disease and novel therapies. We tried to establish a model of bile salt-induced acute necrotizing pancreatitis in rats. METHODS: Acute pancreatitis was induced by retrograde infusion of bile salt into the cannulated pancreatobiliary duct. Twenty-six rats wee divided into 3 groups. Group I (n = 8) received 0.2 ml of glycodeoxycholic acid (GDOC) 10 mmol/l; group II (n = 10) 0.2 ml of 2.5% sodium taurodeoxycholate (NaTDC); group III (n = 8) the mixture of 0.2 ml GDOC 10 mmol/l and 10 U enterokinase. Serum levels of amylase and lipase, hematocrit, mean arterial pressure and heart rate were determined at baseline and 5 hours later. Then the pancreas was removed for histopathology and grading (0-3; absent-severe) with regard to leukocyte infiltration, edema, necrosis, hemorrhage and acinar cell vacuolization. RESULTS: Serum levels of amylase and lipase increased significantly in 5 hours in all the groups. Serum amylase levels were significantly lower in group III than in group II. No significant difference of serum lipase was found among the groups. Group II had the highest scores of necrosis and acinar cell vacuolization, whereas group III had the highest scores of leukocyte infiltration and edema. The degree of necrosis was significantly more severe in group II than in group I. The hematocrit increased significantly in 5 hours in groups I and II. The mean arterial pressure in 5 hours decreased significantly in group I. There was no significant difference of the changes of heart rate in 5 hours among 3 groups. CONCLUSIONS: Intraductal infusion of NaTDC was a good method to induce moderate acute necrotizing pancreatitis in rats. GDOC caused mild pancreatitis, and pancreatic injury was aggravated when enterokinase was added. The severity of pancreatic histopathology was not correlated with the changes of serum levels of pancreatic enzymes, hematocrit or mean arterial pressure at the early stage of pancreatitis.

Acute Disease↗
PubMed1994

YC-1, a novel activator of platelet guanylate cyclase.

YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole] inhibited the aggregation of and ATP release from washed rabbit platelets induced by arachidonic acid (AA), collagen, U46619, platelet-activating factor (PAF), and thrombin in a concentration-dependent manner. YC-1 also disaggregated the clumped platelets caused by these inducers. The thromboxane B2 formation caused by collagen, PAF, and thrombin was inhibited by concentrations of YC-1 that did not affect formation of thromboxane B2 and prostaglandin D2 caused by AA. YC-1 suppressed the increase of intracellular Ca2+ concentration and generation of inositol 1,4,5-trisphosphate caused by these five aggregation inducers. Both the cAMP and cGMP contents of platelets were increased by YC-1 in a concentration- and time-dependent manner. Like sodium nitroprusside, YC-1 potentiated formation of cAMP caused by prostaglandin E1 but not that by 3-isobutyl-1-methylxanthine. Adenylate cyclase and cAMP phosphodiesterase activities were not altered by YC-1. Activity of cGMP phosphodiesterase was unaffected by YC-1. Activities of guanylate cyclase in platelet homogenate and cytosolic fraction were activated by YC-1, whereas particulate guanylate cyclase activity was unaffected. The antiplatelet effect of sodium nitroprusside but not that of YC-1 was blocked by hemoglobin and potentiated by superoxide dismutase. After intraperitoneal administration for 30 minutes, YC-1 prolonged the tail bleeding time of conscious mice. These data indicate that YC-1 is a direct soluble guanylate cyclase activator in rabbit platelets. It may also possess antithrombotic potential in vivo.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Insulin-like growth factor I regulation of Swarm rat chondrosarcoma chondrocytes in culture.

Insulin-like growth factor I (IGF-I) is anabolic for chondrocytes and is thought to be important in regulating such normal cartilaginous tissues as the epiphyseal growth plate. In the present studies, we have investigated the role of IGF-I in the regulation of neoplastic cartilage. Chondrocytes cultured from a transplantable rat chondrosarcoma were analyzed for responsiveness to IGF-I with respect to DNA and glycosaminoglycan synthesis as determined by labeling with radioactive thymidine and sulfate, respectively. Stimulation of [3H]thymidine and [35S]sulfate incorporation by IGF-I was two to four times that in serum-free controls, with half-maximal stimulation at 1 x 10(-9) M. The efficacy of IGF-I was approximately one-half of that of serum in stimulating [3H]thymidine incorporation and was comparable to that of serum for [35S]sulfate incorporation. When Swarm rat chondrosarcoma chondrocytes were cultured in the presence of IGF-I and exposed to graded concentrations of anti-IGF-I antibody, [3H]thymidine incorporation and [35S]sulfate incorporation were attenuated in a dose-dependent fashion to 29 and 25% of antibody-free controls, respectively. Nonspecific antibody not raised against IGF-I was not inhibitory. These observations suggest that the majority of IGF-I action on these cells is susceptible to immunoinhibition. To estimate the contribution of IGF-I to the regulation of these cells by serum, Swarm rat chondrosarcoma chondrocytes were cultured with graded concentrations of either calf serum or fetal calf serum in the presence of anti-IGF-I antibody, nonspecific antibody, or no other additives. Specific antibody attenuated the effect of calf serum on both [3H]thymidine and [35S]sulfate incorporation with overall inhibition of 52% (P < 0.01) and 48% (P < 0.001), respectively. Nonspecific antibody super-imposed small, variably stimulatory or inhibitory effects on those of calf serum. When chondrosarcoma chondrocytes were incubated with fetal calf serum, anti-IGF-I antibody exerted a minimal inhibitory effect, reducing both [3H]thymidine and [35S]sulfate incorporation by less than 25%. The immunoinhibition of both pre- and postnatal serum could be overcome in a dose-dependent fashion by increasing serum concentrations. These results suggest that the factors influencing Swarm rat chondrosarcoma chondrocytes may be developmentally regulated and that the contribution of IGF-I to the action of serum increases between fetal and post-natal life. These data support the hypothesis that chondrosarcoma is a somatomedin-responsive neoplasm and suggest that this tumor may be susceptible to interventions directed toward mechanisms that block insulin-like growth factor action.

Animals↗
PubMed1994

Cytogenetic studies, ras mutation, and clinical characteristics in primary myelodysplastic syndrome. A study on 68 Chinese patients in Taiwan.

Cytogenetics and clinical features were studied for 68 Chinese patients with primary myelodysplastic syndrome (MDS). Ras mutation was analyzed in 25 of them. Thirty-four patients (50%) had clonal chromosomal abnormalities at initial analysis. The most common cytogenetic aberrations were -7, +8, 5q-, and 20q-, which occurred in 11 (16.2%), seven (10.3%), five (7.4%) and three patients, respectively. The incidence of -7 was higher and that of 5q- lower in our patients than in patients from most other geographic areas. The 17 patients with multiple chromosomal abnormalities had a significantly shorter median survival (9 months) than the 34 patients with normal karyotype (33 months) and the 17 patients with patients with single anomalies (26 months). Evolution to acute leukemia occurred in 20 patients (29%) after a median interval of 8 months following the diagnosis. Patients with multiple cytogenetic changes at initial analysis or in subsequent studies had a significantly higher frequency of acute transformation than others (55% vs. 18.6%, p = 0.007); the same was not true if only the data of initial study were considered. Serial cytogenetic studies are important in patient follow-up. N-ras mutation was detected in 5 (20%) of 25 patients within the study. There was no correlation between the gene mutation and acute transformation. But combing the data of N-ras mutation and cytogenetics, patients with either the N-ras mutation or clonal chromosomal abnormalities were at significantly higher risk for developing acute leukemia than those with neither of the changes (77% vs. 25%).

Adolescent↗
PubMed1994

Effects of octreotide on postprandial systemic and hepatic hemodynamics in patients with postnecrotic cirrhosis.

The effects of octreotide on postprandial hemodynamic responses were evaluated in 20 patients with postnecrotic cirrhosis. They were randomly assigned to receive either a 100-micrograms bolus with a 100-micrograms/h infusion of octreotide or a placebo. Placebo administration did not affect any of the hemodynamic values. However, after a liquid meal of 500 kcal, postprandial increases in the hepatic venous pressure gradient and hepatic blood flow were observed in patients receiving placebo, while the systemic hemodynamic values remained unchanged. In contrast, in patients receiving octreotide, the hepatic blood flow was significantly decreased 30 min after administration, while the hepatic venous pressure gradient and the systemic hemodynamic values were not affected. After ingestion of a meal, the mean values of the hepatic blood flows were not significantly different from basal values. Moreover, the wedged hepatic venous pressure, the hepatic venous pressure gradient and the systemic hemodynamic values were not affected by meal ingestion. However, during octreotide infusion, hepatic blood flow 30 min after the meal had a tendency to increase compared to before the meal. In conclusion, octreotide inhibited the postprandial increase in portal pressure in patients with postnecrotic cirrhosis. In addition, octreotide decreased hepatic blood flow in the fasting state. When given before a meal, the increase in blood flow induced by the meal restored the hepatic blood flow to basal levels.

Adult↗
PubMed1994

A double-blind randomized controlled trial of colchicine in patients with hepatitis B virus-related postnecrotic cirrhosis.

The preliminary results of a prospective double-blind controlled trial of colchicine in 100 patients with hepatitis B virus-related cirrhosis are reported. The patients, 94 males and 6 females, aged 32-80, were assigned to receive either 1 mg of colchicine or an identical placebo orally on a daily basis. The duration of the follow up ranged from 15 to 51 months (median 26 months). Seventy percent had histological proof of cirrhosis. On entry, 80 patients were in Child-Pugh class A, 19 were in class B, and one was in class C. Compared to the placebo group, there was no improvement in the colchicine group after a 24-month follow up in any of the biochemistry data, for example, serum albumin, alkaline phosphatase, alanine and aspartate aminotransferase, bilirubin, and prothrombin time. The difference in the cumulative survival rates at 51 months did not reach statistical significance (p = 0.8) in either group. There was no histological improvement in 30 patients who were willing to undergo repeated liver biopsies. No trend toward improvement of the hepatic pressure gradient was observed in these patients. The serum levels of aminopropeptide of type III procollagen increased significantly in patients in both groups after 24 months of therapy (1.07 +/- 0.06 vs. 1.36 +/- 0.06 U/ml in the colchicine group, 0.93 +/- 0.09 vs. 1.25 +/- 0.07 U/ml in the placebo group; p < 0.05). In addition, neither the clinical deterioration of cirrhosis nor death was prevented in patients receiving colchicine therapy. This report indicates that colchicine has no effect in the treatment of HBV-related postnecrotic cirrhosis.

Adult↗
PubMed1994

Endoscopic injection for the treatment of bleeding ulcers: local tamponade or drug effect?

Fifty-two patients with Forrest Ia or Ib bleeding ulcers were randomized to receive endoscopic injection therapy with either 1:10,000 epinephrine in water (Group I) or distilled water (Group II). Twenty-five out of 27 patients in group I, versus 22 out of 25 patients in group II, achieved initial hemostasis after endoscopic injection therapy (p > 0.05). Five patients who did not respond to local injection had bleeding controlled by heater probe thermocoagulation or surgical intervention. Three patients in each group developed rebleeding after initial hemostasis. Four of these patients had bleeding controlled by surgical intervention, while the other two died of underlying diseases. No change in systemic blood pressure, but a significant drop in the pulse rate were noted in both groups after injection therapy. Patients with shock at admission or ulcer size greater than 2 cm had a significantly higher rebleeding rate after initial hemostasis than patients with normal blood pressure and ulcers under 2 cm (p < 0.05). No serious complications were observed after injection therapy, and no significant difference in the amounts of solution required for successful hemostasis was noted between the two groups. We conclude that a local tamponade with distilled water is as effective and safe as diluted epinephrine solution for endoscopic injection therapy.

Double-Blind Method↗
PubMed1994

Study on the vascular reactivity and alpha 1-adrenoceptors of portal hypertensive rats.

1. Vascular hyporesponsiveness in portal hypertension has been demonstrated to various vasoconstrictors including noradrenaline (NA). The present study aimed to determine whether the attenuated vascular responsiveness to NA is due to a change in the affinity or the number of alpha 1-adrenoceptors. 2. Partial portal vein ligation (PVL) was performed in Sprague-Dawley rats to produce portal hypertension. Vascular responsiveness to NA was assayed in portal vein, mesenteric artery or tail artery. The affinity and number of alpha 1-adrenoceptors were determined by specific binding of [125I]-HEAT (2-beta-4-hydroxy-3-iodophenyethyl-aminomethyltetralone). 3. In the presence of yohimbine (10(-7) M, an alpha 2-adrenoceptor antagonist), propranolol (10(-6) M, a beta-adrenoceptor antagonist), and two catecholamine uptake inhibitors, desipramine (10(-7) M) and normetanephrine (10(-6) M), the maximum responses to NA were decreased in all three blood vessels of PVL rats: 45% decrease in portal vein, 25% in mesenteric artery and 18% in tail artery. 4. The EC50 values of NA and the pA2 values of prazosin, an alpha 1-adrenoceptor antagonist, in all three blood vessels were not significantly different between sham-operated and PVL rats. 5. The KD and Bmax values for specific binding of [125I]-HEAT or the Ki values for NA in the crude membrane preparations of either mesenteric artery or tail artery were also not significantly different between the two groups. 6. It is concluded that the vascular hyporesponsiveness to NA in the mesenteric artery or tail artery of PVL rats is not due to changes in the affinity or number of alpha 1-adrenoceptors.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

Clinical courses and predictors for rebleeding in patients with peptic ulcers and non-bleeding visible vessels: a prospective study.

Detailed characterisation of non-bleeding visible vessels in terms of colour, size evolution, and time of rebleeding is important in determining the natural history of these lesions. The colour and size of non-bleeding visible vessels were observed endoscopically every day for three days and then every other day until rebleeding or flattening of visible vessels occurred in 140 patients. Rebleeding happened in 61 (44%) patients. Of them, 59 (97%) rebled within 72 hours. Flattening of visible vessels happened in 79 (56%) patients and 77 of 79 (98%) had flattening of visible vessels within 72 hours. Rebleeding rate increased with increasing length of exposed vessels (r = 0.96, p < 0.001). Coffee ground fluid or blood retention in the stomach and ulcer size > or = 2.0 cm were independent predictors for rebleeding using multivariate analysis. It is suggested that patients with non-bleeding visible vessels and independent predictors for rebleeding may need early aggressive treatment.

Adult↗
PubMed1994

Nitric oxide modulates hepatic vascular tone in normal rat liver.

This study investigated whether nitric oxide (NO) plays a role in the intrahepatic portal circulation in normal rat livers perfused in situ. N omega-nitro-L-arginine (NNA), a specific NO biosynthesis inhibitor, significantly increased baseline portal pressure compared with controls (P < 0.05). Concentration-effect curves to norepinephrine (NE) were performed. Perfusate flow was maintained as constant, and perfusion pressure was continuously measured. NNA markedly enhanced the responsiveness to NE. This effect was abolished by the addition of L-arginine, a specific NO substrate. Presence of indomethacin did not alter the response to NE. The response to NE in the presence of indomethacin and NNA was significantly more than the response to NE in the presence of NNA alone. In vivo, intraportal infusion of NNA significantly enhanced the portal pressure compared with vehicle. This study demonstrates that NO contributes to the basal vascular tone and attenuates the response to NE in intrahepatic portal vascular bed of normal rats. These results support a functional role of NO in the regulation of the intrahepatic portal circulation in normal rats. This study also suggests a synergistic, albeit limited, role of prostacyclin in the intrahepatic circulation.

Animals↗
PubMed1994

Characteristics of patients with bleeding peptic ulcer requiring emergency endoscopy and aggressive treatment.

OBJECTIVES: Patients with an ulcer and active bleeding or a nonbleeding, visible vessel are high-risk for further bleeding and should receive aggressive therapy. In this study, we tried to identify clinical parameters that predict these high-risk groups. METHODS: Over a 7-month period, 16 clinical parameters were analyzed prospectively in 316 patients with bleeding peptic ulcer. A multivariate analysis was used to find the independent predictors for the high-risk patients. RESULTS: A total of 114 patients (36%) was found to have a spurting hemorrhage (eight patients), oozing hemorrhage (27 patients), or a nonbleeding visible vessel (79 patients). Using an univariate analysis, a statistically significant predictor was the appearance of coffee ground fluid or blood from the nasogastric tube. This predictor also emerged as an independent factor (odds ratio, 0.4333; 95% confidence interval, 0.263-0.714). CONCLUSIONS: Patients with bleeding peptic ulcer who have coffee ground fluid or blood from the nasogastric tube should receive an emergency endoscopy and aggressive treatment.

Emergencies↗