BACKGROUND/AIMS: The variceal bleeding has high rebleeding rate, and mortality rate was higher in gastrix varix. Managements of variceal bleeding were included such as drugs, endoscopic procedures, surgical management and radiological intervention. Recently histoacryl(R) injection method has been introduced. We have compared the effects of the endoscopic ligation and Histoacryl(R) injection therapy (HAI) in patient with gastric variceal bleeding. METHODS: We analyzed the effects of hemostasis, complications, rebleeding rates, and survival rates in gastric varix bleeding of 22 patients with Histoacryl(R) injection therapy and 20 patients with endoscopic ligation therapy, from January 1995 to March 1999. RESULTS: There were no difference in the complication rate between the 2 stretigies (12/14). Most common complication was chest pain in EVL group, but fever was common in HAI group. Also early and post rebleeding rates were not different in both groups. The main cause of death during follow up period was rebleeding in both groups. The survival rates were 65.0% in EVL group and 77.0% in HAI group (p>0.05, duration: 23+/-2, 28+/-4 month), and there was no difference in mortlity rate (p=0.77). CONCLUSIONS: There were no difference in the hemostatic effect, complications, rebleeding rate and survival rate in EVL group and HAI group. However, evaluation of larger numbers of patients and prospective studies were needed to define the effectiveness and complications of these therapies.
Cause of Death ; Chest Pain ; Esophageal and Gastric Varices* ; Fever ; Follow-Up Studies ; Hemorrhage* ; Hemostasis ; Humans ; Ligation* ; Mortality ; Survival Rate ; Varicose Veins

BACKGROUND/AIMS: Laterally spreading tumors (LST) were growthed along the colonic wall. These tumors were high malignant potential compared to colon polyp. We analyzed clinicopathological characteristics of these tumors. METHODS: From June 1996 to June 2001, twenty nine patients were diagnosed by colonoscopy. These lesions were classificated macroscopic (granular type and nongranular type) and microscopic findings. RESULTS: 20 male and 9 female were enrolled (mean age, 68.1). Among the LST, 41.4% were 20~30 mm in diameter, and 7% were larger than 30 mm. According to macroscopic findings granular types were 72.4% (21/29) and nongranular types were 27.6% (8/29). In macroscopic findings, tubular types were 48.4% (14/29), malignant changes were 31.3% (9/29). Tumor size was only significant factor in malignant potential of LST (p=0.004). Endoscopic mucosal resection was performed in 72.4% (21/29), operation in 8 (27.6%). Rate of submucosal invasion in LST was 3.4% (1/29, sm1). Recurrent rate of endoscopic treatment group was 9.5% (2/21). CONCLUSIONS: Most of LST were good indication for endoscopic treatment, but larger tumor size and irregular surface of tumor were suspected to be submucosal invasion. Therefore these lesions were performed other procedures as endoscopic ultrasound or computerized tomography for invasion depth.
Colon ; Colonoscopy ; Female ; Humans ; Male ; Polyps ; Ultrasonography

BACKGROUND/AIMS: After colorectal cancer surgery, colonoscopic surveillance should be done for prevention and early detection of secondary cancer. This study aimed to identify the group with high risk of developing colorectal adenoma after curative surgery of colorectal cancer. METHODS: We retrospectively investigated the medical records of the subjects of 130 patients who had been examined using colonoscopy before and after the curative surgery. RESULTS: The average age was 59.4 years. Synchronous adenomas were in 42 patients (32.3%). The occurrence rate was significantly high in men (38.8%) than women (22.0%). After the operation, the mean interval of examining colonoscopy was 11.6 months (3-24 months) and metachronous adenomas were detected in 26 patients (20.0%). The patients who have both metachronous and synchronous adenomas were observed in 13/42 (30.9%) and the patients of metachronous adenomas without synchronous adenomas were observed in 13/88 (14.8%). The occurrence rate of metachronous adenomas with synchronous adenomas was significantly high. The frequency of synchronous adenomas didn't increase with age. However, the frequency of metachronous adenomas increased with age: 0/9 (0%) under 40 years, 7/49 (14.3%) in 41-61 years and 19/72 (26.4%) over 61 years. The occurrence rate was higher in men (26.3%) than women (10.0%). CONCLUSIONS: The occurrence rate of metachronous adenomas after colorectal cancer surgery was higher in the patients with synchronous adenomas, male gender and old aged patients.
Adenoma/*diagnosis ; Adult ; Aged ; Colonoscopy ; Colorectal Neoplasms/*surgery ; English Abstract ; Female ; Humans ; Male ; Middle Aged ; Neoplasms, Multiple Primary/diagnosis ; Neoplasms, Second Primary/*diagnosis ; Risk Factors

Kaposi's sarcoma, a rare tumor, usually presents itself with skin lesions. There is, however, an increased incidence in patients using immunosupressive drugs and with the acquired immunodeficiency syndrome (AIDS). Gastrointestinal Kaposi's sarcoma is usually asymptomatic, but may cause massive intestinal hemorrhage, perforation, intestinal obstruction, intussusception, protein-losing enteropathy, or sepsis. The gastroscopic appearances of Kaposi's sarcoma range from reddish purple maculopapules to polypoid, umbilicated nodule. In Korea, 3 case's of gastrointestinal kaposi's sarcoma have been reported so far. We experienced a 45-year-old man, who was positive for human immunodeficiency virus (HIV) antibodiy and developed Kaposi's sarcoma. A case of gastrointestinal Kaposi's sarcoma treated with paclitaxel is herein reported with the endoscopic findings before and after chemotherapy.
Acquired Immunodeficiency Syndrome ; Drug Therapy ; Duodenum* ; Hemorrhage ; HIV ; Humans ; Incidence ; Intestinal Perforation ; Intussusception ; Korea ; Middle Aged ; Paclitaxel ; Protein-Losing Enteropathies ; Sarcoma, Kaposi* ; Sepsis ; Skin ; Stomach*

PURPOSE: Thiazide diuretics exert their hypotensive efficacy through a combined vasodilator and diuretic effect. The present study was conducted to assess the inhibitory effect of thiazide diuretic, hydrochlorothiazide, and the thiazide-like diuretics, indapamide and chlorthalidone on contractile responses to norepinephrine and arginine vasopressin in aortic rings from 2K1C renal hypertensive and sham-clipped normotensive rats. METHODS: 2K1C hypertension was made by clipping the left renal artery and age-matched control rats received a sham treatment. Changes in the tension of aortic ring preparations were measured isometrically. RESULTS: Indapamide inhibits the contractile responses to norepinephrine and vasopressin in aortic rings from 2K1C rats, while it did not modify in control rats. The inhibitory effect of indapamide was abolished by endothelium removal. Hydrochlorothiazide or chlorthalidone did not affect the vasoconstriction induced by norepinephrine and vasopressin either in sham or in 2K1C hypertensive rats. CONCLUSION: These results suggest that indapamide inhibits the contractile responses to norepinephrine and vasopressin via an endothelium-dependent mechanism in 2K1C renal hypertension.
Animals ; Aorta ; Arginine Vasopressin ; Chlorthalidone ; Diuretics ; Endothelium ; Hydrochlorothiazide ; Hypertension ; Hypertension, Renal ; Indapamide ; Norepinephrine ; Placebos ; Rats ; Renal Artery ; Salicylamides ; Sodium Chloride Symporter Inhibitors ; Vasoconstriction ; Vasodilation ; Vasopressins

BACKGROUND: Endothelial dysfunction is linked to exaggerated production of superoxide anions. This study was conducted to examine the effects of oxidative stress on endothelial modulation of contractions in chronic two-kidney, one-clip (2K1C) renal hypertensive rats. METHODS: The 2K1C hypertension was induced by clipping the left renal artery; age-matched rats receiving sham treatment served as controls. Thoracic aortae were isolated and mounted in tissue baths for measurement of isometric tension. RESULTS: Norepinephrine-induced contraction was augmented by the removal of the endothelium, which was more pronounced in sham rats than in 2K1C rats. Nomega-nitro-L-arginine methyl ester, an inhibitor of nitric oxide production, had a similar augmenting effect. Vitamin C inhibited the contraction in aortic rings with intact endothelium from 2K1C rats but not from sham rats. The contraction was also suppressed by treatment with diphenyleneiodonium or apocynin, inhibitors of nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate (NADH/NADPH) oxidase, in the aortae with intact endothelium from 2K1C rats but not in those from sham rats. Superoxide anions generated by xanthine oxidase/hypoxanthine enhanced the contraction in the aortae with intact endothelium from sham rats, but had no effect in 2K1C rats. Enhanced contractile responses to norepinephrine by xanthine oxidase/hypoxanthine in sham rats were reversed by vitamin C. CONCLUSION: These results suggest that the effect on endothelial modulation of endothelium-derived nitric oxide is impaired in 2K1C hypertension. The impairment is, at least in part, related to increased production of superoxide anions by NADH/NADPH oxidase.
Adenine ; Animals ; Aorta* ; Aorta, Thoracic ; Ascorbic Acid ; Baths ; Endothelium ; Hypertension ; Hypertension, Renal ; Niacinamide ; Nitric Oxide ; Norepinephrine ; Oxidative Stress* ; Oxidoreductases ; Placebos ; Rats* ; Renal Artery ; Superoxides ; Xanthine

BACKGROUND: Ferulic acid (FA) is a naturally occurring nutritional compound. Although it has been shown to have antihypertensive effects, its effects on vascular function have not been intensively established. The aim of this study was to assess the vasoreactivity of FA in chronic two-kidney, one-clip (2K1C) renal hypertensive rats. METHODS: Hypertension was induced in 2K1C rats by clipping the left renal artery and age-matched rats that received a sham treatment served as a control. Thoracic aortas were mounted in tissue baths to measure isometric tension. The effects of FA on vasodilatory responses were evaluated based on contractile responses induced by phenylephrine in the aortic rings obtained from both 2K1C and sham rats. Basal nitric oxide (NO) bioavailability in the aorta was determined by the contractile response induced by NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). RESULTS: FA induced concentration-dependent relaxation responses which were greater in 2K1C hypertensive rats than in sham-clipped control rats. This relaxation induced by FA was partially blocked by the removal of endothelium or by pretreating with L-NAME. L-NAME-induced contractile responses were augmented by FA in 2K1C rats, while no significant differences were noted in sham rats. FA improved acetylcholine-induced endothelium-dependent vasodilation in 2K1C rats, but not in sham rats. The simultaneous addition of hydroxyhydroquinone significantly inhibited the increase in acetylcholine-induced vasodilation by FA. CONCLUSION: These results suggest that FA restores endothelial function by altering the bioavailability of NO in 2K1C hypertensive rats. The results explain, in part, the mechanism underlying the vascular effects of FA in chronic renal hypertension.
Animals ; Aorta ; Aorta, Thoracic ; Baths ; Biological Availability ; Coumaric Acids ; Endothelium ; Hydroquinones ; Hypertension ; Hypertension, Renal ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Nitric Oxide Synthase ; Phenylephrine ; Placebos ; Rats ; Relaxation ; Renal Artery ; Salicylamides ; Vasodilation

BACKGROUND/AIMS: Tamoxifen is a widely used anticancer drug for breast cancer with frequent gastrointestinal side effects. Changes in gastrointestinal motility is associated with altered activities of membrane ion channels. Ion channels have important role in regulating membrane potential and cell excitability. This study was performed to investigate the effects of tamoxifen on the membrane ionic currents in colonic smooth muscle cells. METHODS: Murine colonic smooth muscle cells were isolated from the proximal colon using collagenase, and the membrane currents were recorded using a whole-cell patch clamp technique. RESULTS: Two types of voltage-dependent K+ currents were recorded (A-type and delayed rectifier K+ currents). Tamoxifen inhibited both types of voltage-dependent K+ currents in a dose-dependent manner. However, tamoxifen did not change the half-inactivation potential and the recovery time of voltage-dependent K+ currents. Chelerythrine, a protein kinase C inhibitor or phorbol 12, 13-dibutyrate, a protein kinase C activator did not affect the voltage-dependent K+ currents. Guanosine 5'-O-(2-thio-diphosphate) did not affect the tamoxifen-induced inhibition of voltage-dependent K+ currents. Tamoxifen inhibited voltage-dependent Ca2+ currents completely in whole-test ranges. CONCLUSIONS: These results suggest that tamoxifen can alter various membrane ionic currents in smooth muscle cells and cause some adverse effects on the gastrointestinal motility.
Animals ; Antineoplastic Agents, Hormonal/*pharmacology ; Calcium Channels/drug effects ; Colon/*drug effects/physiology ; English Abstract ; In Vitro ; Membrane Potentials ; Mice ; Myocytes, Smooth Muscle/*drug effects/physiology ; Potassium Channels/*drug effects ; Tamoxifen/*pharmacology

PURPOSE: S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide (NO) donor, is thought to relax vascular smooth muscle by stimulation of soluble guanylate cyclase, accumulation of its product cyclic GMP (cGMP) level. Evidence has emerged that NO-induced vasodilatation is also mediated by stimulating Ca2+-activated K+ (KCa) channels directly or indirectly through cGMP. The aim of the present study was to investigate possible involvement or alteration of KCa channels in the mechanism of vasodilation induced by SNAP in two-kidney, one-clip (2K1C) hypertensive rats. METHODS: 2K1C hypertension was made by clipping the left renal artery and age-matched control rats received a sham treatment. Using rings prepared from thoracic aortae, we studied changes in isometric tension of the rings in response to SNAP to evaluate effects of a soluble guanylate cyclase inhibitor methylene blue (MB), and a specific blocker of KCa channel iberiotoxin (ITX). RESULTS: Aortic rings from 2K1C hypertensive and sham-clipped control rats precontracted with phenylephrine showed similar relaxation to SNAP. MB markedly suppressed the SNAP-induced relaxation in both groups, leaving about 30% of MB-resistant relaxation. ITX nearly completely eliminated the MB-resistant relaxation in control rats, but it did not affect 2K1C rats. CONCLUSION: These results suggest that SNAP-induced vasorelaxation is mediated through cGMP- dependent and cGMP-independent KCa channel involving mechanisms, the latter may be altered in 2K1C renal hypertension.
Animals ; Aorta* ; Aorta, Thoracic ; Cyclic GMP ; Guanylate Cyclase ; Humans ; Hypertension ; Hypertension, Renal ; Methylene Blue ; Muscle, Smooth, Vascular ; Nitric Oxide ; Phenylephrine ; Placebos ; Potassium Channels, Calcium-Activated ; Rats* ; Relaxation* ; Renal Artery ; S-Nitroso-N-Acetylpenicillamine ; Tissue Donors ; Vasodilation

BACKGROUND: Cells rely on gap junctions for intercellular communication, which is important for growth and contractility. The present study was conducted to test the hypothesis that contractile responses in aortic rings from two-kidney, one clip (2K1C) hypertensive rats are more dependent on gap junctional communication compared to those from normotensive rats. METHODS: 2K1C hypertension was induced by clipping the left renal artery and age-matched rats received a sham operation. Heptanol and octanol were used as inhibitors of gap junctional activity. RESULTS: The contraction induced by phenylephrine or KCl was completely reversed by either heptanol or octanol, and the relaxant response to inhibitors was more enhanced in 2K1C hypertensive rats compared to sham-operated rats. Vessels from hypertensive rats also relaxed more to nifedipine when precontracted with KCl, although it did not differ in aortic segments contracted with phenylephrine in between normotensive and hypertensive rats. CONCLUSION: These results suggest that gap junctional communication and voltage-operated calcium channels are differentially regulated in 2K1C renal hypertension.
Rats ; Animals