Several models of experimental ulcerative colitis have been reported previously. However, none of these models showed the optimum characteristics. Although dextran sulfate sodium-induced colitis results in inflammation resembling ulcerative colitis, an obvious obstacle is that dextran sulfate sodium is very expensive. The aim of this study was to develop an inexpensive model of colitis in rats. Sprague-Dawley rats were treated with 2% dextran sulfate sodium in drinking water for 3 d followed by an intracolonic administration of 30% ethanol. The administration of 2% dextran sulfate sodium followed by 30% ethanol induced significant weight loss, diarrhea and hematochezia in rats. Severe ulceration and inflammation of the distal part of rat colon were developed rapidly. Histological examination showed increased infiltration of polymorphonuclear leukocytes, lymphocytes and existence of cryptic abscesses and dysplasia. The model induced by dextran sulfate sodium at lower concentration followed by 30% ethanol is characterized by a clinical course, localization of the lesions and histopathological features similar to human ulcerative colitis and fulfills the criteria set out at the beginning of this study.
Acute Disease ; Administration, Rectal ; Animals ; Colitis, Ulcerative ; chemically induced ; pathology ; Dextran Sulfate ; administration & dosage ; Disease Models, Animal ; Drug Administration Schedule ; Ethanol ; administration & dosage ; Female ; Rats

OBJECTIVES: The effects of ethanol and phenobarbital,which are known to affect metabolism of xenobiotics, on the formation of benzidine-and its metabolites-plasma protein adducts in rats administered benzidine were evaluated. METHODS: The experimental rats were divided into the control,ethanol and phenobar-bital groups. The experimental groups (ethanol and phenobarbital group)were pretreated with ethanol (1g/kg)or phenobarbital (80mg/kg)24 hours prior to the oral administration of benzidine (0.5mmol/kg). Blood samples were obtained from the vena cava from 5 rats in each group; and at 30 min,3 h,6 h,9 h,12 h,24 h,48 h,72 h,96 h,and 144 h after the administration of benzidine using heparin treated syringes.The plasma protein levels were separated immediately after taking blood samples. The adducts were underwent basic hydrolysis to convert them into aromatic amines. The hydrolyzed benzidine, monoacetylbenzidine, and 4-aminobiphenyl were analyzed by reverse-phased liquid chro-matography with an electrochemical detector. The quantitative amount of the metabolites was expressed by the plasma protein binding index(PBI). RESULTS: Similar to the hemoglobin adducts,the levels of the plasma protein adducts of the ethanol and phenobarbital groups (benzidine-, monoacetylbenzidine-, and 4-amino-biphenyl-PBI)were higher than those of the control group. These results are attributable to the fact that ethanol and phenobarbital induced to the plasma protein adduct formation. The N-acetylation ratio in the control group was highest at 72 h with 2.34.In the ethanol group,it was highest at 72 h with a ratio of 2.46 and was highest in the phenobarbital group at 72 h with a ratio of 2.43. The N-acetylation ratio of the plasma protein adducts was relatively lower than that of the hemoglobin adducts.The level of the plasma protein adduct increased more rapidly than the hemoglobin adducts in all experimental groups regardless of the pretreatment,and decreased rapidly after reaching the maximum level. CONCLUSION: The above results indicate that ethanol and phenobarbital increased the level of plasma protein adduct formation. The plasma protein adducts tended to decrease more rapidly than the hemoglobin adducts in the body after benzidine exposure. This results in this study result suggests that the effects of ethanol or phenobarbital need to be considered in the biochemical monitoring,and that the level of the plasma protein adducts be a more proper biomarker than the hemoglobin adducts for assessing the short term exposure to a benzidine and benzidine based dye.
Administration, Oral ; Amines ; Animals ; Environmental Monitoring* ; Ethanol* ; Heparin ; Hydrolysis ; Metabolism ; Phenobarbital* ; Plasma* ; Protein Binding ; Rats* ; Xenobiotics

Catheter Ablation ; methods ; Ethanol ; administration & dosage ; Humans ; Liver Neoplasms ; diagnostic imaging ; surgery ; Tomography, X-Ray Computed

OBJECTIVES: To evaluate the effects on the formation of benzidine-hemoglobin, and benzidine metabolite-hemoglobin adducts, caused by pretreatment with the known xenobiotic metabolism effectors, ethanol and phenobarbital, in rats administered Direct Black 38 dye. METHODS: The experimental rats were divided into three groups: a control group, an ethanol group and a phenobarbital group. Rats were pretreated with ethanol (1g/kg) or phenobarbital (80mg/kg) 24 hours prior to the oral administration of Direct Black 38 (0.5mmol/kg), with the control group being administered the same amount of distilled water. Blood samples were obtained from the vena cava of 5 rats from each group prior to, and at 30 min, 3 h, 6 h, 9 h, 12 h, 24 h, 48 h, 72 h, 96 h, and 144 h following the oral administration of Direct Black 38. Directly after sampling the blood was separated into hemoglobin and plasma, with the adducts being converted into aromatic amines by basic hydrolysis. Hydrolyzed benzidiene, monoacetylbenzidine and 4-aminobiphenyl were analyzed by reverse-phase liquid chromatography with an electrochemical detector. The quantitative amount of the metabolites was expressed by the hemoglobin binding index (HBI). RESULTS: In the ethanol group, benzidine-, monoacetylben-zidine-, and 4-aminobiphenyl-HBI were increased to a greater extent than those in the control group. These results were attributed to the ethanol inducing N-hydroxylation, which is related to the formation of the hemoglobin adduct. In the phenobarbital group, all the HBIs, with the exception of the benzidine-HBI, were increased to a greater extent than those of the control group. These results were attributed to the phenobarbital inducing N-hydroxylation related to the formation of the hemoglobin adduct. The N-acetylation ratio was only increased with the phenobarbital pretreatment due to the lower benzidine-HBI of the phenobarbital group compared to those of the control and ethanol groups. The N-acetylation ratios for all groups were higher than 1 for the duration of the experimental period. Although the azo reduction was unaffected by the ethanol, it was inhibited by the phenobarbital. The ratio of the benzidine-HBI in the phenobarbital group was lower than those of the ethanol the control groups for the entire experiment. CONCLUSION: Our results indicate that both ethanol and phenobarbital increase the formation of adducts by the induction of N-hydroxylation, but also induced N-acetylation. Phenobarbital decreased the formation of benzidine-HBI due to the decrease of the azo reduction. These results suggest that the effects of ethanol and phenobarbital need to be considered in the biochemical monitoring of Direct Black 38.
Administration, Oral ; Amines ; Animals ; Chromatography, Reverse-Phase ; Ethanol* ; Hydrolysis ; Metabolism ; Phenobarbital* ; Plasma ; Rats* ; Water

OBJECTIVE: We wanted to determine whether transcatheter Ethiodol-based capillary embolization in combination with carboplatin could improve the efficiency of a 1:1 Ethiodol-ethanol mixture (EEM) to ablate kidneys that been inoculated with VX-2 carcinoma. MATERIALS AND METHODS: The right kidney in 34 New Zealand white rabbits were inoculated with fresh VX-2 tumor fragments. One week later, the kidneys were subjected to transarterial treatment (4-5 rabbits/group): Saline infusion (Group 1); carboplatin infusion (5 or 10 mg, Groups 2A and 2B); carboplatin-Ethiodol (CE) alone (Group 3) and followed by main renal artery occlusion with ethanol (RAO) (Group 4); carboplatin-EEM (C-EEM) followed by RAO (Group 5); carboplatin infusion followed by EEM plus RAO (Group 6); and EEM followed by RAO (Group 7). The animals were followed for up to 3-weeks. The treated kidneys were evaluated angiographically and macroscopically. The kidneys that showed successful embolization macroscopically were entirely cut into serial sections, and these were examined microscopically. Histologically, the kidneys were evaluated on the basis of the residual tumor found in the serial sections. RESULTS: The results obtained with carboplatin infusion alone (Groups 2A and 2B) and CE without RAO (Group 3) were similar to those of the control animals (Group 1). Kidneys from Groups 4-7 demonstrated macroscopically successful embolization with histologically proven complete renal parenchyma infarction; however, some residual tumor was evident in all but one animal. CONCLUSION: None of the Ethiodol-based modalities combined with locoregional carboplatin were more efficacious for tumor ablation than EEM alone.
Angiography ; Animals ; Carboplatin/*administration & dosage ; Chemoembolization, Therapeutic/*methods ; Ethanol/*administration & dosage ; Ethiodized Oil/*administration & dosage ; Injections, Intra-Arterial ; Kidney Neoplasms/*therapy ; Rabbits ; Statistics, Nonparametric

OBJECTIVETo summarize the management of infant vascular tumors with Kasabach-Merritt phenomenon (KMP) and to evaluate the effect of drug combined with sclerotherapy.

METHODSFrom Feb. 2007 to Nov. 2014, 25 cases with KMP, who underwent drug therapy combined with sclerotherapy, were retrospectively studied. Oral corticosteroids (2 mg/kg per day) was used as the first-line therapy on all of the patients and intravenous vincristine (1.5 mg/m2 every week) was added when the platelet counts didn't recover obviously after 2-3 weeks. After the recovery of the platelet counts, the patients were admitted for sclerotherapy (average, 4.56 sessions per case) with 100% alcohol (1-3 ml per session), Lauromacrogol (1.25-5 ml per session) and betamethasone (0.25-1 ml per session). All the patients were followed up for 42 months ( range, 9 months to 6.5 years). Therapeutic outcomes were assessed by evaluating platelet counts, size of lesion, function of trunk and limb.

RESULTSAll the 25 cases got obvious recovery in the platelet counts [average, (94.3 ± 18.5) x 10(9)/L] after drug therapy, of which 16 were treated by single oral corticosteroids for 4-7 weeks and 9 were treated by corticosteroids plus intravenous vincristine for 2-5 weeks. Meantime, 11 cases received platelet transfusions, of which 3 were coupled with gamma globulin intramuscularly. During the first admission, each of the 25 cases received 1-4 sessions of sclerotherapy (average, 2.6 sessions each case). One week after the sclerotherapy, the platelet counts returned to (167-312) x 10(9)/L (average, (258.5 ± 34.4) x 10(9)/L). The hemoglobin and blood coagulation function returned to normal within 1-5 weeks. Meanwhile the mental condition, appetite, body weight, sleeping were greatly improved. The size of the lesions decreased gradually after the combined therapy including 13 cases within 3-12 months and 13 cases within 13-36 months. Long term follow-up indicated that only 1 case need treatment for recurrent decrease of platelet counts, and all of the 25 cases kept the normal weight, height, immunity as well as the growing development.

CONCLUSIONSOral corticosteroids plus intravenous vincristine combined with sclerotherapy is a reliable management with high cure rate, short course and minor side-effect.

Administration, Oral ; Betamethasone ; administration & dosage ; Combined Modality Therapy ; methods ; Ethanol ; administration & dosage ; Glucocorticoids ; administration & dosage ; Humans ; Infant ; Injections, Intravenous ; Kasabach-Merritt Syndrome ; blood ; therapy ; Platelet Count ; Polyethylene Glycols ; administration & dosage ; Retrospective Studies ; Sclerotherapy ; methods ; Vincristine ; administration & dosage

Erectile dysfunction (ED) is a highly prevalent disorder that affects millions of men and considered to be an early symptom of atherosclerosis and a precursor of various systemic vascular disorders. The aim of the present study was to prepare ginsenoside Re enriched fraction (GS-F3K1, ginsenoside Re 10%, w/w) from ginseng berries flesh and to investigate the enhanced activities of GS-F3K1 on alcohol-induced ED. GS-F3K1 was prepared by the continuous liquid and solid separating centrifugation and circulatory ultrafiltration from ginseng berries flesh. GS-F3K1 was administered for 5 weeks in ethanol-induced ED rat by oral administration of 20% ethanol. To investigate the effects of GS-F3K1 on ED model, the levels of nitrite expression, cyclic guanosine monophosphate (cGMP) and erectile response of the penile corpus cavernosum of rat were measured. The erectile response of the corpus cavernosum was restored after GS-F3K1 administration, to a level similar to the normal group. The level of nitrite and cGMP expression in the corpus cavernosum of GS-F3K1-administered male rats was increased significantly compared to positive control group. GS-F3K1 from ginseng berries should effectively restore ethanol-induced ED in male rats and could be developed as a new functional food for the elderly men.
Administration, Oral ; Aged ; Animals ; Atherosclerosis ; Centrifugation ; Erectile Dysfunction* ; Ethanol ; Fruit* ; Functional Food ; Guanosine Monophosphate ; Humans ; Male ; Panax* ; Rats ; Ultrafiltration

Carcinoma, Hepatocellular ; pathology ; therapy ; Chemoembolization, Therapeutic ; Combined Modality Therapy ; Ethanol ; administration & dosage ; Hepatectomy ; Humans ; Injections, Intralesional ; Liver Neoplasms ; pathology ; therapy

The effects of halothane anesthesia on the liver function were investigated in 78 male Sprague-Dawley rats pretreated with ethyl alcohol. Blood sampling was done before intravenous administration of ethyl alcohol(400 mg/kg, 5 ml/kg, 9.99 vol %) or saline(5 ml/kg)through tail vein of the rat. Twentyfour hours later, all rats were randomly assigned to receive one of two anesthetic managements for two hours; 1) halothane -N2O-O2 2)N2O-O2 Bood sample and hepatic tissue were obtained 24 or 96 hours after anestheia Measurements of hepatic function(protein, albumin, cholesterol, bilirubin, blood urea nitro- gen, creatinine) were made and hepatic tissue was examined with light microscopy. The results are as follows; 1) There was no siginificant difference in the laboratory findings between the alcohol and saline groups. 2) There was no significant difference in the laboratory findings between the halothane and nitrous oxide anesthesia. 3) No difference in histologic injury was found between alcohol and saline groups. 4) No difference in histologic injury was found between halothane-nitrous oxide-oxygen and nitrous oxide-oxygen ansthesia groups.
Administration, Intravenous ; Anesthesia* ; Animals ; Bilirubin ; Cholesterol ; Ethanol* ; Halothane* ; Humans ; Liver ; Male ; Microscopy ; Nitrous Oxide ; Rats* ; Rats, Sprague-Dawley ; Urea ; Veins

OBJECTIVETo establish a new animal model of osteonecrosis of the femoral head by local ethanol injection in emu.

METHODSEight milliliter ethanol was injected slowly to the operated femoral head with customized probe in twenty adult male emus. Postoperatively, hip magnetic resonance imaging was performed at 1, 4, 8, 12 weeks. After emus were sacrificed, the femurs were collected for micro-computed tomography and histological analysis.

RESULTSNo emu demonstrated signs of infection or died unexpectedly. Magnetic resonance imaging examination showed broad edema at proximal femur at 1(th) week, and the edema decreased with time, till local edema at femoral head at the 12(th) week. Histological images showed human-like osteonecrotic changes with active bone repair. There were significant differences in trabecular structure and bone mineral density between the operated and intact femoral heads. No collapse was found 6 months after the operation.

CONCLUSIONSThis emu model of femoral head osteonecrosis by local ethanol injection can progress to early stage osteonecrosis. The different repair methods may have certain correlation with the results of osteonecrosis of the femoral heads.

Animals ; Disease Models, Animal ; Dromaiidae ; Ethanol ; administration & dosage ; toxicity ; Femur Head ; pathology ; Injections ; Male ; Osteonecrosis ; chemically induced