No abstract available.
Drug Therapy* ; Stomach Neoplasms*

No abstract available.
Delusions* ; Hallucinations* ; Humans

No abstract available.
Delusions* ; Hallucinations* ; Humans

To investigate the effect of hyperoxia on EKG findings and to evaluate the applicability of EKG as noninvasive monitoring index of oxygen toxicity, 38 rabbits were continuously exposed to 6 different conditions-3 hyperbaric oxygenations (HBO-2.5, 3.5 and 5ATA, 100% O2), normobaric oxygenation (NBO, 100% O2), hyperbaric aeration (HBA-5ATA, 21% O2) and normobaric aeration (NBA, 21% O2)-for 120 minutes and their EKG and time to dyspnea and convulsion were recorded. Dyspnea and death were observed in exposure conditions of HBO-3.5 and HBO-5 (Positive rate of dyspnea; 10%, 100%, death; 10%, 25%, respectively) only, and convulsion in 4 oxygenation groups (NBO; 20%, HBO-2.5; 20%, HBO-3.5; 20%, HBO-5; 88%). Abnormal EKG findings included arrhythmia and ST-T changes and the incidences was increasing with doses(partial pressure of oxygen). In addition to EKG change, findings observed during exosure were dyspnea and convulsion in the order of appearence and when non specific ST-T change was accepted as positive (abnormal) finding, the frequency of abnormal EKG was statistically significant(p<0.01), but when it was excluded from positive results, the frequency of EKG change was not significant(p>0.05). These results suggest that the effect of hyperoxia on heart is myocardial ischemia and arrhythmia, that oxygenation more than 3.5ATA causes myocardial damage in 120 minutes exposure, and that EKG is valuable as monitoring index of oxygen toxicity.
Arrhythmias, Cardiac ; Dyspnea ; Electrocardiography* ; Heart ; Hyperbaric Oxygenation ; Hyperoxia* ; Incidence ; Myocardial Ischemia ; Oxygen ; Rabbits* ; Seizures

PURPOSE: To evaluate the radiological patterns of vascular invasion in peripheral cholangiocarcinomas. MATERIALS AND METHODS: Hepatic arteriography and portography in 20 cases with cholangiocarcinoma including 12 cases with anglographic CT were retrospectively analized. RESULTS: The arteriography showed no arterioportal shunt, hypertrophy of tumor vessel, or tumor staining extending to central portion of the mass in all cases. However, doughnut shaped peripheral tumor staining was seen until late hepatogram phase in 12 cases and compensatory hyperperfusion around the mass was seen in six cases(eight cases if include arterial CT). Encasement of tumor vessel was seen in 12 cases, and hypertrophy of feeding vessel in nine cases. On portogrphy, the filling defect on segmental portal branch could be demonstrated only in 11 cases. Shape of the portal defect was tapered narrowing in six cases, abrupt narrowing in two cases but intraluminal nodular filling defect was not seen. Remainning three cases were difficult to define the shape. On seven cases of CT during arterial portography, three cases showed mass shaped defect and four showed segmental defect but three of them could demonstrate the partially preserved portal flow in defective portal area. CONCLUSION: Hepatic arteriography in peripheral cholagiocarcinoma showed no evidence of hypertrophy of tumor vessels and tumor stain extending to central portion but peripheral staining on late hepatogram phase and compensatory hyperperfusion could be seen. Portal vein was more commonly involved through perivascular connective tissue invasion rather than by direct extension into the portal lumen.
Angiography* ; Cholangiocarcinoma* ; Connective Tissue ; Hypertrophy ; Portal Vein ; Portography ; Retrospective Studies

PURPOSE: To evaluate the radiological patterns of vascular invasion in peripheral cholangiocarcinomas. MATERIALS AND METHODS: Hepatic arteriography and portography in 20 cases with cholangiocarcinoma including 12 cases with anglographic CT were retrospectively analized. RESULTS: The arteriography showed no arterioportal shunt, hypertrophy of tumor vessel, or tumor staining extending to central portion of the mass in all cases. However, doughnut shaped peripheral tumor staining was seen until late hepatogram phase in 12 cases and compensatory hyperperfusion around the mass was seen in six cases(eight cases if include arterial CT). Encasement of tumor vessel was seen in 12 cases, and hypertrophy of feeding vessel in nine cases. On portogrphy, the filling defect on segmental portal branch could be demonstrated only in 11 cases. Shape of the portal defect was tapered narrowing in six cases, abrupt narrowing in two cases but intraluminal nodular filling defect was not seen. Remainning three cases were difficult to define the shape. On seven cases of CT during arterial portography, three cases showed mass shaped defect and four showed segmental defect but three of them could demonstrate the partially preserved portal flow in defective portal area. CONCLUSION: Hepatic arteriography in peripheral cholagiocarcinoma showed no evidence of hypertrophy of tumor vessels and tumor stain extending to central portion but peripheral staining on late hepatogram phase and compensatory hyperperfusion could be seen. Portal vein was more commonly involved through perivascular connective tissue invasion rather than by direct extension into the portal lumen.
Angiography* ; Cholangiocarcinoma* ; Connective Tissue ; Hypertrophy ; Portal Vein ; Portography ; Retrospective Studies

No abstract available.
Carbon Monoxide* ; Carbon*

BACKGROUND: The purpose of this study was to investigate the mechanism of endothelium-dependent and independent responses to endothelins (ETs) in porcine coronary artery. METHODS: The vascular rings of left anterior descending artery or left circumflex artery from 7 pigs were suspended in conventional organ chambers for the measurement of isometric force. To evaluate relaxation responses, vascular rings with endothelium were exposed to ET-1 and ET-3. To evaluate contraction responses, vascular rings with and without endothelium were exposed to ET-1 and ET-3 in the presence or absence of BQ 123 (ET(A) receptor antagonist) or TAK-044 (ET(A) and ET(B) receptor antagonist). RESULTS: Transient relaxation responses of vascular rings occurred after exposure of ET-1 and ET-3. These transient responses disappeared after preincubation with N-nitro-L arginine. There was an increased contractions of vascular rings according to increasing concentration of ET-1 and ET-3. The initial responses were enhanced in vascular rings without endothelium in ET-1 and ET-3. In vascular rings with endothelium, the contraction responses were more reduced in vascular rings with preincubation of BQ 123 than in vascular rings without BQ 123 in ET-1. In vascular rings without endothelium, the contraction responses were more reduced in vascular rings with preincubation of TAK-044 than in vascular rings without TAK-044 in ET-1. CONCLUSION: ET(B) receptor on the endothelium might mediate the transient vasodilator responses to ET-1 and ET-3 through release of nitric oxide in porcine coronary artery. ET(A) and ET(B) receptor on vascular smooth muscle cells might mediate vasoconstrictor responses to ETs.
Arginine ; Arteries ; Coronary Vessels* ; Endothelins* ; Endothelium ; Muscle, Smooth, Vascular ; Nitric Oxide ; Receptors, Endothelin ; Relaxation ; Swine

No abstract available.
Magnesium Sulfate* ; Magnesium* ; Torsades de Pointes*

Mutation of the p53 tumor-suppressor gene in exons 4 through 9 was examined in 34 cases of primary advanced gastric cancer using PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) and the results were compared with p53 protein expression as determined by immunohistochemistry (IHC) using a monoclonal antibody(DO-1). p53 protein detected by IHC was observed in 14 cases (41.2%) and genotypic mutation detected by PCR-SSCP in exons 4-9 was observed in 13 cases (38.2%) One case showed an aberrant band on PCR-SSCP both in Exon 7 and Exon 8/9. p53 alteration detected by either IHC or PCR-SSCP was observed in 19 cases (55.9%), but only 8 cases (23.5%) showed both p53 mutation and protein expression. We also tried to obtain the correlation between relative intensity of the shifted bands on PCR-SSCP and percentage of positive cells by IHC, but a significant correlation was not seen between relative intensity of shifted bands on PCR-SSCP and positve cell ratio. A discrepancy between p53 protein expression and p53 mutation is observed in primary gastric carcinomas. The reason for this discrepancy are not apparent. However, examination of gastric carcinomas for mutations in other exons may identify a better correlation with protein overexpression. The results obtained in this study suggest that the negative reaction for p53 immunohistochemistry may not necessarily mean no genetic alteration of the p53 locus.
Exons ; Immunohistochemistry* ; Stomach Neoplasms