BACKGROUND: Clinical and experimental studies have suggested that brain death may cause hemodynamic, electrocardiographic, functional or histopathologic changes of the heart. METHODS: Brain death was induced by increasing intracranial pressure(ICP) abruptly by intermittent bolus injection of saline(model ) or gradually by continuous infusion of saline(model ) to the epidural catheter in 5 mongrel dogs, respectively. Hemodynamic and biochemical changes during the process of brain death and histopathologic changes of the myocardium were analyzed and compared in two brain death models, and the association of apoptosis was also evaluated. RESULTS: 1) Two predominant subsets of acute contraction band lesion were produced in both brain death models : paradiscal and holocystic contraction band lesions. Both contraction band lesions were more prevalent in brain death model . 2) The frequency of both contraction band lesions was lowest in the epicardial layer and highest in the endocardial layer in both models, but no correlation was observed between the degree of contraction band lesions and ICP, LV maximum +dp/dt or catecholamine levels. There was no statistical difference between any of the LV circumferential blocks and either type of contraction band lesion, and transaxial distribution was not also different in both models. 3) There was no remarkable histopathologic changes in the analysis of major epicardial coronary arteries. Apoptotic cells were suggested in the scattered myocytes in the light microscopy and apoptosis was detected by in situ nick end labeling method. Electron microscopy revealed a condensation of nuclear chromatin and convolution of nuclear membrane in those myocytes. CONCLUSIONS: Myocardial changes due to brain were observed frequently, and few apoptotic cells were found in the brain death heart. Studies on the treatment strategy to minimize damages of myocardial structure and function caused by brain death should be followed in the near future.
Animals ; Apoptosis ; Brain Death* ; Brain* ; Catheters ; Chromatin ; Coronary Vessels ; Dogs ; Electrocardiography ; Heart ; Hemodynamics ; In Situ Nick-End Labeling ; Microscopy ; Microscopy, Electron ; Muscle Cells ; Myocardium* ; Nuclear Envelope

BACKGROUND: Overstimation of blood pressure(BP) by clinic measurements occur in about 20 to 30% of subjects(white-coat hypertension) who may, consequently, be misdiagnosed as hypertensives and received unnecessary medications. The clinical significance of white-coat hypertension and its effects on the cardiovascular wystem have not been studied systematically.This study was designed to evaluate the influences of white-coat hypertension and white-coat effect, defined as difference between clinic and ambulatory BP, on the LV mass and diastolic function. METHODS: LV mass index was calculated and LV systolic and diastolic function were assessed by the analysis of mitral and pulmonary venous flow velocity in 45 untreated essential hypertensives and 20 normotensives(NT). Ambulatory BP monitoring classified hypertensives as white-coat hypertensives(WCHT,n=20) and sustained hypertensives(SHT, n=25). RESULTS: 1) Left ventricular systolic indices were not different among the three groups. 2) Left ventricular mass inedx of WCHT(114.5+/-36.3g/m2) was similar to that of SHT(115.6+/-34.9g/m2) and was significantly greater than that of NT(86.5+/-37.7g/m2)(p<0.05). 3) Some of left ventricular diastolic parameters(isovolumic relaxation time, E/A ratio, A velocity, pulmonary systolic fraction, ratio of systolic to diastolic forward flow velocity) of WCHT and SHT were significantly different from those of NT(p<0.05), but there were no differences between two hypertensive groups. 4) Even though both systolic and diastolic white-coat effect in WCHT were significantly greater than those of SHT(o<0.05),white-coat effect did not influence on the left ventricular mass or function in both groups. CONCLUSION: An increased left ventricular mass and diastolic dysfunction in WCHT suggests that white-coat hypertension could not be considered as an entirely innocuous clinical condition.
Blood Pressure Monitoring, Ambulatory ; Hypertension* ; Relaxation

Split hand split foot(SHSF) is a rare human developmental defect characterized by mi-ssing digits, fusion of remaining digits, and a deep median cleft in the hands and feet. Cy-togenetic studies of deletions and translocations associated with this disorder have indicated that an autosomal dominant split hand/split foot locus maps to 7q21-q22. We have experienced a case of ectrodactyly in a 25-year-old primigravida woman and her baby and reported out our experience with a review of related literature.
Adult ; Female ; Fetus* ; Foot ; Hand ; Human Development ; Humans

No abstract available.
Paget Disease, Extramammary*

PURPOSE: To investigate the prognostic factors for neovascular glaucoma after vitrectomy in eyes with proliferative diabetic retinopathy. METHODS: In the present study we retrospectively reviewed intraindividual and interocular differences in 14 patients (28 eyes) who underwent pars plana vitrectomy for proliferative retinopathy with vitreous hemorrhage and having only 1 eye neovascular glaucoma. The patients underwent vitrectomy between March 2008 and July 2014 at Maryknoll Hospital. The patient clinical data on preoperative, intraoperative and postoperative factors were compared. Statistical analysis was performed using the Wilcoxon matched-pairs signed-rank (Mann-Whitney) test and chi-square test to evaluate the significance of differences within the patient groups. RESULTS: The decrease of photopic b-wave amplitudes on the preoperative electroretinogram significantly correlated with the development of neovascular glaucoma after vitrectomy for proliferative retinopathy with vitreous hemorrhage (p > 0.05). CONCLUSIONS: Based on the results from the present study, decreased photopic b-wave amplitudes on preoperative electroretinogram is an effective prognostic factor for the development of neovascular glaucoma after vitrectomy for proliferative retinopathy with vitreous hemorrhage.
Diabetic Retinopathy* ; Glaucoma, Neovascular* ; Humans ; Retrospective Studies ; Vitrectomy* ; Vitreous Hemorrhage

In this study, the ontogeny of the dopamine D1 and D2 receptors on fetal rat retina was investigated by using in situ hybridization technique. The expression of the D1 and D2 receptor mRNAs showed different pattern of appearance, distribution and density. At gestational day(GD) 13.5, D1 receptor was first detected in neuroepithelium of the retina. Both D1 and D2 receptors were detected at GD 15.5 in the ventricular layer and ganglion cell layer of developing retina of the rat, and D1 receptor showed more strong density than that of D2 receptor. At GD 17.5, Both D1 and D2 receptors were detected in the ganglion cell layer, ventricular layer and pigment epithelium. The labelling density of D1 receptor was higher than that of D2 receptor. At GD 19.5, both D1 and D2 receptors were additionally detected in the optic nuclear layer and plexiform layer. These results imply that D1 and D2 receptor may mediate different important function of the retina.
Animals ; Dopamine* ; Epithelium ; Ganglion Cysts ; In Situ Hybridization ; Rats* ; Retina* ; RNA, Messenger*

BACKGROUND: Adaptive remodeling of the wall of diseased arterial segments occurs to compensate for the accumulation of atherosclerotic plaque. Histopathologic studies and intraoperative high-frequency epicardial coronary ultrasound imaging as well as intracoronary ultrasound imaging have shown that human coronary arteries enlarge in parallel with the formation of atherosclerotic plaque. Therefore, the lumen area is preserved until the progressive accumulation of plaque exceeds the compensatory mechanisms of the vessel. In 1995, however, Pastercamp et al. reported that arterial wall constriction (shrinkage) or inadequate enlargement may be a different mechanism associated with the development of severe arterial lumen narrowing in addition to plaque proliferation. The aim of this study is to examine what extent of de novo native coronary arterial stenosis is accompanied by compensatory enlargement and to find the predictors of inadequate remodeling with intravascualr ultrasound. METHODS: Fifty eight patients were enrolled from February 1997 through October 1997. Patients who had the lesion of more than 50% stenosis of minimal luminal diameter in coronary angiography were indicated. The lesion which was located in the ostium or was very tortuous or angulated was excluded. The lesion which had the history of balloon angioplasty or stent insertion was also excluded. We used 20 MHz endosonic intravascular ultrasound catheter. We measured EEM area (External Elastic Membrane area), lumen area and plaque plus media area and analysed plaque characteristics. RESULTS: 1) Fifty-eight consecutive patients (43 men, 15 women; mean age 55.4 years, range 33 to 78) who had not undergone previous catheter intervention were studied with a single intravascular ultrasound system. 2) Among 58 patients, 20 patients (35%) had acute myocardial infarction, 30 patients (52%) unstable angina, 6 patients (10%) stable angina and 2 patients (3%) old myocardial infarction. Lesions were located at the left anterior descending arteries in 29 patients (50%), right coronary arteries in 21 patients (36%) and left circumflex coronary artery in 8 patients (14%). 3) Compensatory enlargement was observed in 19 (32%) of 58 lesions and inadequate compensatory enlargement in 39 (68%). 4) EEM and plaque areas at lesion site of compensatory enlargement group were significantly larger than those of inadequate enlargement group (p<0.05). 5) Risk factors for coronary arterial disease including diabetes mellitus, hypertension, hypercholesterolemia (serum cholesterol<0A65B>240 mg/dl), smokings and plaque characteristics were not statistically related with inadequate enlargement. Although there was no statistical significance, there was a tendency of inadequate enlargement in patients with diabetes mellitus and calcified plaque. 6) The only predictor of inadequate remodeling was the postmenopausal female (p<0.05). CONCLUSION: Adaptive compensatory coronary arterial remodeling was occured less frequently in patients with acute coronary syndromes than in patients with stable angina. The only statistically significant predictor of adaptive compensatory coronary arterial remodeling was postmenopausal women. Inadequate compensatory coronary arterial remodeling was occured more frequently in patients with diabetes mellitus or calcified plaque but without statistical significance.
Acute Coronary Syndrome ; Angina, Stable ; Angina, Unstable ; Angioplasty, Balloon ; Arteries ; Catheters ; Constriction ; Constriction, Pathologic ; Coronary Angiography ; Coronary Vessels ; Diabetes Mellitus ; Female ; Humans ; Hypercholesterolemia ; Hypertension ; Male ; Membranes ; Myocardial Infarction ; Phenobarbital ; Plaque, Atherosclerotic ; Risk Factors ; Smoke ; Stents ; Ultrasonics* ; Ultrasonography

BACKGROUND: Many autopsy studies have shown that the extent of extracranial carotid and coronary artherosclerosis is correlated and B-mode ultrasonographic intima-media thickness(IMT) and histologic IMT have been good correlation. In recent years. as it has been reported that IMT of carotid artery had something to do with risk factors of atherosclerosis and occurrence of coronary artery disease, in this study, we tried to investigate if the grade of atherosclerosis in B-mode ultrasonography of carotid artery could predict coronary artery disease and have something to do with the severity of coronary artery disease. METHODS: We classified the patients who were examined coronary angiography into control group without significant(>50%) stenosis(11 patients) and coronary artery disease(CAD) group(45 patients) according to the existence of significant stenosis, and we subdivided CAD group into single vessel disease(SVD) group(25 patients) and multivessel disease(MVD) group(20 patients). Practicing B-mode ultrasonography of common carotid artery(CCA), carotid artery bifurcation(BIF) and internal carotid artery(ICA), we measured IMT and IMT/L(lumen diameter) of each segment. Adding all values of each segment, we got mean aggregated IMT and mean aggregated IMT/L. RESULTS: 1) As IMT of left BIF in both six segments, control group was 0.55+/-0.16mm, SVD group was 0.71+/-0.36mm and MVD group was 1.02+/-0.61mm. So compared with control group and SVD, MVD group were significantly thick. As IMT/L, control group was 0.07+/-0.02, SVD group 0.08+/-0.05 and MVD group was 0.13+/-0.08. So compared with control group and SVD, MVD group was ignificantly high. 2)IMT of BIF in three segments, control group was 0.59+/-0.16mm, CAD group was 0.82+/-0.47mm and MVD group was 0.90+/-0.54mm. So compared with control group and CAD, MVD group were significantly thick. Also as IMT/L of BIF, compared with control group(0.07+/-0.02) and CAD(0.10+/-0.06), MVD(0.11+/-0.07) group was high.= 3) As mean aggregated IMT, control group was 0.57+/-0.34mm, CAD group was 0.69+/-0.45mm, SVD group was 0.63+/-0.12mm and MVD group was 0.74+/-0.21mm. So CAD group was thicker than control group and MVD group was thicker than SVD group. As mean aggregated IMT/L, control group was 0.07+/-0.03, CAD group was 0.10+/-0.05, SVD group was 0.09+/-0.01 and MVD group was 0.11+/-0.03. So CAD group was higher than control group and MVD group was higher than SVD group. CONCLUSION: These data support use of the mean aggregated B-mode ultrasonographic IMT and IMT/L in carotid bifurcation for correlation with the status of coronary atherosclerosis.
Atherosclerosis ; Autopsy ; Carotid Arteries* ; Constriction, Pathologic ; Coronary Angiography ; Coronary Artery Disease* ; Coronary Vessels* ; Humans ; Risk Factors ; Ultrasonography

BACKGROUND AND OBJECTIVES: Mechanisms of restenosis following successful coronary angioplasty (PTCA) are knownasvascularsmoothmuscle cells(VSMCs)proliferationandmigration, elastic recoil or vascular wall remodeling. Paclitaxel whose effect on the stabilization of microtubles leads to cell death is highly lipophilic, permitting easy pass through cell membrane, and has a long-term antiproliferative effect. This study was performed to evaluate effect of paclitaxel on VSMCs proliferation and whether locally delivered paclitaxel can prevent stenosis and neointimal formation in rat carotid artery injury model. MATERIALS AND METHODS: Cultured VSMCs were exposed to sequential concentrations of paclitaxel in vitro, and proliferation inhibition was analyzed with 3H-thymidine incorporation. Paclitaxel of a suitable concentration was applied to the endothelium-denuded carotid artery of Fisher 344 inbred rats for 20 minutes. Angiogram and morphometric analysis of carotid artery was performed after 2 weeks. RESULTS: 3H-thymidine incorporation in cultured VSMCs was decreased dose-dependently from the concentration of 0.1 micromol/L (2,454+/-149cpm/ microgram protein) to 100 micromol/L (1,323+/-69cpm/ microgram protein) of paclitaxel by single and 20-minute exposure in the presence of platelet-derived growth factor (p<0.005). In the absence of platelet-derived growth factor, the decrement of 3H-thymidine incorporation was evident above the concentration of 5 micromol/L of paclitaxel. To evaluate in vivo effect, paclitaxel (0.1 or 1 micromol/L) was administered into the endothelium-denuded carotid artery by balloon injury and incubated for 20 minutes. Percent stenoses (32.2+/-9.8%) of paclitaxel-treated group was less than those (46.3+/-7.5%) of control group on histologic analysis (p<0.01). Paclitaxel-treated group also had wider lumen on carotid angiogram and less neointimal thickening than control on histologic examination (p<0.005). CONCLUSION: Proliferation of VSMCs was effectively inhibited and neointimal formation and luminal stenosis was prevented in rat carotid artery injury model by single, brief and local delivery of low-dose paclitaxel. This strategy could be applied to clinical settings for the prevention of restenosis after PTCA.
Angioplasty ; Animals ; Carotid Arteries* ; Carotid Artery Injuries ; Cell Death ; Cell Membrane ; Constriction, Pathologic ; Neointima ; Paclitaxel* ; Phenobarbital ; Platelet-Derived Growth Factor ; Rats*

No abstract available.
Diagnosis ; Seizures ; Tomography, Emission-Computed, Single-Photon