This study was designed to assess the antihypertensive efficacy and overall tolerance of doxazosin in patients with mild-to-moderate essential hypertension. Doxazosin was administered in once-daily dose from 1 to 3mg to 97 patients both in a general hospital and a local clinic in rural area. These patients are composed of three groups. One group has 49 Patients treated with doxazosin monotherapy, another group with 31 patients treated with doxazosin as well as other antihypertensive drugs combined and a third group is composed of 17 patients with renal insufficiency n addition to hypertension. The patients in the third group with renal insufficiency had 2.5mg/dl-5.0mg/dl in serum creatinine. Results are as follows : 1) The study sample is composed of 37 males (38.1%) and 60 females (61.9%) with mean age 51.4 years. Among three subasmples no statistically significant difference is observed in age, sex, mean body weight and heigh at 0.05 error level. 2) A total of 47 patients (48.5%) of the 97 patients have completed twelve-week doxazosin antihypertensive treatment. At a mean dose of 4.4+/-0.4mg at twelfth week, 37 patients (78.7%) responded to doxazosin therapy. Twenty-nine(61.7% patients achieved "excellent" blood pressure control(mean sitting DBP of < or =90mmHg), and 8 patients (17.0%) showed "good respone" (10mmHg or more DBP reduction from baseline). Whereas remaining 10 patients (21.3%) showed only "fair response" (5-9mmHg DBP reduction) or "failed"(0-4mmHg DBP reduction). In doxazosin monotherapy group thirteen(68.4%) of nineteen patients showed "excellent" or "good response" at a mean dose of 4.8mg/day. Combination therapy group with eighteen patients showed 100% therapeutic success. This group had fourteen(77.8%) "excellent" and four(22.2%) "good respinse" at a mean daily dose of doxazosin 3.9mg. Renal insufficiency group with ten patients showed six(60.0%) "excellent" and four (40.0%) "failure"cases at a mean daily dose of 4.6mg. 3) The mean baseline sitting blood pressures of doxazosin monotherapy group were 175/109 whose blood pressure at twelfth week were 150/94 at a mean daily dose of 4.8mg. The baseline blood pressure of combined therapy group 180/111 were reduced to 145/91 at twelfth week at a mean daily dose of 3.9mg. Those of renal insufficiency group were 177/112 and 156/98 respectively at a mean doxazosin daily dose of 4.6mg. 4) Of the 97 study cases, adverse effect were reported in 19.6%. The most prevalent adverse effects were dizziness(11.3%), blurred vision(9.3%), headache(5.2%), most of which were mild or moderate and disappeared with or were tolerated on continued therapy. But three cases(3.1%) had to refrain from doxazosin administration due to blurred vision, dizzines, and headache. 5) The change of lipid analysis between before and after treatment in the monotherapy group with doxazosin showed 3.8% decrease of total cholesterol and 4.6% increase of HDL cholesterol and 11% increase of triglycerides, which were not statistically significant. In the combination therapy group 0.4% decrease of total cholesterol, 24.1% decrease of HDL cholesterol and 44.3% increase of triglycerides were observed. In the renal insufficiency group 4.9% decrease of total cholesterol, 22.1% decrease of HDL cholesterol, 0.1% decrease of triglycerides were observed. But all these findings have limitation in generalization due to small number of sample and a short period of observation. 6) Laboratory chemistry test results revealed no apparent treatment-related abnormalities.
Antihypertensive Agents ; Blood Pressure* ; Body Weight ; Chemistry ; Cholesterol ; Cholesterol, HDL ; Creatinine ; Doxazosin* ; Female ; Generalization (Psychology) ; Headache ; Hospitals, General ; Humans ; Hypertension ; Male ; Renal Insufficiency ; Triglycerides

No abstract available.
Animals ; Liver* ; Metals, Heavy* ; Rats*

Parkinsonism secondary to intracranial mass lesions usually results from compression or distortion of the basal ganglia. Secondary parkinsonism due to midbrain infiltration or compression is rare and generally associated with other neurologic signs caused by pyramidal tract and/or cranial nerve involvement. We report a case of 30-year-old woman in whom mild parkinsonism was the major clinical manifestation of an astrocytoma in the anterior third ventricle and hypothalamus. She underwent surgical resection, ventriculoperitoneal shunt and radiation therapy. All symptoms of parkinsonism were completely recovered 3 months after the treatment. Brain tumors can be manifested only by the symptoms of parkinsonism. This case emphasizes the significance of neuroimaging in the evaluation of parkinsonism.
Adult ; Astrocytoma ; Basal Ganglia ; Brain Neoplasms ; Cranial Nerves ; Female ; Humans ; Hypothalamus ; Mesencephalon ; Neuroimaging ; Neurologic Manifestations ; Parkinson Disease, Secondary ; Parkinsonian Disorders ; Pyramidal Tracts ; Third Ventricle ; Ventriculoperitoneal Shunt

Malignant lymphoma in the eye and its adnexa can occur rarely as a primary tumor as well as a part of disseminated malignant lymphoma. A case of bilateral conjunctival involvement in the disseminated lymphocytic type malignant lymphoma in a 60 year-old male patient is reported because of its rarity and review of the literature is made. Other organ involvement includes cervical, axillary, hilar and inguinal lymphnodes, liver, spleen and bone marrow.
Bone Marrow ; Conjunctiva* ; Humans ; Liver ; Lymphoma ; Lymphoma, Non-Hodgkin* ; Male ; Middle Aged ; Spleen

OBJECTIVE: To investigate the neuropathic changes induced by nucleus pulposus and possible role of nitric oxide (NO) in the pathogenesis of painful radiculopathy. METHOD: Autologous nucleus pulposus was harvested from the rat coccygeal intervertebral disc and grafted to the sciatic nerve. Pain behavior, neurophysiologic and pathologic changes were compared between autografted and sham operated group during 14-day-period. Western immunoblotting and immunohistochemistry with anti-nitrotyrosine mouse monoclonal antibody were used to compare the NO production and nerve damage in autografted and sham operated nerve tissues. RESULTS: Mechanical allodynia and thermal hyperalgesia were observed 2 days after autograft of nucleus pulposus and persisted during 14-day-period (p<0.05). Motor nerve conduction latency was delayed and compound muscle action potential amplitude was decreased 5 days after autograft (p<0.05). Histologically, nucleus pulposus induced severe inflammatory reaction with fibroblast proliferation and foamy macrophage infiltration, which were persisted during 14-day- period. More nitrated proteins were detected consistently in nerve tissues with autograft of nucleus pulposus and immunohistochemical staining of nitrotyrosine was prominent around foamy macrophages. CONCLUSION: These data suggest that nucleus pulposus induce mechanical allodynia, thermal hyperalgesia and nerve dysfunction through inflammatory reaction with macrophage infiltration. NO and NO related tissue injury may play an important role in the pathogenesis of painful radiculopathy.
Action Potentials ; Animals ; Autografts* ; Blotting, Western ; Fibroblasts ; Hyperalgesia ; Immunohistochemistry ; Intervertebral Disc ; Macrophages ; Mice ; Nerve Tissue ; Neural Conduction ; Neuralgia ; Nitric Oxide* ; Radiculopathy ; Rats* ; Sciatic Nerve* ; Transplants

No abstract available.
Brain ; Brain Injuries ; Spinal Cord ; Wallerian Degeneration

Adriamycin (ADR) is a potent anticancer drug that causes often severe cardiomyopathy. Previous reports have demonstrated that zinc accumulation is shown in rat myocardial cells following ADR treatment. However, the mechanism and role of zinc accumulation in ADR-induced cardiomyopathy are not yet elucidated. Zinc may be one of the key executors in ADR-induced cardiomyopathy. To test this hypothesis, we examined the cytotoxic effects of zinc on various cell lines including H9c2 cardiomyoblast cells, HL-60, U937, and C(6)-glial cells. Zinc induced significant the death of H9c2 cells at 0.125 mM in a dose-dependent manner. However, zinc did not induce any cytotoxic effect on both promyelocytic leukemic HL-60 cells and monoblastoid U937 cells. The nuclear morphology of Zn(2+)-treated H9c2 cells displayed apparent chromatin condensation, but no formation of chromatin fragmentation. In addition, phosphatidylserine (PS) externalization was observed by annexin-V staining. Zinc markedly decreased the intracellular GSH level in a time-dependent manner. Exposure to 0.2 mM ZnCl(2) for 6 hr decreased the intracellular GSH content to 13% of control value. Zinc-induced death of H9c2 cells and the intracellular GSH depletion were completely prevented by the addition of exogenous GSH and NAC. These result suggests that intracellular GSH depletion is directly involved in zinc-induced cardiomyopathy.
Animals ; Cardiomyopathies ; Cell Death* ; Cell Line ; Chromatin ; Doxorubicin ; Free Radicals ; HL-60 Cells ; Humans ; Rats ; U937 Cells ; Zinc

In order to examine the neurotoxic mechanism of oxygen radicals on cultured bovine oligodendrocytes, cytoxic effect of oxygen radicals was examined when cultures were treated with various concentrations of xanthine oxidase (XO) and hypoxanthine (HX) in culture medium. In addition, the neuroprotective effect of iron-chelators against the neurotoxicity induced by oxygen radicals was evaluated by MTT assay. Cell viability was remarkably decreased in a time-dependent manner after exposure of cultured bovine oligodendrocytes to 20mU/ml XO and 0.1mM HX for 4 hours. In the neuroprotective effect of iron-chelators on oxidant-induced neurotoxicity, tetrakis (2-pyridylmethyl)ethylenediamine (TPEN) blocked the neurotoxicity induced by oxygen radicals, while DFX was not effective in blocking oxidant-induced neurotoxicity in these cultures. These results suggest that oxygen radicals are toxic in cultured bovine oligodendrocytes, and also selective iron-chelators such as TPEN are effective in blocking the neurotoxicity induced by oxygen radicals.
Allopurinol* ; Cell Survival ; Hypoxanthine ; Neuroprotective Agents ; Oligodendroglia ; Reactive Oxygen Species ; Xanthine Oxidase

In order to elucidate the cardiotoxicity of FeSO4 in cultured myocardial cells derived from neonatal rat, cardiotoxicity was measured by MTT assay when cultured cells were treated with various concentrations of FeSO4. In addition, the cardioprotective effect of antioxidants, glutathione and ascorbic acid was evaluated by MTT assay in these cultrures. Cell viability was remakably decreased in a dose -dependent manner after exposure of cultured rat myocardial cells to 20 microM FeSO4 for 48 hours. In the cardioprotective effect of antioxidants on FeSO4 -induced toxicity, glutathione blocked the cardiotoxicity induced by FeSO4, while ascorbic acid was not effective in blocking FeSO4 -induced cardiotoxicity in these cultures. These results suggest that FeSO4 is toxic in cultured myocardial cells from neonatal rat and selective antioxidants such as glutathione are effective in blocking the cardiotoxicity induced by FeSO4.
Animals ; Antioxidants* ; Ascorbic Acid ; Cell Survival ; Cells, Cultured ; Glutathione ; Rats

In order to elucidate the neurotoxic effect of oxygen radicals on cultured mouse cerebral neurons, the neurotoxicity induced by xanthine oxidase (XO) and hypoxanthine (HX), was evaluated by MTT assay. The neuroprotective effect of allopurinol against oxidant -mediated neurotoxicity was also examined in these cultures by MTT assay and neurofilament enzymeimmunoassay (EIA) with light microscopy. The results were as follows: 1. Oxygen radicals induced degenerative changs such as the decrease of cell number and the loss of neurites in cultured mouse cerebral neurons. 2. The value of midcytotoxicity value (MTT50) of oxygen radicals was estimated at a concentration of 20 mU/ml XO and 0.1 mM HX for 4 hours in these cultures. 3. Cell viability of cultured mouse cerebral neurons was significantly decreased by XO/HX in a dose -and time -dependent manners. 4. Allopurinol was very effective in blocking the neurotoxicity induced by XO/HX at a concentration of 30 microM as determined by MTT assay and neurofilament enzymeimmunoas-say. From the above results, it is suggested that oxygen radicals show neurotoxicity, and the selective antioxidant such as allopurinol are very effective in blocking oxidant -mediated neurotoxicity on cultured mouse cerebral neurons.
Allopurinol* ; Animals ; Antioxidants* ; Cell Count ; Cell Survival ; Hypoxanthine ; Mice* ; Microscopy ; Neurites ; Neurons* ; Neuroprotective Agents ; Oxygen* ; Reactive Oxygen Species ; Xanthine Oxidase