Atropine (2.5 mg/kg), hexamethonium (1 mg/kg), Trasylol (1,000 u/kg), acetazolamide (100 mg/kg), cortisone (5 mg /kg) or procaine (5 mg/kg) were injected intraperitoneally once a day for 21 days into rats (both sexes) fed a low protein diet. The rats were fasted and sacrificed 24 hr after the last injection. Atropine and cortisone, but not the other agents, cause a significant increase in both pancreatic weight and enzymes. Serum amylase increased markedly in the cortisone group and serum GOT and GPT increased but slightly in the atropine group. Enlargement of the pancreatic acini, cellular hypertrophy and increases of zymogen granules were observed in all the groups except the procaine and normal control group. The hypertrophy of acini was more prominent in the atropine and cortisone groups. None of drugs used could induce decrease or depress the enzyme formation and weight of pancreas. This data indicates that long-term administration of these drugs, particularly atropine, cortisone or even other Ragents may induce preferential formation of pancreatic enzymes to exocrine secretions and consequently may cause enlargement of the pancreatic acini.
Acetazolamide/administration & dosage* ; Alanine Transaminase/blood ; Amylases/blood ; Animal ; Aprotinin/administration & dosage* ; Aspartate Aminotransferases/blood ; Atropine/administration & dosage* ; Cortisone/administration & dosage* ; Female ; Hexamethonium Compounds* ; Lipase/blood ; Male ; Organ Weight ; Pancreas/drug effects* ; Pancreas/enzymology ; Procaine/administration & dosage* ; Rats ; Time Factors

This study was undertaken to clarify the effects of glucocorticosteroids on intraocular pressure and the combined effects of acetazolamide and glucocorticosteroid on ocular pressure. Male and female rabbits, weighing 1.7-2.2kg, were divided into 5 groups: 1) saline-treated group, 2) hydrocortisone (0.5 %)-treated group, 3) prednisolone (0.5 %)-treated group, 4) fludrocortisone (0.1% )-treated group, 5) dexamethasone (0.1% )-treated group. Drugs were instilled 4 times a day for 3 weeks, and ocular pressure was checked in each group on second and third week. Following 3 weeks instillation of glucocorticoids, ocular pressure was checked in each animal at 15, 30, 60, and 120 minutes after intravenous administration of acetazolamide (10mg/kg). Under 0.5% tetracaine anesthesia, facility of outflow and flow rate of the aqueous humor were also measured with a tonometer. The results of the experiments were as follows: 1) The mean ocular pressure rose significantly in all glucocorticoid-treated groups, and the rise was especially marked in the dexamethasone-treated group. 2) The mean facility of outflow of the aqueous humor decreased significantly in the dexamethasonetreated group, but it remained with little change in the other glucocorticoidtreated group. 3) The ocular pressure-lowering action of acetazolamide was suppressed significantly at 30 minutes after the treatment with acetazolamide in the hydrocortisone and prednisolonetreated groups, but it was not suppressed in the fludrocortisone and the dexamethasonetreated groups. 4) The flow rate of the aqueous humor was suppressed significantly (36.2 %) at 30 minutes after the treatment with acetazolamide in the control group, but it was not suppressed significantly in g]ucocorticoid-treated groups.
Acetazolamide* ; Administration, Intravenous ; Adrenal Cortex Hormones* ; Anesthesia ; Animals ; Aqueous Humor ; Dexamethasone ; Female ; Fludrocortisone ; Glucocorticoids ; Humans ; Hydrocortisone ; Intraocular Pressure* ; Male ; Prednisolone ; Rabbits ; Tetracaine

Bietti crystalline retinal dystrophy is a rare, inherited disorder whose hallmark is the presence of retinal crystal deposits associated with later chorioretinal degeneration. This condition may rarely be complicated by the development of cystoid macular oedema leading to rapid visual decline. Currently, treatment options for this complication of Bietti dystrophy are limited and the visual prognosis is poor. Here, we present a case of cystoid macular oedema associated with Bietti dystrophy that was successfully diagnosed using multimodal imaging techniques including optical coherence tomography and fluorescein angiography. These modalities confirmed the diagnosis of macular oedema and excluded other possible causes of oedema such as choroidal neovascularisation. In this patient, cystoid macular oedema was resolved with oral acetazolamide therapy, a treatment that has not been previously reported in this context. Acetazolamide treatment resulted in oedema resolution and improvement in visual function, and can be considered a therapeutic option for other patients with Bietti dystrophy who develop cystoid macular oedema.
Acetazolamide/*administration & dosage ; Administration, Oral ; Adult ; Corneal Dystrophies, Hereditary/*drug therapy/pathology ; Diuretics/*administration & dosage ; Humans ; Macular Edema/*drug therapy/pathology ; Male ; Retinal Diseases/*drug therapy/pathology ; Tomography, Optical Coherence ; Treatment Outcome

PURPOSE: Although time-of-flight (TOF)-magnetic resonance angiography (MRA) can clearly depict intracranial arteries, the arterial flow of middle cerebral artery (MCA) is occasionally not detected. We evaluated this phenomenon with reference to cerebrovascular dynamics. MATERIALS AND METHODS: Seventeen patients with suspected occlusion of MCA or internal carotid artery on TOF-MRA were enrolled. All patients underwent CT angiography (CTA) and quantitative cerebral blood flow (CBF) examination for measurement of resting CBF and cerebrovascular reactivity (CVR). Depending on appearance, patients were categorized into three groups. Group A (n=6) had MCA delineation on both MRA and CTA, while groups B (n=6) and C (n=5) had no signal on MRA, but Group B had a MCA delineation on CTA.
Acetazolamide/administration & dosage ; Aged ; Aged, 80 and over ; Carotid Artery, Internal/physiopathology ; Cerebrovascular Circulation ; Computed Tomography Angiography ; Female ; Humans ; Magnetic Resonance Angiography ; Male ; Middle Aged ; Middle Cerebral Artery/diagnostic imaging

An 11-year-old female presenting diplopia only at distance was found to have comitant esotropia of 20 prism diopters (PD) at distance and normal alignment at nearer proximity. Other ocular movement, including abduction, was normal and a thorough neurologic examination was also normal. The deviation angle of esotropia was increased to 35 PD in 6 months, and a brain magnetic resonance imaging with venogram at that time demonstrated no intracranial lesion. A lumbar puncture showed increased opening pressure but the cerebrospinal fluid composition was normal. The patient was diagnosed as having idiopathic intracranial hypertension and treated with oral acetazolamide. Three months after treatment, the deviation angle decreased to 10 PD. This is a case report of divergence insufficiency in pediatric idiopathic intracranial hypertension, with an increasing deviation angle of esotropia. Although sixth cranial nerve palsy is a common neurologic manifestation in intracranial hypertension, clinicians should be aware of the possibility of divergence insufficiency. Also, ophthalmoparesis may not be apparent and typical at first presentation, as seen in this case, and therefore ophthalmologists should be aware of this fact, while conducting careful and proper evaluation, follow-up, and intervention.
Acetazolamide/administration & dosage ; Administration, Oral ; Child ; Diagnosis, Differential ; Diuretics/administration & dosage ; Esotropia/diagnosis/*etiology/physiopathology ; Exotropia/diagnosis/*etiology/physiopathology ; Eye Movements ; Female ; Follow-Up Studies ; Humans ; Intracranial Pressure ; Magnetic Resonance Imaging ; Pseudotumor Cerebri/*complications/diagnosis/drug therapy ; Spinal Puncture/methods ; Vision, Binocular ; Visual Acuity