Delayed recovery from paralysis by succinylcholine in patient with preoperatively unrecognized and inherited pseudocholinesterase deficiency / 대한마취과학회지

No abstract available.

Nitric Oxide Synthase Inhibitor Inhibits Platelet Activating Factor: Induced Microvascular Leakage in Rat Nasal and Tracheal Mucosa / 대한이비인후과학회지

BACKGROUND AND OBJECTIVE: Platelet-activating factor (PAF), a potent chemical mediator in inflammation and allergic reaction, induces microvascular leakage in several tissues. In rat airways, PAF-induced microvascular leakage is not dependent on cyclooxygenase or lipoxygenase products nor on circulating platelets, and it is probably mediated by receptors on vascular endothelium. Nitric oxide (NO), first identified as endothelium-derived relaxing factor, has been reported recently to be an important mediator of the neurogenic vascular exudative process. The aim of this study was to investigate the role of NO in PAF-induced microvascular leakage in rat nasal and tracheal mucosa. METHODS: PAF (1 ug/kg) was injected intravenously to induce microvascular leakage. The degree of microvascular leakage was measured with the amount of extravasated Evans blue (30 mg/kg) using both spectrophotometry and fluorescence microscopy. Five Sprague-Dawley rats were pretreated with Nw-nitro-L -arginine methyl ester (L-NAME, 10 mg/kg, intravenously, 1 hour before the injection of PAF) to inhibit the NO synthase, while four control rats(n=4) were pretreated with normal saline. RESULT: The average amounts of extravasated Evans blue in the nasal mucosa and trachea of the control rats were 24.789 and 28.238 ug/mg wet tissue, and those of the L-NAME pretreated rats were 6.643 and 6.987 ug/mg wet tissue respectively. Tissue sections of the L-NAME pretreated rats showed a definitely decreased extravasation of Evans blue under fluorescence microscopy. CONCLUSION: Pretreatment with L-NAME clearly inhibited PAF-induced microvascular leakage in the nasal and tracheal mucosa of rat. This finding implies that NO may mediate PAF-induced microvascular leakage in rat airways.

Megadose Steroids and Intranasal Optic Nerve Decompression in the Treatment of Traumatic Optic Neuropathy

BACKGROUND AND OBJECTIVES: Traumatic optic neuropathy (TON) is a relatively rare complication associated with closed head injury. However, it represents an extremely poor prognosis, and its management remains controversial. We present the treatment results of 15 patients with immediate and complete TON who were treated with megadose steroids (MDS), and, in cases where MDS produced no response, intranasal optic nerve decompression (OND). PATIENTS AND METHODS: The diagnosis of TON was based on evidence of the following : complete loss of vision, absence of direct pupillary light reflex and intact consensual response. All of the patients underwent high resolution CT scans of the orbit and received a complete neuro-opthalmologic examination. MDS was started immediately after the diagnosis. If no response occurred by 48 hours, an intranasal OND was conducted. RESULTS: Two of the 15 patients exhibited improved vision after treatment with MDS, and six of the remaining 13 patients who were unresponsive to MDS demonstrated improved vision after OND. Overall, eight out of the 15 patients experienced improved vision. CONCLUSION: This study is uncontrolled, but suggests that our protocol of MDS and, in cases where this produced no response, OND may be an effective and valid treatment modality for patients with immediate complete TON, which is generally believed to represent an extremely poor prognosis regardless of treatment.

Expression of Inducible Nitric Oxide Synthase in Rat and Guinea PigRespiratory Epithelium after Capsaicin Treatment / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: Nitric oxide (NO) production in the respiratory epithelium and the demonstration of inducible nitric oxide synthase in ciliated epithelium of the upper airway have recently been reported. The aim of this study was to investigate the expression of inducible nitric oxide synthase in the nasal epithelium after capsaicin treatment, which stimulates the substance P innervation. MATERIALS AND METHODS: In vivo treatment -Capsaicin (112 nM) was applied to the nasal cavities of the rat and guinea pig, and 30 nl of normal saline was applied for the control groups. After 2 hours, animals were sacrificed with cardiac perfusion of 4% paraformaldehyde and septal mucosa were removed. The 8 nm serial frozen tissue sections were made, and the expression of inducible nitric oxide synthase was determined using nicotinamide adenine diphosphate-diaphorase histochemistry. In vitro treatment- The nasal septum of the rats and the trachea of the guinea pigs were incubated in DMEM culture media with or without 112 nM capsaicin for experimental or control groups. After 0, 30 or 120 minutes of incubation, the tissues were fixed and processed for nicotinamide adenine diphosphate-diaphorase histochemistry. RESULTS: Both in vivo and in vitro studies demonstrated that the strong positive histochemical reactivity were observed in the respiratory epithelium of the rats and guinea pigs after capsaicin treatment compared to control groups. CONCLUSION: These data imply that capsaicin induces the expression of inducible nitric oxide synthase and that the substance P innervation of the nasal mucosa may have a protective role in the airway defense mechanism through nitric oxide production.

A Case of Neurofibromatosis Type II / 대한이비인후과학회지

Neurofibromatosis affects primarily cell growth of neural tissues and can cause tumors to grow on nerves at any time and any location. it is a heritable disease that is transmitted as an autosomal-dominant trait. Neurofibromatosis type II is characterized by bilateral acoustic neuromas with high incidence of other tumors. Hearing loss is the most common symptom in patients with neurofibromatosis type II. The other symptoms may be tinnitus, facial weakness, and dizziness. Audiometric test and MRI are essential to diagnose neurofibromatosis type II. Most cases of neurofibromatosis type II may need for surgical procedures. We experienced a case of neurofibromatosis type II having cervical spinal cord neuroma, multiple intracranial meningiomas, and bilateral acoustic neuromas. There was positive family history. Her two brothers also had neurofibromatosis type II, confined by MRI. Her acoustic neuroma on left side was removed successfully via translabyrinthine approach and cervical spinal cord neuroma by cervical laminectomy was removed.