Enhancement of Microvascular Leakage in the Nasal Mucosa after Re-exposure to Capsaicin in a Rat Model Challenged/Rechallenged with Capsaicin

It has been suggested that the role of neurogenic inflammation is to protect the airway from various noxious irritants in inhaled air. Repeated exposure to various irritating stimuli has become very common in daily life. However, the process that occurs in neurogenic inflammation after repeated exposure to irritating stimuli is not yet clearly understood. The aim of this study was to investigate the changes of microvascular leakage in the airways after re-exposure to capsaicin in an experiment using a rat model challenged/rechallenged with capsaicin. Twenty-four Sprague-Dawley rats were divided into four groups : a capsaicin-challenged group (10 microgram/kg of capsaicin, intravenous, n=6) and three capsaicin-rechallenged groups (10 microgram/kg of capsaicin, intravenous, n=6 in each group) corresponding to time intervals of 1, 3, or 6 hours after capsaicin-challenge. The amount of microvascular leakage in the nasal mucosa and trachea of the animal in each group was measured with extravasation of Evans blue dye (30 mg/kg, intravenous) using a spectrophotometer. In the nasal mucosa, a significant enhancement of microvascular leakage with capsaicin-rechallenge was observed at 3 hours after capsaicin-challenge (AVOVAR, * : p<0.01). However, there was no significant changes in the trachea. In conclusion, the protective mechanisms against repeated irritating stimuli in the nasal mucosa and trachea are different. After exposure to a noxious irritant, the airway defense mechanism mediated by an axon reflex in the nose may be up- regulated, while that in the trachea may not be changed.

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.

Propofol and ketamine attenuate antigen-induced bronchoconstriction and microvascular leakage in rats / 中华麻醉学杂志

Objective To investigate the effects of propofol and ketamine on antigen-induced bronehoconstriction and microvascular leakage in rats.Methods Thirty SD rats of both sees weighing 150-200 g were sensitized with ovalbumin 1 mg, aluminium hydroxide 200 mg and devitalized Bordetella pertusis (6 ? 109 ) adminisered intraperitoneally 2 weeks before experiment. The animals were anesthetized with pentobarbital 30 mg ? kg-1 ip, tracheotomized and mechanically ventilated (VT = 10 ml? kg-1 , RR = 70 bpm) . The animals were randomly divided into 5 groups with 6 animals in each group: group I received normal saline iv group II propofol 50 mg?kg-1?h-1 iv group III propofol 100 mg?kg-1?h-1 iv group IV ketamine 50 mg?kg-1?h-1 iv; and group V ketamine 100 mg? kg-1? h-1 iv. Two minutes after propofol or ketamine administration Evan's blue 30 mg?kg-1 was given iv. Five minutes after dye injection ovalbumin 15 mg?kg-1 was injected iv to trigger asthmatic attack which was maintained for 30 min when airway pressure was measured. Then the animals were sacrificed by bleeding. Heart and lungs were removed for determination of lung coefficient( wet lung weight/body weight) , wet lung/dry lung ratio, lung extravascular water content [ (wet lung weight - dry lung weight/wet lung weight ? 100% ] and lung Evans blue content (formamide extraction method) . Results Propofol and ketamine significantly attenuated ovalbumin-induced bronchoconstiction( P