Humans ; Nitrogen Oxides ; poisoning ; Pulmonary Edema ; chemically induced

The aim of this study was to determine whether formalin reliably provokes a paw edema and pain behavior. The paw of male Sprague-Dawley rats were injected with 100 microliter of formalin with 2.5% (F2.5), 5% (F5), and 10% (F10) concentrations. Following the formalin (n=8) or saline (control, n=6) injection, the flinching or licking of the paw was recorded for the phase 1 response (0-5 min after injection) and phase 2 response (20-60 min). The formalin-induced paw edema was assessed by measuring the diameters of the injected paws at 4 hr after injection. As for flinching, phase 1 and 2 of all three groups showed higher frequency than those of the control group (p<0.05). As for licking, phase 1 cumulative time of the F2.5 and F10 groups, and phase 2 cumulative time of the F2.5 and F5 groups showed a longer duration than those in the control group (p<0.05). The diameters of the paw in the F10 group were significantly larger than those in the control group (p<0.05). Flinching behavior was more reliably expressed the biphasic response than licking response at all formalin concentrations. Peak of the licking was reached at 2.5% and that of flinching was reached at 5%, whereas the paw edema peaked at 10% concentration. This suggests that there may be some dissociation of nociception from the edema formation.
Animals ; *Behavior, Animal ; Edema/*chemically induced ; Extremities ; Formaldehyde/*adverse effects ; Male ; Pain/*chemically induced ; Rats ; Rats, Sprague-Dawley

Humans ; Male ; Middle Aged ; Occupational Diseases ; complications ; Pulmonary Edema ; chemically induced ; Trimethylsilyl Compounds ; poisoning

Burns, Inhalation ; complications ; Humans ; Male ; Middle Aged ; Nitric Acid ; adverse effects ; Pulmonary Edema ; chemically induced ; therapy

Administration, Oral ; Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; therapeutic use ; Aspirin ; adverse effects ; therapeutic use ; Brain Edema ; chemically induced ; Child ; Coma ; chemically induced ; Female ; Humans ; Liver ; drug effects ; pathology ; physiopathology ; Reye Syndrome ; chemically induced ; Treatment Outcome

Topical phenylephrine, an agent used to facilitate nasotracheal intubation and prevent nasal mucosal bleeding, can cause severe hypertension in some patients, secondary to its stimulation of alpha-adrenergic receptors. Moreover, a high incidence of pulmonary edema is found in patients whose phenylephrine administration is followed by treatment with beta-blocking agents. We report a case of acute pulmonary edema in a pediatric patient who developed severe hypertension after the inadvertent administration of a large dose of topical nasal phenylephrine, followed by beta-adrenergic antagonists (esmolol).
Administration, Intranasal ; Adolescent ; *Anesthesia, General ; Dentigerous Cyst/surgery ; Humans ; Male ; Phenylephrine/*adverse effects ; Pulmonary Edema/*chemically induced/radiography ; Radiography, Thoracic

OBJECTIVETo establish the rats model of acute pulmonary edema induced by inhalation of high concentrations of nitrogen dioxide (NO2).

METHODS38 SD rats were divided into the experimental group (n = 30) and the control group (n = 8). 30 rats in the experimental group were exposed to (6747.47 ± 25.24) mg/m(3) NO2 in the exposure system. At the time point of 6, 12, 18, 24 h, chest X-ray examination was taken for the experimental group. And at each time point, 6 rats were sacrificed after taking blood samples. After sacrificing, the lung of rats was taken for pathological examination and calculated lung wet/dry weight ratio. Erythrocyte superoxide dismutase (SOD) activity and plasma atrial natriuretic peptide (ANP) concentration of blood samples were detected.

RESULTSAcute pulmonary edema was successfully induced by exposure to NO2 in 30 rats within 24 hours. There were some cloudy shadows without clear edge on the chest X-ray. To the time point of 12 hours, shadows combined with each other, and to the time point of 18 hours, the whole lung became "white" on the X-ray. The situation stabilized but not improved at the time point of 24 hours. HE staining of the lung tissue showed that to the time point of 6 hours, the alveolar gap increased and small amount of eosinophilic liquid leaked into alveolar. To the time point of 12 hours, alveolar combined with each other and eosinophilic liquid increased in amount. To the time point of 18 hours, the whole alveolar was filled with eosinophilic liquid and the situation stabilized till the time point of 24 hours. Wet/dry weight ratio of the experimental group at each time point were 5.6 ± 0.20, 6.89 ± 0.25, 8.03 ± 0.47, 7.81 ± 0.45. There was significant difference compared with the control group which was 4.72 ± 0.06 (P < 0.01). There was statistical difference between 12, 18, 24 h and 6 h time points (P < 0.01). Moreover, statistical difference was observed between 18, 24 h and 12 h time points for wet/dry weight ratio (P < 0.01). The erythrocyte SOD activity reduced significantly. Compared with the control group, there was a statistical difference (P < 0.01) at each time point. After exposure of 18 and 24 hours, plasma ANP concentration (136.66 ± 35.37) and (134.10 ± 60.41) ng/ml respectively, which were higher than (31.31 ± 13.06) ng/ml of control group and (34.71 ± 13.42) ng/ml of 6 hours time point and (47.98 ± 7.86) ng/ml. The differences were significant (P < 0.01).

CONCLUSIONHigh concentrations of NO2 can induce acute pulmonary edema model successfully in SD rats.

Animals ; Disease Models, Animal ; Female ; Nitrogen Dioxide ; administration & dosage ; toxicity ; Pulmonary Edema ; chemically induced ; Rats ; Rats, Sprague-Dawley

To investigate the role of AQP9 in brain edema, the expression of AQP9 in an infectious rat brain edema model induced by the injection of lipopolysaccharide (LPS) was examined. Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis demonstrated that the expressions of AQP9 mRNA and protein at all observed intervals were significantly increased in LPS-treated animals in comparison with the control animals. Time-course analysis showed that the first signs of blood-brain barrier disruption and the increase of brain water content in LPS-treated animals were evident 6 h after LPS injection, with maximum value appearing at 12 h, which coincided with the expression profiles of AQP9 mRNA and protein in LPS-treated animals. The further correlation analysis revealed strong positive correlations among the brain water content, the disruption of the blood-brain barrier and the enhanced expressions of AQP9 mRNA and protein in LPS-treated animals. These results suggested that the regulation of AQP9 expression may play important roles in water movement and in brain metabolic homeostasis associated with the pathophysiology of brain edema induced by LPS injection.
Aquaporins/genetics ; Aquaporins/*metabolism ; Blood-Brain Barrier/metabolism ; Brain/drug effects ; Brain/physiology ; Brain Edema/chemically induced ; Brain Edema/*metabolism ; Lipopolysaccharides ; Rats, Sprague-Dawley ; Water/physiology

The precise relationship between the degree of pain and the degree of inflammation in the individual remains debated. A quantitative analysis simultaneously applied to the immediate and prolonged painful consequences of inflammation has not yet been done. Thus, the correlations between edema, nociception and hypersensitivity following an inflammatory insult were assessed in rodents. To better understand the therapeutic value of modifying specific aspects of inflammation, the effects of an anti-inflammatory drug were compared to the results. Inbred strains of mice and outbred rats received an intraplantar injection of honeybee venom and the between-group and within-group correlations were calculated for spontaneous nociceptive measures, thermal and mechanical hypersensitivity, and edema and temperature. The effect of indomethacin on the pain and inflammation measures was examined. Edema correlated with spontaneous flinching, licking and lifting of the injected paw (P< or =0.003), and not with thermal or mechanical hypersensitivity. Indomethacin affected edema and spontaneous nociception dose-dependently, and affected hypersensitivity only at the highest dose tested (P< 0.05). These results suggest that edema may contribute only to immediate spontaneous nociceptive responses to an inflammatory insult, and not to the more clinically relevant prolonged hypersensitivity. This analysis represents a method for determining which inflammatory processes are the most promising therapeutic targets against the multiple painful consequences of inflammation.
Animals ; Anti-Inflammatory Agents, Non-Steroidal ; pharmacology ; Bee Venoms ; Edema ; chemically induced ; complications ; Indomethacin ; pharmacology ; Inflammation ; chemically induced ; complications ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nociceptors ; physiology ; Pain ; etiology ; physiopathology ; Pain Measurement ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the regulatory mechanism of immune response of guinea pigs sensitized by trichloroethylene (TCE), and the expression level of 3-arrestin, and the activity of NF-kappaB and AP-1 in peripheral blood mononuclear cells (PBMC) of guinea pigs sensitized by TCE.

METHODSGuinea pigs were treated with TCE based on the guinea pig maximum response test (GPMT); Blank control group and DNCB positive control group were established. Scores of skin reaction were evaluated and used to determine whether or not allergy in guinea pig. Then TCE treated group was divided into sensitized group or un-sensitized group. The expression levels of beta-arrestin protein, activity of NF-kappaB and AP-1 in PBMC were detected by Western Blotting and EMSA, respectively. TNF-alpha level in serum was detected by ELISA kits.

RESULTSNo erythema or edema was found in the control group; part of guinea pigs treated with TCE developed erythema and edema, while obvious erythema and edema could be found in DNCB group. The sensitization rates were 71.4% and 100% in TCE and DNCB group, respectively. Compared with TCE un-sensitized group, expression of beta-arrestin and AP-1 activity were not significantly different in TCE sensitized group (P > 0.05). While the NF-kappaB activity was elevated obviously (P < 0.05). Compared with blank control groups [(32.118 +/- 12.550) pg/ml], serum TNF-alpha levels in TCE sensitized groups [(55.485 +/- 8.732) pg/ml] significantly elevated (P < 0.05);

CONCLUSIONIn guinea pigs, beta-arrestin and AP-1 may not be activated, while the NF-kappaB activation is significant, and plays a immune regulatory role in the immune reaction of allergy induced by TCE.

Animals ; Arrestins ; blood ; Edema ; chemically induced ; Erythema ; chemically induced ; Female ; Guinea Pigs ; Hypersensitivity ; blood ; Leukocytes, Mononuclear ; drug effects ; immunology ; metabolism ; NF-kappa B ; blood ; Transcription Factor AP-1 ; blood ; Trichloroethylene ; toxicity ; Tumor Necrosis Factor-alpha ; blood ; beta-Arrestins