43 Exposure to low-vapor levels can involve the eyes, nose, and airways. Visual disturbances, rhinorhea, and/or dyspnea can develop seconds to several minutes
after exposure. Eye contact with vapor causes miosis that may be accompanied by deep eye pain, conjunctival irritation, and visual disturbances. Inhalaltion of high-vapor concentration can induce consciousness within one or two minutes and then cause seizures, flaccid paralysis, and apnea and the victims may die within 30 minutes in the absence of immediate medical Inhibitors,research,lifescience,medical care.44 Cholinergic clinical manifestations of OPs are as a result of excessive ACh receptors (muscarinic and nicotinic) stimulation, which appear during the first few hours after exposure.28 Muscarinic receptors include dizziness, nausea, vomiting, abdominal pain, diarrhea, miosis, blurred vision, salivation, lacrimation, urination and respiratory dysfunctions. Major effects on the respiratory system include bronchoconstriction and increased bronchial secretion Inhibitors,research,lifescience,medical leading to respiratory failure, which is the main cause of mortality. Nicotinic effects include easy fatigue, weakness, muscle cramp, fasciculations,
skeletal muscle twitching, convulsions and flaccid paralysis. Inhibitors,research,lifescience,medical Central nervous system effects include: irritability, nervousness, giddiness, ataxia, fatigue, and generalized weakness, depression of respiratory and circulatory centers with dyspnea, cyanosis, hypoventilation and hypotension, lethargy, impairment
of memory, confusion, convulsions, coma and respiratory depression.45-48 Consequently, depression of respiratory and vasomotor centers in the brain can Inhibitors,research,lifescience,medical occur and deteriorate the clinical picture.49 With moderate to large doses of OPs, Inhibitors,research,lifescience,medical nicotinic and central stimulation predominates over most muscarinic effects. Death is usually due to respiratory and cardiovascular failure.50 The most life-threatening complication is respiratory failure, that is the most severe result of the nerve agents.51,52 One of the remarkable problems in the nerve agent poisoning is hypoxia, which may lead to cerebral edema, convulsions, and histopathological brain damage. Cardiovascular complications are sometimes severe and life threatening.53,54 Acute OP poisoning is associated with ventricular arrhythmias, tachycardia or bradycardia, and mild myocardial ischemia.55 Exaggerated Dacomitinib cholinergic stimulation increases the vagal nerve http://www.selleckchem.com/products/BAY-73-4506.html influence on heart rate and induces bradycardia and slowed cardiac conduction, leading to a decrease in cardiac output. However, in practice, tachycardia is usually observed as a result of fear and anxiety. Electrocardiogram abnormalities consist of idioventricular dysrhythmias, atrial fibrillation, multiform ventricular extra systoles, ventricular fibrillation, and complete heart block.52,56-58 Intermittent ST-T wave alterations and second-degree atrioventricular heart block also occurs.