Mohammad Hossein Boskabady
Mashhad University of Medical Sciences, Iran
Posters & Accepted Abstracts: J Pulm Respir Med
Increased airway responsiveness to diff erent stimuli is the main characteristic feature of asthma. However, airway hyper responsiveness is reported in COPD patients and smokers. In a series of studies airway responsiveness to various pharmacological agonists and antagonists were examined. In animal studies, increased tracheal responsiveness to histamine as histamine concentration caused 50% of maximum response (EC50) and hisataminie (H1) receptor blockade by chlorpheniramine as shift in concentration response to histamine (CR-1) in guinea pig model of COPD by their exposing to cigarette smoke as well as in sensitized animals was shown. Tracheal responsiveness to both isoprenaline and beta-adrenoreceptor blockade by propranolol in cigarette smoke exposed and sensitized guinea pigs and a close correlation in responsiveness to isoprenaline and propranolol between COPD and asthmatic animals were demonstrated. Increased tracheal responsiveness to methacoline and muscarinic receptor blockade by atropine in an animal model of COPD was also reported. Tracheal hyper responsiveness to methacholine in sulfur mustard exposed guinea pigs was also shown. In human studies, increased airway responsiveness to methacholine and salbutamol and the relationship between the two was demonstrated in smokers. Airway hyper responsiveness to salbutamol in COPD patients was also shown. Airway hyper responsiveness to methacholine as well as to salbutamol in chemical war victims were also shown in two studies. Increased airway responsiveness to diff erent pharmacological agonists and antagonists in exposed animal to cigarette smoke and sulfur mustard, smokers, COPD patients and chemical war victims were documented.
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