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dc.contributor.authorGaspari, Romolo Joseph
dc.contributor.authorPaydarfar, David
dc.date2022-08-11T08:08:57.000
dc.date.accessioned2022-08-23T16:13:51Z
dc.date.available2022-08-23T16:13:51Z
dc.date.issued2007-05-01
dc.date.submitted2008-09-11
dc.identifier.citationNeurotoxicology. 2007 May;28(3):664-71. Epub 2007 Feb 11. <a href="http://dx.doi.org/10.1016/j.neuro.2007.02.002">Link to article on publisher's site</a>
dc.identifier.issn0161-813X (Print)
dc.identifier.doi10.1016/j.neuro.2007.02.002
dc.identifier.pmid17350689
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33724
dc.description.abstractOrganophosphate (OP) poisoning causes a cholinergic crisis with a wide range of clinical effects including central apnea, pulmonary bronchoconstriction and secretions, seizures, and muscle weakness. The morbidity and mortality from acute OP poisoning is attributed to respiratory failure but the relative contributions of the central and peripheral effects in producing collapse of the respiratory system are unclear. In this study we used a novel adult rat model of acute OP poisoning to analyze the pathophysiology of acute OP poisoning. We found that poisoning caused rapidly lethal central apnea. In animals sustained with mechanical ventilation, we found that following central apnea there ensued progressive pulmonary insufficiency that was variable in timing and severity. Our findings support the hypothesis that OP poisoning in this animal model causes a sequential "two hit" insult, with rapid central apnea followed by delayed impairment of pulmonary gas exchange with prominent airway secretions.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17350689&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2041827/pdf/nihms25955.pdf
dc.subjectAcute Disease; Algorithms; Anesthesia, General; Anesthesia, Inhalation; Animals; Blood Gas Analysis; Blood Pressure; Carbon Dioxide; Cholinesterase Inhibitors; Data Interpretation, Statistical; Dichlorvos; Heart Rate; Male; Pesticides; Pulmonary Gas Exchange; Rats; Rats, Wistar; Respiration, Artificial; Respiratory Insufficiency
dc.subjectLife Sciences
dc.subjectMedical Toxicology
dc.subjectMedicine and Health Sciences
dc.subjectNeurology
dc.subjectNeuroscience and Neurobiology
dc.subjectPharmacology, Toxicology and Environmental Health
dc.titlePathophysiology of respiratory failure following acute dichlorvos poisoning in a rodent model
dc.typeJournal Article
dc.source.journaltitleNeurotoxicology
dc.source.volume28
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/387
dc.identifier.contextkey627224
html.description.abstract<p>Organophosphate (OP) poisoning causes a cholinergic crisis with a wide range of clinical effects including central apnea, pulmonary bronchoconstriction and secretions, seizures, and muscle weakness. The morbidity and mortality from acute OP poisoning is attributed to respiratory failure but the relative contributions of the central and peripheral effects in producing collapse of the respiratory system are unclear. In this study we used a novel adult rat model of acute OP poisoning to analyze the pathophysiology of acute OP poisoning. We found that poisoning caused rapidly lethal central apnea. In animals sustained with mechanical ventilation, we found that following central apnea there ensued progressive pulmonary insufficiency that was variable in timing and severity. Our findings support the hypothesis that OP poisoning in this animal model causes a sequential "two hit" insult, with rapid central apnea followed by delayed impairment of pulmonary gas exchange with prominent airway secretions.</p>
dc.identifier.submissionpathgsbs_sp/387
dc.contributor.departmentDepartment of Neurology
dc.contributor.departmentDepartment of Emergency Medicine
dc.source.pages664-71
dc.contributor.studentRomolo Gaspari


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