title: The effect of euthanasia technique on vascular arachidonic acid metabolism and vascular and intestinal smooth muscle contractility.
abstract: This study was designed to determine the effects that specific euthanasia methods have on vascular arachidonic acid metabolism and vascular and intestinal smooth muscle contractility. Rats were euthanatized by decapitation (DC), pentobarbital overdose (PB), or anesthesia with CO2, methoxyflurane or ether followed by DC (CO2-DC, Met-DC, Ether-DC, respectively). Rabbits were killed by a similar protocol, but CO2 overexposure replaced Ether-DC. The rat and rabbit aortas produced mainly 6-keto PGF1 alpha, the prostacyclin metabolite, and lesser amounts of PGE2. No qualitative differences were seen in arachidonate metabolites. However, aortic tissue from rabbits and rats killed by Met-DC produced more prostacyclin. In contrast, aorta from rabbits euthanatized by CO2-DC produced less prostacyclin than controls, whereas aorta from rats killed in the same way yielded greater amounts of prostacyclin. Aortic tissue from rabbits killed by Met-DC and CO2-OD was less responsive to acetylcholine (ACH). Intestinal contractility to ACH was increased in rabbits when Met-DC was used as the method of euthanasia, while colon from rats sacrificed by Met-DC showed decreased responsiveness to ACH. Colon from rats killed by intraperitoneal PB exhibited altered contractility to ACH and norepinephrine. The results of this study show that methoxyflurane, carbon dioxide (rabbit) and pentobarbital (rat) alter the vascular synthesis of prostacyclin and smooth muscle contractility. We conclude that the method of euthanasia affects certain physiologic parameters and careful consideration should be given to the selection of a particular euthanasia technique.
authors.affiliation: Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75235.
authors.forename: M M
authors.initials: MM
authors.lastname: Butler
authors.forename: S M
authors.initials: SM
authors.lastname: Griffey
authors.forename: F J
authors.initials: FJ
authors.lastname: Clubb
authors.forename: L W
authors.initials: LW
authors.lastname: Gerrity
authors.forename: W B
authors.initials: WB
authors.lastname: Campbell
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis*; D000280:Administration, Inhalation; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000032:analysis / Q000378:metabolism*; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000633:toxicity; D002851:Chromatography, High Pressure Liquid; D011464:Epoprostenol / Q000096:biosynthesis; D005065:Euthanasia / Q000662:veterinary*; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects / Q000201:enzymology; D008084:Lipoxygenase / Q000378:metabolism; D008297:Male; D008733:Methoxyflurane / Q000008:administration & dosage / Q000633:toxicity; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D010424:Pentobarbital / Q000008:administration & dosage / Q000633:toxicity; D011451:Prostaglandin-Endoperoxide Synthases / Q000032:analysis / Q000378:metabolism; D011817:Rabbits; D011897:Random Allocation; D051381:Rats; D011919:Rats, Inbred Strains; D013047:Specific Pathogen-Free Organisms
chemical_list: D001095:Arachidonic Acids; D002245:Carbon Dioxide; D016718:Arachidonic Acid; D008733:Methoxyflurane; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D008084:Lipoxygenase; D011451:Prostaglandin-Endoperoxide Synthases; D010424:Pentobarbital