title: Exposure of rats to hyperoxia enhances relaxation of isolated aortic rings and reduces infarct size of isolated hearts.
abstract: Exposure of rats to hyperoxia before organ harvesting protected their isolated hearts against global ischaemia-reperfusion injury in a previous study. The present study investigates whether hyperoxia influences vasomotor function and regional ischaemia of the heart. Isolated rings of the thoracic aorta were obtained from rats immediately or 24 h after in vivo exposure to 60 min of hyperoxia (>95% O2), and the in vitro dose-response to phenylephrine (PHE), prostaglandin F2alpha (PGF2alpha) and endothelin-1 (ET-1), acetylcholine (Ach) and sodium nitroprusside (SNP) was assessed. Hyperoxia in vivo increased the relaxation of aortic rings to Ach and SNP, while it delayed contraction to PHE. The effect was more evident when the vessels were harvested immediately rather than 24 h after hyperoxic exposure. In separate experiments rat hearts were isolated immediately after hyperoxia, buffer-perfused, and subjected to 30 min of regional ischaemia and reperfused for 120 min. Infarct size was determined by triphenyl tetrazolium chloride staining. Hyperoxia significantly reduced infarct size. In normoxic controls 23.0 +/- 8.3% of the area at risk was infarcted, while in hyperoxic animals infarct size was 14.8 +/- 5.6% of the area at risk (P = 0.012). Exposure of rats to hyperoxia modifies the vasomotor response of isolated aortic rings, and reduces the infarct size of isolated rat heart. These novel aspects of hyperoxic treatment require further studies to explore the potential of its clinical application.
authors.affiliation: Crafoord Laboratory for Experimental Surgery, Karolinska Hospital, Stockholm, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Tähepõld
authors.forename: P
authors.initials: P
authors.lastname: Elfström
authors.forename: I
authors.initials: I
authors.lastname: Eha
authors.forename: J
authors.initials: J
authors.lastname: Kals
authors.forename: G
authors.initials: G
authors.lastname: Taal
authors.forename: A
authors.initials: A
authors.lastname: Talonpoika
authors.forename: G
authors.initials: G
authors.lastname: Valen
authors.forename: J
authors.initials: J
authors.lastname: Vaage
authors.forename: J
authors.initials: J
authors.lastname: Starkopf
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology; D015237:Dinoprost / Q000494:pharmacology; D019332:Endothelin-1 / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D018496:Hyperoxia / Q000503:physiopathology*; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology; D016276:Ventricular Function
chemical_list: D019332:Endothelin-1; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D015237:Dinoprost