title: Hypoxia and ischaemia in buffer-perfused toad hearts.
abstract: Previous studies on the effects of ischaemia or hypoxia in ectothermic vertebrate hearts have generally used preparations that were not performing at physiological levels of pressure and flow. The conclusions that ischaemia or hypoxia are not stressful to these organisms were examined in another species, Bufo marinus, in which a buffer-perfused heart was performing physiological levels of work. The in situ preparation demonstrated the Frank-Starling relationship and mechanical characteristics similar to the hearts of intact animals. The hearts recovered from 60 min of ischaemia and reperfusion with no reduction in pressure, flow or heart rate parameters. Hearts exposed to 30 min of hypoxia at physiological filling and diastolic afterload pressures ceased generating a continuous cardiac output during the hypoxia. In most cases, there was a gradual reduction of cardiac output to zero, but in 27% of the hearts studied, intermittent beating was observed. During reoxygenation, the hearts recovered 50-90% of their prehypoxic function and were damaged. Hearts exposed to hypoxia with reduced filling and diastolic afterload continued to develop a cardiac output throughout the hypoxia and demonstrated an overshoot phenomena with the onset of reoxygenation. If demand is in the normal range at the onset of hypoxia, the hearts intrinsically reduce demand either by reducing pressure development or by conversion to intermittent beating. Toad hearts appear not to be damaged by ischaemia, a condition in which demand is low.
authors.affiliation: Department of Biological Sciences, University of Idaho, Moscow 83844-3051, USA.
authors.forename: T
authors.initials: T
authors.lastname: McKean
authors.forename: A
authors.initials: A
authors.lastname: Scherzer
authors.forename: H
authors.initials: H
authors.lastname: Park
mesh_terms: D000818:Animals; D002021:Buffers; D002024:Bufo marinus / Q000502:physiology*; D002302:Cardiac Output; D006321:Heart / Q000502:physiology* / Q000503:physiopathology; D006339:Heart Rate; D000860:Hypoxia / Q000503:physiopathology; D066298:In Vitro Techniques; D007511:Ischemia / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000503:physiopathology; D010477:Perfusion; D013045:Species Specificity
chemical_list: D002021:Buffers