title: Cardiac ATP breakdown and mechanical function during recurrent periods of anoxia.
abstract: The effect of repeated short anoxic or ischemic periods on ATP breakdown and cardiac function remains controversial. To analyze this issue further and to study the regulation of adenine nucleotide breakdown during recurrent cardiac anoxia, we compared two different protocols of intermittent anoxia. Four rat hearts, perfused according to Langendorff, were exposed to 12 periods of anoxia, each lasting 1 minute, with reoxygenation periods of 3 minutes (protocol A). A second group of 8 hearts were made anoxic for 6 periods of anoxia, each lasting 1 minute, followed by 6 periods of anoxia, each lasting 2 minutes, with the same reoxygenation periods (protocol B). Adenosine production was studied with high performance liquid chromatography, ventricular contraction was monitored using a force transducer. During anoxia a substantial vasodilation and immediate fall in strength of ventricular contraction occurred. They were most pronounced during the first anoxic period and during the change from 1 to 2 minute periods of anoxia. Adenosine production was about 1 nmol/min during the first 1-minute anoxic period, decreasing during the following 1-minute anoxic periods. During the first 2-minute anoxic period, a new and much higher adenosine peak was observed (6 nmol/min), decreasing during the following 2-minute anoxic periods. Total purine release followed a pattern similar to that of adenosine. The concentration of ATP at the end of protocol B was 18.5 mumol/g dry tissue, which is significantly lower than that in protocol A (21.6 mumol/g). The results show that ATP breakdown during intermittent anoxia gradually decreases, notwithstanding the presence of substantial amounts of ATP.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Thoraxcenter, Erasmus University Rotterdam, The Netherlands.
authors.forename: I K
authors.initials: IK
authors.lastname: De Scheerder
authors.forename: A A
authors.initials: AA
authors.lastname: Maas
authors.forename: A S
authors.initials: AS
authors.lastname: Nieukoop
authors.forename: P
authors.initials: P
authors.lastname: van der Meer
authors.forename: T
authors.initials: T
authors.lastname: Huizer
authors.forename: J R
authors.initials: JR
authors.lastname: Roelandt
authors.forename: J W
authors.initials: JW
authors.lastname: de Jong
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002851:Chromatography, High Pressure Liquid; D004734:Energy Metabolism / Q000502:physiology; D000860:Hypoxia / Q000378:metabolism*; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D011687:Purines / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D000227:Adenine Nucleotides; D011687:Purines; D000255:Adenosine Triphosphate