Post-ischemic contractile dysfunction does not correlate with an elevated intracellular free [Mg2+]: a 31P-NMR study on isolated rat and rabbit hearts.
The aim of this study was to investigate whether intracellular free Mg2+ (Mgr), which increases during myocardial ischemia due to hydrolysis of ATP, remained elevated during reperfusion after a relatively short period of ischemia and thereby could account for temporary post-ischemic contractile dysfunction, often referred to as stunning. 31P-magnetic resonance (31P-NMR) spectroscopy was used to follow creatine phosphate, adenosine triphosphate, intracellular inorganic phosphate, intracellular pH and Mgr simultaneously with left ventricular developed pressure (LVDP) and coronary flow in isolated rat and rabbit hearts, which were perfused (37 degrees C) according to Langndorff. LVDP was measured in an isovolumic way by means of an intraventricular latex balloon. Rat hearts (300 beats/min) were made globally ischemic for 15 min and rabbit hearts (180 beats/min) for 15 or 20 min. All hearts were reperfused for 60 min. Control hearts were perfused for 75 min without being made ischemic. During ischemia Mgr (mmol/l) increased from 0.76 +/- 0.20 to 4.34 +2- 1.99 in the rat hearts, and from 0.72 +/- 0.22 to 2.18 +/- 1.06 (15 min) and 2.35 +/- 1.26 (20 min) in the rabbit hearts. During reperfusion Mgr in the three groups returned to the level of the control hearts within 7.5 min, and LVDP within 25 min. At the end of the reperfusion period ATP content amounted to 56 +/- 17% (rat hearts), 66 +/- 10% (rabbit hearts; 15 min ischemia group) and 61 +/- 7% (rabbit hearts; 20 min ischemia group) of the pre-ischemic levels. The results confirm that in vitro stunning is a short-lived phenomenon and indicate that an increased Mgr is not involved in this temporary mechanical dysfunction.
Schreur
J H
JH
Interuniversity Cardiology Institute of The Netherlands, Department of Cardiology, University Hospital, Utrecht.
de Beer
R
R
Van Echteld
C J
CJ
Ruigrok
T J
TJ
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D006321:Heart / Q000503:physiopathology; D008274:Magnesium / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism
D000255:Adenosine Triphosphate; D008274:Magnesium