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SUPEROXIDE DISMUTASE ATTENUATED POST‐ISCHAEMIC CONTRACTILE DYSFUNCTION IN A MYOCARDIAL XANTHINE OXIDASE DEFICIENT SPECIES
Author(s) -
Ooiwa Hitoshi,
Miura Tetsuji,
Iwamoto Toshihiro,
Ogawa Takashi,
Ishimoto Row,
Adachi Takeo,
Iimura Osamu
Publication year - 1992
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1992.tb00430.x
Subject(s) - myocardial stunning , xanthine oxidase , superoxide dismutase , ischemia , medicine , coronary occlusion , cardiology , chemistry , anesthesia , oxidative stress , biochemistry , enzyme
SUMMARY 1. We assessed the effect of polyethylene glycol conjugated superoxide dismutase (PEG‐SOD) on myocardial stunning in the rabbit heart in which xanthine oxidase level is extremely low. 2. In open‐chest anaesthetized rabbits, the left marginal branch of the coronary artery was occluded for 10 min and then reperfused for 30 min. A group of rabbits (PEG‐SOD group) received 1000 units/kg of PED‐SOD and another group (control group) was given saline 15 min before the coronary occlusion. 3. Regional systolic thickening fraction (TF) was similarly reduced to approximately ‐ 25% of baseline value during ischaemia in both groups. However recovery of TF after reperfusion was significantly better in the PEG‐SOD group ( n = 9) and TF at 30 min after reperfusion was 70.1 ±3.9% of baseline value compared with 44.9 ±3.4% in the control group ( n = 9; P < 0.05). Rate‐pressure products, left ventricular pressure, and LV dP/dt max were not significantly different between the PEG‐SOD treated and untreated control rabbits at any time during the experiment. PEG‐SOD did not modify the regional myocardial blood flow (coloured microsphere method) during ischaemia/reperfusion, which was assessed by using separate groups of rabbits. 4. These findings indicate that oxygen free radicals are important in the pathogenesis of myocardial stunning in xanthine oxidase deficient hearts.