AJP - Heart and Circulatory Physiology, Vol 264, Issue 3 783-H790, Copyright © 1993 by American Physiological Society
Mechanisms of antifibrillatory effect of acidic reperfusion: role of perfusate bicarbonate concentration
C. Ibuki, D. J. Hearse and M. Avkiran
Rayne Institute, St. Thomas' Hospital, London, United Kingdom.
Transient (2 min) acidic (pH 6.6) reperfusion with low [HCO3-] solution
suppresses reperfusion-induced ventricular fibrillation (VF) in the
isolated rat heart. Using this preparation, we tested whether the effect
was mediated by the high [H+] or the low [HCO3-] of perfusate. Left and
right coronary beds were independently perfused with HCO3(-)-containing
(25.0 mmol/l) solution at pH 7.4. Regional ischemia was then induced by
stopping flow to the left coronary bed for 10 min. Hearts were subsequently
assigned to four groups (n = 12 hearts/group), and the left coronary bed
was reperfused with either HCO3(-)-containing (25.0 or 4.0 mmol/l) or
HCO3(-)-free (5.0 mmol/l HEPES) solution, at pH 7.4 throughout (control
reperfusion) or at pH 6.6 for the first 2 min and at pH 7.4 from 2 to 5 min
(acidic reperfusion). Regardless of the buffer, controls exhibited a high
(92 and 100%) incidence of VF; this was reduced to 42% in both of the
acidic reperfusion groups (P < 0.05). There were no intergroup
differences in heart rate, coronary flow, or size of ischemic zone. Thus
high [H+], rather than low [HCO3-], appears to mediate the antifibrillatory
effect of transient acidic reperfusion.
