PREVENTION OF EXTRACELLULAR K- SALUTARY ANTIARRHYTHMIC EFFECTS OF ENHANCED MYOCARDIAL HYDRATION( INHOMOGENEITY ACROSS THE ISCHEMIC BORDER BY CORONARY VENOUS OBSTRUCTION IN THE DOG )
Ac. Kralios et al., PREVENTION OF EXTRACELLULAR K- SALUTARY ANTIARRHYTHMIC EFFECTS OF ENHANCED MYOCARDIAL HYDRATION( INHOMOGENEITY ACROSS THE ISCHEMIC BORDER BY CORONARY VENOUS OBSTRUCTION IN THE DOG ), Journal of Molecular and Cellular Cardiology, 26(10), 1994, pp. 1349-1356
Partial coronary sinus obstruction (CSO) in the dog prevents or delays
the predictable ventricular fibrillation (VF) of the early phase of a
cute ischemia, by normalizing regional electrophysiological disparitie
s which presumably reflect inhomogeneous extracellular potassium ([K+]
(o)) accumulation. To clarify whether CSO indeed affects [K+](o) inhom
ogeneity, we determined in 12 chloralose anesthetized dogs the dynamic
[K+](o) changes occurring early during reversible coronary artery occ
lusion (CAO) involving the mid-left anterior descending branch, These
changes were compared to those observed during CAO preceded by CSO suf
ficient to increase the coronary sinus pressure to 40 mmHg. [K+](o) wa
s determined using valinomycin coated electrodes implanted within the
ischemic (IZ) and the normal (NZ) zones, as well as immediately inside
(BZi) and outside (BZo) the visible border. [K+](o) increased rapidly
within the IZ and the BZi reaching plateau 5 min after CAO, at about
three-ford control (11.89 +/- 1.12 mEq/l). Unexpectedly, [K+](o) also
increased initially outside the border (BZo) but declined after 3 min
to a lower level (7.00 +/- 0.40 mEq/l), thus creating a steep gradient
of up to 5.54 +/- 0.20 mEq/l, P < 0.001) across the visible border. I
n four trials, the gradient coincided with VF. With CSO preceding CAO,
the development of this border zone gradient was entirely prevented.
Moreover, [K+](o) reached a significantly lower and similar level in t
he IZ, BZi and BZo (9.5 +/- 0.89 mEq/l, P < 0.001) and no VP was obser
ved. Thus the beneficial electrophysiologic and antiarrhythmic effects
of CSO in acute ischemia may be explained by [K+](o) equalization, Pr
evention of ''patchy'' [K+](o) sequestration probably reflects higher
dilution, facilitation of diffusion and possibly enhanced lymphatic wa
shout of extracellular solutes mediated through enhanced tissue hydrat
ion.