Prevention of Extracellular K+ Inhomogeneity Across the Ischemic Border by Coronary Venous Obstruction in the Dog: Salutary Antiarrhythmic Effects of Enhanced Myocardial Hydration

Partial coronary sinus obstruction (CSO) in the dog prevents or delays the predictable ventricular fibrillation (VF) of the early phase of acute ischemia, by normalizing regional electrophysiological disparities which presumably reflect inhomogeneous extracellular potassium ([K+]o) accumulation. To clarify whether CSO indeed affects [K+]o inhomogeneity, we determined in 12 chloralose anesthetized dogs the dynamic [K+]o changes occurring early during reversible coronary artery occlusion (CAO) involving the mid-left descending branch. These changes were compared to those observed during CAO preceded by CSO sufficient to increase the coronary sinus pressure to 40 mmHg. [K+]owas 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+]oincreased rapidly within the IZ and the BZi reaching plateau 5 min after CAO, at about three-fold control (11.89 ± 1.12 mEq/1). Unexpectedly, [K+]o also increased initially outside the border (BZo) but declined after 3 min to a lower level (7.00 ± 0.40mEq/1), thus creating a steep gradient of up to 5.54 ± 0.20 mEq/1, P > 0.001) across the visible border. In four trials, the gradient coincide 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 the IZ, BZi and BZo (9.5 ± 0.89 mEq/1, P > 0.001) and no VF was observed. Thus the beneficial electrophysiologic and antiarrhythmic effects of CSO in acute ischemia may be explained by [K+]o equalization. Prevention of "patchy" [K+]o sequestration probably reflects higher dilution, facilitation of diffusion and possibly enhanced lymphatic washout of extracellular solutes mediated through enhanced tissue hydration.