PREVENTION OF EXTRACELLULAR K- SALUTARY ANTIARRHYTHMIC EFFECTS OF ENHANCED MYOCARDIAL HYDRATION( INHOMOGENEITY ACROSS THE ISCHEMIC BORDER BY CORONARY VENOUS OBSTRUCTION IN THE DOG )

Citation
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
Citations number
34
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00222828
Volume
26
Issue
10
Year of publication
1994
Pages
1349 - 1356
Database
ISI
SICI code
0022-2828(1994)26:10<1349:POEKSA>2.0.ZU;2-5
Abstract
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.