title: Ultrastructural-functional basis for spontaneous termination of ventricular fibrillation in mammals.
abstract: Ventricular fibrillation in humans is generally sustained (SVF), but it can be also transient (TVF), reverting spontaneously to sinus rhythm. In previous studies we have shown that: a) TVF appears in all young mammals and varies according to age and species; b) it requires synchronization of myocardial cell activity; c) infusion of certain drugs may change the type of ventricular fibrillation from sustained into transient. We hypothesize that the synchronization required for TVF depends on the electrical conductivity of intercellular structures. These intercellular couplings differ among species and decrease with age. Comparison between the inter- and intra-specific variations of intercellular connective structure described in the literature with the type of ventricular fibrillation found in our previous studies on various animals of different ages showed a clear relationship between these histological variations and the changes in the type of ventricular fibrillation. In this study we examined intercellular connective structures ultrastructurally in 3 groups of cats: a. control, untreated cats exhibiting sustained ventricular fibrillation; b. untreated cats exhibiting transient ventricular fibrillation; c. treated cats exhibiting sustained ventricular fibrillation before infusion of a defibrillating drug and transient ventricular fibrillation thereafter. It was found that the intercellular connective structure in cats exhibiting sustained ventricular fibrillation differs significantly from that in cats exhibiting transient fibrillation. In hearts exhibiting sustained ventricular fibrillation, many intercellular connective structures are widened and the degree of widening is pronounced, forming a continuous line, while in hearts exhibiting transient ventricular fibrillation the widened junctions are rare and isolated and the widening is relatively small. These preliminary results strongly support our above-mentioned hypothesis, providing an explanation for the origin of transient ventricular fibrillation and a tool for the development of new defibrillating drugs.
authors.affiliation: Department of Physiology, Tel Aviv Medical School, Israel.
authors.forename: Y
authors.initials: Y
authors.lastname: Blayer
authors.forename: L
authors.initials: L
authors.lastname: Reisin
authors.forename: M
authors.initials: M
authors.lastname: Manoach
mesh_terms: D000818:Animals; D002415:Cats; D008854:Microscopy, Electron; D009206:Myocardium / Q000648:ultrastructure*; D014693:Ventricular Fibrillation / Q000473:pathology*