{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,13]],"date-time":"2025-11-13T12:20:25Z","timestamp":1763036425248},"reference-count":39,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2009,12]]},"abstract":"<jats:p> The atrioventricular (AV) node filters atrial impulses. Underlying rate-dependent refractory properties are assessed with the effective (ERPN; longest nonconducted atrial cycle length) and functional (FRPN; shortest His bundle cycle) refractory period determined with premature protocols at different basic rates. Fast rates prolong ERPN and shorten FRPN, but these effects vary with subjects, age, and species. We propose that these opposite and variable effects reflect the net sum of concurrent cumulative and noncumulative effects associated with basic (BCL) and pretest cycle length (PTCL), respectively. To test this hypothesis, we assessed selective and combined effects of five BCL (S<jats:sub>1<\/jats:sub>S<jats:sub>1<\/jats:sub>) and six PTCL (S<jats:sub>1<\/jats:sub>S<jats:sub>2<\/jats:sub>) on ERPN, FRPN, and their subintervals (ERPN = A<jats:sub>2<\/jats:sub>H<jats:sub>2<\/jats:sub> + H<jats:sub>2<\/jats:sub>A<jats:sub>3<\/jats:sub> and FRPN = H<jats:sub>2<\/jats:sub>A<jats:sub>3<\/jats:sub> + A<jats:sub>3<\/jats:sub>H<jats:sub>3<\/jats:sub>, where A is atrium and H is His bundle) with S<jats:sub>1<\/jats:sub>S<jats:sub>2<\/jats:sub>S<jats:sub>3<\/jats:sub> protocols in six rabbit heart preparations. At control BCL, PTCL shortenings prolonged ERPN (113 \u00b1 12 vs. 101 \u00b1 14 ms, P &lt; 0.01) as a net result of prolonged A<jats:sub>2<\/jats:sub>H<jats:sub>2<\/jats:sub> and curtailed H<jats:sub>2<\/jats:sub>A<jats:sub>3<\/jats:sub>. At control PTCL, BCL shortenings increased ERPN (127 \u00b1 20 vs. 101 \u00b1 14 ms, P &lt; 0.01) by prolonging A<jats:sub>2<\/jats:sub>H<jats:sub>2<\/jats:sub>. FRPN did not vary with BCL but decreased (163 \u00b1 6 vs. 175 \u00b1 10 ms, P &lt; 0.01) with PTCL that curtailed H<jats:sub>2<\/jats:sub>A<jats:sub>3<\/jats:sub>. Equal BCL and PTCL shortenings as in standard protocols prolonged ERPN but left FRPN unchanged. Notably, ERPN and FRPN significantly correlated through their H<jats:sub>2<\/jats:sub>A<jats:sub>3<\/jats:sub> subinterval. In conclusion, BCL and PTCL are both important determinants of AV nodal refractoriness and together account for rate-induced changes in ERPN and FRPN observed during standard premature protocols. ERPN and FRPN are related variables. Similar functional rules may govern nodal refractory behavior during supraventricular tachyarrhythmias. <\/jats:p>","DOI":"10.1152\/ajpheart.00712.2009","type":"journal-article","created":{"date-parts":[[2009,10,9]],"date-time":"2009-10-09T22:00:11Z","timestamp":1255125611000},"page":"H2136-H2143","source":"Crossref","is-referenced-by-count":7,"title":["Rate-dependent AV nodal refractoriness: a new functional framework based on concurrent effects of basic and pretest cycle length"],"prefix":"10.1152","volume":"297","author":[{"given":"Rafik","family":"Tadros","sequence":"first","affiliation":[{"name":"D\u00e9partement de physiologie, Facult\u00e9 de m\u00e9decine, Universit\u00e9 de Montr\u00e9al, Montreal, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jacques","family":"Billette","sequence":"additional","affiliation":[{"name":"D\u00e9partement de physiologie, Facult\u00e9 de m\u00e9decine, Universit\u00e9 de Montr\u00e9al, Montreal, 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