title: Postrest shortening of the action potential duration in rabbits: in vitro and in vivo correlation.
abstract: Previous evidence has shown that the action potential duration of rabbit ventricular muscle cells shortens after a rest period (postrest shortening). However, there has not been much research on postrest shortening in the intact heart. We recorded transmembrane action potentials (TAPs) of isolated papillary muscle from rabbit ventricle with glass microelectrodes and monophasic action potentials (MAPs) of the rabbit left ventricular endocardium with contact electrodes. In the in vitro experiments, repetitive regular stimuli (S1) at a cycle length of 1 sec were followed by a single extrastimulus (S2) at coupling intervals (S1S2) ranging between 0.5 sec and 8 sec. The increase in the S1S2 interval resulted in a progressive shortening of the duration of TAP elicited by the S2, which was abolished by the simultaneous application of 1 mmol/L 4-aminopyridine and 2 micromol/L ryanodine. In the in vivo experiments, regular right ventricular pacing (S1) at a cycle length of 0.35 sec was followed by a single extrastimulus (S2) with coupling intervals (S1S2) ranging between 0.25 sec and 3 sec. The increase in the S1S2 interval also resulted in a progressive shortening of the duration of MAP elicited by the S2. This is the first report to demonstrate postrest shortening in the intact heart, which probably occurs because of a mechanism analogous to that observed in the isolated ventricular muscle.
authors.affiliation: Department of Internal Medicine I, School of Medicine, Oita Medical University, Hasama, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Ishida
authors.forename: N
authors.initials: N
authors.lastname: Takahashi
authors.forename: T
authors.initials: T
authors.lastname: Saikawa
authors.forename: T
authors.initials: T
authors.lastname: Iwao
authors.forename: T
authors.initials: T
authors.lastname: Fujino
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: H
authors.initials: H
authors.lastname: Yonemochi
authors.forename: M
authors.initials: M
authors.lastname: Ito
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002118:Calcium / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000187:drug effects; D017136:Ion Transport / Q000187:drug effects; D008297:Male; D010210:Papillary Muscles / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000502:physiology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology; D024683:Potassium Channels, Tandem Pore Domain; D011817:Rabbits; D012433:Ryanodine / Q000494:pharmacology; D019837:Ryanodine Receptor Calcium Release Channel / Q000187:drug effects / Q000502:physiology; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors; D014630:Vagus Nerve / Q000502:physiology; D016276:Ventricular Function
chemical_list: D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024683:Potassium Channels, Tandem Pore Domain; D019837:Ryanodine Receptor Calcium Release Channel; D012433:Ryanodine; D015761:4-Aminopyridine; D011188:Potassium; D002118:Calcium