title: Transmembrane potential changes caused by shocks in guinea pig papillary muscle.
abstract: To study transmembrane potential (Vm) changes (delta Vm) caused by extracellular field stimulation, Vm was recorded in 10 guinea pig papillary muscles by a double-barrel microelectrode. A 10-ms shock was delivered during the action potential plateau or during diastole. Six shock strengths (1.8 +/- 0.4, 3.8 +/- 0.7, 5.6 +/- 0.9, 7.2 +/- 1.1, 11.1 +/- 1.9, and 17.8 +/- 1.5 V/cm) were given with both polarities. The tissue was then treated with either 30 microM tetrodotoxin (TTX; n = 5) or 30 microM TTX plus Ca(2+)-free (n = 5) perfusion. For shocks during the action potential plateau, delta Vm caused by the six potential gradients was 22.4 +/- 9.6, 43.6 +/- 17.4, 54.7 +/- 17.9, 60.4 +/- 18.1, 65.4 +/- 13.7, and 66.4 +/- 12.2 mV for shocks causing depolarization and 41.1 +/- 16.5, 68.3 +/- 22, 80.5 +/- 20.4, 84.0 +/- 19.5, 93.6 +/- 16.3, and 98.9 +/- 15.4 mV for shocks causing hyperpolarization. The relationship between delta Vm and shock potential gradient was not linear. During diastole, hyperpolarizing shocks induced initial hyperpolarization, then depolarization followed again by hyperpolarization. A new depolarization upstroke occurred immediately after the shock. After TTX or TTX plus Ca(2+)-free perfusion, point stimuli 10 times diastolic threshold could not induce an action potential, but a shock field of 1.8 +/- 0.2 V/cm still induced action potentials. The peak value of depolarization measured with respect to resting potential (-87 +/- 5 mV) during the hyperpolarizing shock decreased from +14 +/- 22 before to -66 +/- 30 mV with TTX perfusion (P < 0.01). The fast upstroke rate of depolarization both during and immediately after the end of hyperpolarizing shocks was inhibited by TTX perfusion. Thus 1) the relationship between delta Vm and shock potential gradient is not linear; 2) field but not point stimulation can induce an action potential when Na+ channels are inactivated; and 3) during diastole Na+ channels are activated twice by a 10-ms hyperpolarizing shock, once during shock-induced hyperpolarization and again immediately after the end of the shock.
authors.affiliation: Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
authors.forename: X
authors.initials: X
authors.lastname: Zhou
authors.forename: W M
authors.initials: WM
authors.lastname: Smith
authors.forename: D L
authors.initials: DL
authors.lastname: Rollins
authors.forename: R E
authors.initials: RE
authors.lastname: Ideker
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D004597:Electroshock; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D010210:Papillary Muscles / Q000187:drug effects / Q000502:physiology*; D010477:Perfusion; D011930:Reaction Time; D026941:Sodium Channel Blockers; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D026941:Sodium Channel Blockers; D013779:Tetrodotoxin; D002118:Calcium