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J C Bailey

Publications and source records attributed to J C Bailey.

At least 19 recordsLinked to original sources
PubMed1989

Action potential duration alternans in dog Purkinje and ventricular muscle fibers. Further evidence in support of two different mechanisms.

An abrupt shortening of cycle length causes action potential duration (APD) alternation in both canine Purkinje (P) and ventricular (V) muscle fibers. Our recent study suggested that APD alternans is determined by the process controlling APD during electrical restitution in P but not in V fibers. In the latter, alternans was attributed to changes in the availability of intracellular calcium [Ca2+]i. We examined this hypothesis further with the following pharmacologic probes known to alter restitution or action of [Ca2+]i: tetradotoxin (0.5-3.0 microM), lidocaine HCl (2.0-12.0 micrograms/ml), sotalol (10 microM), nicorandil (10-20 microM), 4-amino-pyridine (0.5 microM), ryanodine (10 microM), caffeine (2 mM), and ARL 115 BS (100 microM). Alternans in P fibers persisted under all studied conditions but varied in magnitude depending on the time constant and amplitude of restitution. In V fibers, the magnitude of alternans did not correlate with APD changes during restitution, and APD alternans was associated with the alternans of action potential shape and alternans of developed tension. Alternans in V was suppressed by caffeine at 2.0 mM [Ca2+]o when tension was increased and by ryanodine at 1.0 mM [Ca2+]o when tension was decreased. Alternans in V was not altered by changes in [Ca2+]o within the range of 1.0-4.0 mM; by ARL 115 BS, a compound that increases myofibrillar sensitivity to calcium; or by any other pharmacologic probes. We concluded that in P fibers, APD alternans was determined by the factors controlling APD in the absence of alternans; V fibers posses an independent mechanism of alternans linked to alternans of tension and controlled by [Ca2+]i; in V fibers, alternans could be suppressed by both positive and negative inotropic interventions; and calcium released from sarcoplasmic reticulum plays an important role in the V alternans.

Action Potentials↗
PubMed1989

Selective parasympathectomy increases the quantity of inhibitory guanine nucleotide-binding proteins in canine cardiac ventricle.

In mammalian heart, vagal stimulation or the direct application of acetylcholine produces profound direct effects on the electro-physiologic characteristics of atrial myocytes. At the tissue level, these effects are observed as shortening of atrial action potential duration. Despite anatomic, biochemical, and physiologic evidence for significant vagal input to the mammalian ventricle, similar direct effects of acetylcholine on the ventricular action potential have been difficult to demonstrate. Chronic denervation via cervical vagotomy is one method that has been shown to render previously unresponsive ventricular myocytes sensitive to acetylcholine, but the molecular mechanism has not been defined. In the experiments described, selective cardiac para-sympathectomy was performed on mongrel dogs. Five to seven days after parasympathectomy, the dogs were sacrificed, electrophysiologic responses to acetylcholine were measured, and sarcolemmal vesicles were prepared. After parasympathectomy, ventricular myocytes were responsive to the effects of acetylcholine, manifested as shortening of the action potential duration. A quantitative and functional assessment of the transmembrane signalling mechanisms of the muscarinic receptor was carried out. After parasympathectomy, the density of muscarinic receptors in the sarcolemma was increased, compared with control ventricles. After parasympathectomy, ventricular sarcolemma displayed significant increases in both basal and oxotremorine-stimulated GTPase activity. ADP-ribosylation revealed significantly increased quantities of the pertussis toxin substrates Gi and Go. The quantity of ADP ribose incorporated was correlated with the increased level of GTPase activity in control and oxotremorine-stimulated membranes. Quantitation of the alpha and beta gamma subunits of the guanine nucleotide-binding proteins by immunoblot confirmed the increase in density of inhibitory guanine nucleotide-binding proteins following parasympathectomy. The results offer new insights into possible mechanisms of altered electrophysiologic responsiveness to acetylcholine following cardiac parasympathectomy.

Acetylcholine↗
PubMed1989

Lipid risk factors in patients requiring arterial reconstruction.

Progressive peripheral atherosclerosis commonly leads to failure of a bypass graft. Lowering blood cholesterol retards coronary atherosclerosis and similar treatment might limit peripheral atherosclerosis. To identify lipid risk factors for peripheral atherosclerosis, 144 patients with peripheral atherosclerosis (98 with severe disease and 46 with stable claudication) and 61 age-matched control subjects were studied. Fasting lipid (cholesterol and triglycerides) and lipoprotein (high-density lipoprotein [HDL], low-density lipoprotein [LDL], and very-low-density lipoprotein [VLDL] cholesterol [C]) levels were measured. The incidence of hypertension and diabetes mellitus, amount of previous tobacco use, and location and severity of the peripheral atherosclerosis were also determined. Patients with peripheral atherosclerosis had higher VLDL-C and lower HDL-C levels than controls had, but serum cholesterol and plasma LDL-C levels were similar. Patients with peripheral atherosclerosis also had a higher incidence of diabetes mellitus and hypertension. Predictors of peripheral atherosclerosis by regression analysis were diabetes mellitus, low HDL-C levels, and tobacco use, with diabetes mellitus being the strongest variable. Peripheral atherosclerosis below the inguinal ligament was strongly predicted by low HDL-C and increased VLDL-C levels but not by increased cholesterol or LDL-C levels. Thus lipid risk factors for peripheral atherosclerosis are different, and attempts at limiting late graft failure by lowering lipid levels should be directed toward these lipoproteins.

Arteriosclerosis↗
PubMed1988

Alternans of action potential duration after abrupt shortening of cycle length: differences between dog Purkinje and ventricular muscle fibers.

The purpose of this study was to determine whether the alternans of action potential duration (APD) occurring in Purkinje and ventricular muscle fibers after an abrupt shortening of cycle length can be explained by the two factors controlling the cycle length-dependent APD changes (i.e., restitution and memory effect). Action potentials were recorded simultaneously from dog Purkinje fibers and ventricular muscle fibers using conventional microelectrode techniques. APD change during alternans was dependent on the preceding diastolic interval in the same manner as during restitution in Purkinje fibers but not in ventricular muscle fibers. The course of memory change was not affected by the presence of alternans in either fiber type. In Purkinje fibers, APD alternans was attenuated by a Ca2+ channel blocker, nisoldipine (2 X 10(-6) M), and augmented by a Ca2+ channel agonist, Bay K 8644 (3 X 10(-8) M). These effects were attributed to the changes in the kinetics and the amplitude of restitution. In ventricular muscle fibers, APD alternans was always preceded and accompanied by alternans of action potential shape. Alternans of both action potential shape and APD was suppressed by nisoldipine (2 X 10(-6) M) and attenuated by Bay K 8644 (3 X 10(-8) M). These results show that in Purkinje fibers, APD during alternans can be explained by restitution and memory effect. However, in ventricular muscle fibers, the mechanism of APD alternans is linked to factors controlling action potential shape. These findings are compatible with the hypothesis that APD alternans in Purkinje fibers depends on the differences in the recovery of membrane currents generated by the preceding action potential and in ventricular muscle fibers on the differences in the concentration and/or handling of intracellular calcium.

Action Potentials↗
PubMed1985

Effects of acetylcholine on action potential characteristics of atrial and ventricular myocardium after bilateral cervical vagotomy in the cat.

Acetylcholine, the parasympathetic neurotransmitter, shortens the action potential duration of cat atrial muscle cells, but not ventricular muscle cells. In mammalian species, atrial tissue receives a richer cholinergic nerve supply than ventricular tissue. To determine whether chronic withdrawal of cholinergic tone might influence the subsequent response of these tissues to cholinergic stimulation, we examined the effect of acetylcholine on the action potentials of atrial and ventricular myocytes from cats with intact vagi and cats after chronic bilateral cervical vagotomy. Following bilateral cervical vagotomy, physostigmine (10(-6) M) failed to alter atrial tension development or action potential duration. Acetylcholine produced shortening of the action potential duration in atrial muscle from cats with intact vagi and in cats following bilateral cervical vagotomy. However, the degree of shortening produced by acetylcholine after bilateral cervical vagotomy was significantly greater (P less than 0.001). In ventricular muscle from cats with intact vagi, acetylcholine did not alter action potential duration. In ventricular muscle from cats after bilateral cervical vagotomy, acetylcholine shortened the action potential duration. Maximal effect was seen at a concentration of 10(-5) M where acetylcholine shortened action potential duration at 90% repolarization from a control value of 179 +/- 4 to 150 +/- 7 msec. Atropine (10(-6) M) reversed the effects of acetylcholine. Addition of propranolol (10(-6) M) to the superfusate or pretreatment of the animals with reserpine (2 mg/kg, ip) 24 hours before sacrifice failed to alter the response of ventricular muscle cells to acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1979

Acetylcholine antagonism of the electrophysiological effects of isoproterenol on canine cardiac Purkinje fibers.

The purpose of these experiments was to determine whether or not acetylcholine modulated the electrophysiological effects of isoproterenol on canine cardiac Purkinje fibers. Conventional microelectrode techniques were used. Predictably, isoproterenol produced shortening of action potential duration; acetylcholine significantly blunted this effect of isoproterenol. Isoproterenol restored excitability to fibers exposed to 22 mM potassium solutions, and acetylcholine abolished this isoproterenol-restored excitability. Both of these antagonistic effects of acetylcholine were blocked by atropine. Acetylcholine alone did not affect action potential duration in polarized fibers or excitability in potassium-depolarized fibers. Furthermore, acetylcholine had no effect on the decrease in action potential duration induced by premature electrical stimulation or by acetylstrophanthidin administration, or on excitability of fibers exposed to a zero sodium, high calcium superfusant. These data demonstrate a direct cellular basis for cholinergic antagonism of the electrophysiological effects of beta-adrenergic stimulation of canine cardiac specialized intraventricular conducting tissue.

Acetylcholine↗
PubMed1979

Dissociation between the electrophysiological properties and total tissue cyclic guanosine monophosphate content of guinea pig atria.

The purpose of this study was to investigate the role of cyclic guanosine monophosphate (cyclic GMP) in mediating the direct electrophysiological effects of acetylcholine in guinea pig atria. Acetylcholine significantly diminished spontaneous rate of right atria without increasing cyclic GMP content. Reductions in rate following acetylcholine were augmented by pretreatment with physostigmine, but cyclic GMP levels remained unchanged. In left atria, acetylcholine significantly shortened action potential duration within 5 seconds (both with and without physostigmine pretreatment), but cyclic GMP content was not significantly elevated. Cyclic GMP levels in right atria were significantly increased in response to acetylcholine when the Ca2+ content of the buffer was elevated from 1.25 mM TO 2.5 MM; however, reductions in automaticity in the right atria were not augmented in the high Ca2+ buffer. Marked increases in cyclic GMP content were produced by Na nitroprusside superfusion without changing automaticity of right atria or action potential duration of left atria. Finally, both right and left atria were superfused with cyclic GMP analogs (8-bromo cyclic GMP and dibutyryl cyclic GMP) at high concentrations (10(-4)) for 15 minutes without producing significant effects on spontaneous rate or action potential duration. These results failed to show a correlation between total tissue cyclic GMP content and the electrophysiological effects of acetylcholine on guinea pig atria. The reasons for this are either that cyclic GMP does not mediate directly the electrophysiological effects of acetylcholine, or that small changes in cyclic GMP concentrations, undetectable when total tissue nucleotide levels are measured, occur in discrete effector pools of the cardiac cell to mediate the intracellular effects of the choline ester.

Acetylcholine↗
PubMed1978

Slow-channel depolarization: mechanism and control of arrhythmias.

The secondary inward current that flows through the slow channel is probably carried primarily by calcium ions. This current is responsible, in part, for the plateau phase of the cardiac action potential. Inward calcium current through the slow channel is essential to excitation-contraction coupling, and enhancement of this current exerts a positive inotropic effect. Transmembrane electrical potentials generated as a consequence of this slow inward current, so-called slow-channel depolarizations or slow responses, have been useful models in recent studies of cardiac autonomic interactions. The significance of the slow response in ventricular arrhythmias remains controversial and awaits more definitive experiments. The role of slow-channel depolarization as a basis for SA and AV nodal electrical activity is suggested by the electrophysiological similarities between these tissues and slow responses produced in vitro. This hypothesis is supported by the responses of these nodal tissues to interventions that augment of impede the slow inward current. More direct evidence in support of this notion may not be obtainable in the near future, since the critical voltage-clamp studies of ionic currents in SA and AV nodes are not technically feasible at this time.

Action Potentials↗
PubMed1978

Effects of aprindine HCl on slow channel action potentials and transient depolarizations in canine Purkinje fibers.

The electrophysiologic effects of aprindine hydrochloride were studied on normal Purkinje fibers, on Purkinje fibers superfused with Tyrode's solution containing 22 mM KCl and isoproterenol (1 X 10(-5) M) and on transient depolarizations induced by exposure to acetylstrophanthidin (1.7--2 X 10(-7) M). Aprindine (3 X 10(-6) M) significantly reduces the action potential amplitude and dV/dtmax and shortens the action potential duration but does not alter the resting membrane potential. Transient depolarizations were suppressed by aprindine at a dose of 2 X 10(-6) M. Isoproterenol (1 X 10(-5) M) failed to restore the transient depolarizations after suppression with aprindine. Slow responses induced in K-depolarized, isoproterenol-treated fibers were unchanged by aprindine (3 X 10(-6)-1 X 10(-5) M) in the presence as well as in the absence of acetylstrophanthidin. These experiments suggest that aprindine does not have slow channel blocking properties and that an inward current through the slow channel cannot be considered as the sole basis of the digitalis-induced transient depolarization.

Action Potentials↗
PubMed1977

Lack of electrical interaction between proximal bundle branches and subjacent muscle.

Microelectrode techniques were used to assess the importance of subthreshold electrotonic interactions between the canine proximal bundle branches and adjacent septal myocardium, and vice versa. Bundle branch action potential duration, maximal rising velocity of phase O, current threshold requirements for all-or-none depolarization, transmembrane voltage, and spontaneous frequency were not altered by adjacent septal muscle activation. Activation of the proximal bundle branches did not change the transmembrane voltage of immediately subjacent muscle cells; likewise, all-or-none activation of ventricular septal muscle did not effect a voltage change in the overlying proximal bundle branches. We conclude that a high ohmic resistance barrier between proximal bundle branch and subjacent muscle precludes significant electrotonic interactions between these neighboring structures.

Action Potentials↗
PubMed1977

Differences between proximal left and right bundle branch block action potential durations and refractoriness in the dog heart.

To date the electrophysiological mechanism responsible for aberrant intraventricular conduction of critically timed premature supraventricular impulses has not been documented. Microelectrode techniques were used to measure in vitro action potential and refractory period durations of the canine proximal right and left bundle branches equidistant from the distal bundle of His. Both measurements in the right bundle branch were statistically significantly longer than these parameters of the left bundle branch. Transection of the bundle branches immediately distal to the distalmost recording sites effected no change in the proximal right bundle action potential but caused marked prolongation of proximal left bundle branch action potential and refractory period durations. We conclude that functional right bundle branch aberrancy is most likely due to the longer proximal right bundle action potential duration and refractoriness. Our data also suggest that the shorter proximal left bundle branch action potential durations and refractory periods may be due to the proximity of the low ohmic resistance Purkinje fiber-muscle junctions on the left septal surface, effecting electrotonic foreshortening of these proximal left bundle branch parameters.

Action Potentials↗
PubMed1976

Electrophysiological observations on the digitalis-potassium interaction in canine Purkinje fibers.

We studied the effects of elevating potassium concentration on the membrane potential of Purkinje cells exposed to toxic concentrations of acetylstrophanthidin or ouabain. Conventional intracellular microelectrode techniques were employed. Rapid elevation of [K+]o from 2.7 to 5.4 mEq/liter resulted in an initial increase (more negative) in membrane potential of cells demonstrating ouabain-induced phase 4 depolarization. The increase in maximal diastolic potential occurred initially without suppression of phase 4 depolarization. In cells rendered inexcitable by ouabain or acetylstrophanthidin, elevation of [K+]o consistently increased membrane potential and restored excitability. In four experiments automaticity was initiated within 2 minutes after the increase in [K]o. Although automaticity reappeared, as maximal diastolic potential increased, the automatic rate slowed and then pacemaker activity was suppressed. Studies with 3H-ouabain showed that the increase in membrane potential paralleled K+-induced release of 3H-ouabain from Purkinje cells. These studies suggest that elevation of [K+]o reverses digitalis toxic manifestations in canine Purkinje fibers by causing release of cardiac glycosides bound to the membrane. The observed increase in membrane potential of ouabain-treated Purkinje fibers that occurred after [K+]o elevation was considered to be mediated in part by restoration of the Na pump and by electrogenic pumping.

Action Potentials↗