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PubMed1994

Late hemodynamic effects of the preserved papillary muscles during mitral valve replacement.

BACKGROUND: The late hemodynamic effects of preserving the papillary muscles during mitral valve replacement have not been evaluated. METHODS AND RESULTS: Sixteen patients who had chronic mitral regurgitation due to myxomatous degeneration were randomized to preservation (Pres group, n = 8) or no preservation (No Pres group, n = 8) of the chordae tendineae and papillary muscles during mitral valve replacement. Rest and exercise nuclear ventriculograms were performed early (3 months) and late (5 years) after surgery. Early after surgery, the No Pres group had lower ejection fractions and stroke work indexes (P < .05 by repeated-measures [rm] ANOVA) than the Pres group did at similar end-diastolic volume indexes. The No Pres group had similar cardiac indexes after exercise because heart rate increased (P < .005 by rm ANOVA). Late after surgery, ejection fraction was greater at similar end-diastolic volume indexes (P < .005 by rm ANCOVA), and preload recruitable stroke work indexes (P < .001 by rm ANCOVA) were better in the Pres group. CONCLUSIONS: Preserving chordal attachments enhanced the late hemodynamic recovery after mitral valve replacement for mitral regurgitation.

Chordae Tendineae↗

PubMed1991

Inotropic and electrophysiological effects of BDF 9148, a congener of DPI 201-106, in guinea-pig atria and papillary muscles.

1. BDF 9148 is a newly synthesized congener of DPI 201-106 in which the piperazidinyl moiety has been replaced by an azetidine-3-oxy-moiety. The inotropic effect of both drugs was studied as well as their influence on the action potential, by use of standard microelectrode techniques. 2. BDF 9148 increased the contractile force of guinea-pig atria and papillary muscles. The EC50 was 1.32 X 10(-7) mol l-1 and 0.7 X 10(-6) mol l-1 respectively. DPI 201-106 was effective in a similar concentration-range, the EC50 being 2.6 X 10(-7) mol l-1 for atria and 2.8 X 10(-7) mol l-1 for papillary muscles. 3. Both drugs caused a concentration-dependent prolongation of the relaxation time of the isometric contraction curve. With 10(-6) mol l-1 BDF 9148, the mean increase was 39.1 +/- 4.4 ms in atria and 39.4 +/- 7.5 ms in papillary muscles while 10(-6) mol l-1 DPI 201-106 caused increases of 56.7 +/- 2.5 ms and 79.3 +/- 11.7 ms, respectively. The effect of BDF 9148 was not prevented by propranolol, but was reversed by 3 X 10(-6) mol l-1 tetrodotoxin. Pretreatment of atria with 3 X 10(-8) mol l-1 BDF shifted the concentration-response curve of ouabain to the left and reduced the EC50 of the glycoside from 3.21 X 10(-7) mol l-1 to 2 X 10(-7) mol l-1. 4. BDF 9148 and DPI 201-106 concentration-dependently increased the action potential duration of papillary muscles and their functional refractory period. The drugs did not modify the resting potential, the action potential amplitude or the maximum depolarization velocity.5. All effects of BDF 9148 persisted after washout. The lipophilic drug accumulated in the tissues and the tissue drug concentration was little reduced by washout of BDF 9148 from the organ bath.6. In contrast to DPI 201-106, which had a prominent negative chronotropic effect in right atria, BDF 9148 caused only a slight reduction of the beating frequency with the largest (3 x 10 5mol 11) concentration.7. The results are consistent with BDF 9148 being a sodium channel activator with much weaker influence on the beating frequency than the parent compound DPI 201-106.

Action Potentials↗

PubMed1977

Maximum rate of tension fall during isometric relaxation at end-systolic fiber length in canine papillary muscle.

We measured the characteristics of the decline in tension during isometric relaxation of canine papillary muscle. In the intact heart, relaxation begins with the isovolumic phase, but in experiments on papillary muscle previously reported the isotonic phase preceded the isometric phase during the course of relaxation. In our experiments, however, the isotonic bar was locked at the instant the muscle reached the end-systolic fiber length in order to hold the fiber at the length during the succeeding relaxation process. Therefore, we obtained a relaxation process similar to that occurring in the intact heart. The major results of these experiments are: (1) Maximum rate of the decline in tension (-dT/dtmax) is linearly related to the magnitude of total load. (2) -dT/dtmax is augmented by positive inotropic interventions and diminished by negative inotropic interventions. (3) An increase in preload results in only a slight increase in -dT/dtmax. (4) End-systolic fiber length itself is not a principal determinant of -dT/dtmax. (5) -dT/dtmax divided by total load is independent of the amount of muscle shortening. We, therefore, suggest that -dT/dtmax divided by total load cand be a useful index of the relaxation characteristics of cardiac muscle.

Animals↗

PubMed1986

Rupture of a left ventricular papillary muscle during acute myocardial infarction: analysis of 22 necropsy patients.

Certain clinical and cardiac morphologic findings are described in 22 patients, aged 45 to 80 years (mean 64) (15 men [68%]), in whom rupture of a papillary muscle occurred during acute myocardial infarction. In most, the acute infarction associated with papillary muscle rupture was a first coronary event (only 18% had a myocardial scar consistent with prior infarction and 29% had angina pectoris). The posteromedial papillary muscle, presumably because of its more tenuous blood supply, ruptured almost three times more frequently than the anterolateral one (73 and 27%, respectively). Quantitative examination of the amounts of narrowing by atherosclerotic plaque in each of the four major epicardial coronary arteries (right, left main, left anterior descending and left circumflex) disclosed less narrowing in the patients with rupture than in the patients with fatal acute myocardial infarction unassociated with rupture. Of the 519 five mm sections of coronary artery examined (11 patients), only 68 sections (13%) were narrowed greater than 75% in cross-sectional area compared with 34% of 1,403 sections from 27 patients with fatal myocardial infarction without rupture.

Adipose Tissue↗

PubMed1995

Papillary muscle displacement causes systolic anterior motion of the mitral valve. Experimental validation and insights into the mechanism of subaortic obstruction.

BACKGROUND: Systolic anterior motion (SAM) of the mitral valve in hypertrophic cardiomyopathy (HCM) has generally been explained by a Venturi effect related to septal hypertrophy, causing outflow tract narrowing and high velocities. Patients with HCM, however, also have primary abnormalities of the mitral apparatus, including anterior and inward or central displacement of the papillary muscles, and leaflet elongation. These findings have led to the hypothesis that changes in the mitral apparatus can be a primary cause of SAM by altering the forces acting on the mitral valve and its ability to move in response to them. Despite suggestive observations, however, it has never been prospectively demonstrated that such changes can actually cause SAM. METHODS AND RESULTS: To test this hypothesis in vivo, anterior papillary muscle displacement was created in 7 dogs studied by echocardiography, with controlled cardiac output and heart rate. In all 7 dogs, papillary muscle displacement caused SAM, with an outflow tract gradient (33 +/- 19 mm Hg) and mitral regurgitation in 6. As in patients with HCM, the mitral valve was displaced anteriorly and the coaptation point shifted toward the insertion of the leaflets, creating longer distal residual leaflets that moved anteriorly. CONCLUSIONS: Primary changes in the mitral apparatus can cause SAM without septal hypertrophy. In this model, SAM appears to be determined by the ability of the leaflets to move anteriorly (papillary muscle displacement causing slack and increased residual leaflet length) and their interposition into the outflow stream by anterior displacement, determining the direction of this motion. Geometric factors observed in HCM and in patients with SAM without HCM can therefore play a primary role in causing SAM.

Animals↗

PubMedDate not supplied

Interaction between sarcomere and mitochondrial length in normoxic and hypoxic rat ventricular papillary muscles.

We hypothesized that the mitochondrial length may be altered according to changes in the sarcomere length, and that this relationship may be affected by exposure to hypoxia. Rat ventricular papillary muscles were isolated and immersed in normoxic or hypoxic solutions for 10 min. Sarcomeres of various lengths were obtained by fixing the papillary muscles in a slack or stretched state, or after exposure to a contracture solution containing saponin and CaCl(2). The mitochondrial length measured using electron microscopy significantly correlated to the length of the adjacent sarcomere in both the normoxic (n=767) and hypoxic (n=1145) groups (P<.0001). The slope of the regression line, however, was significantly less steep, and its intercept was significantly larger in the hypoxic group than in the normoxic group (analysis of covariance). When we analyzed the mitochondrial lengths among the three sarcomere-length subgroups (<1.5, 1.5-2.0, and >2.0 microm), the mitochondrial length was significantly shorter in the hypoxic condition than in the normoxic condition at sarcomere lengths greater than 2.0 microm. Staining for desmin, the major muscle-type intermediate filament, the longitudinal system of which connects the mitochondria with the Z bands of sarcomeres, showed a clear cross-striation pattern in both papillary muscles with and without the exposure to hypoxia, suggesting that desmin was preserved after the exposure to hypoxia. These data indicate that the mitochondrial length changes according to changes in the sarcomere length, suggesting the possible role of mitochondria as an internal load against myocyte contraction. It is also suggested that mitochondria exposed to hypoxia may be more resistive to both compression and stretch in a longitudinal direction than those in the normoxic condition.

Animals↗

PubMedDate not supplied

[Alterations in the passive and active performance of cat papillary muscle induced by variation of preload (author's transl)].

In the isolated cat papillary muscle a rapid change in length induces a viscoelastic process of relaxation, during which the diastolic tension attains its new equilibrium after a delay. Its time course may be approximated both after stretching and releasing by a total of four exponential functions being marked by highly diverse time constants. During the stretch-induced relaxation phase the isometrically active papillary muscle shows a marked increase in mechanogram amplitudes, which is preceded in the first seconds by a short-term decrease. An opposite behavior is to be recorded after abrupt releases. The mechanograms of the stationary state prove to be exclusively a function of the degree of stretch, while the contractions in the early relaxation phases are dependent on the speed, direction and scale of the preceding change in length. The higher the stretching step chosen, the more clearly reduced are the mechanogram amplitudes of the early relaxation phase in comparison to the stationary state. This applies especially right of the optimum of force-development and contradicts a viscoelastic interpretation of the systolic phenomena in the poststretch phase. The findings after abrupt stretching point to either an initial decrease of amplitude or to a delayed approach of the contractions to their stationary state. Stretch-induced changes in the time course of the action potentials would constitute an adequate basis for the interpretation of these phenomena.

Animals↗

PubMed1996

Effects of yew alkaloids and related compounds on guinea-pig isolated perfused heart and papillary muscle.

The mechanical and electrical effects of selected yew alkaloids were studied on two different cardiac preparations: the isolated coronary perfused heart and the isolated papillary muscle of the guinea-pig. In the isolated heart, the Winterstein acid type alkaloids 1, 2 and 3 induced electrical and mechanical effects similar to those reported after yew intoxication (negative inotropic effect, block of atrio-ventricular conduction), but the coronary flow was unchanged. Taxine B (1), the most potent compound of this group, reduced cardiac contractility and the maximum rate of depolarisation of the action potential in the isolated papillary muscle, acting as a class I antiarrhythmic drug. In the isolated heart, the cinnamates 4 and 5, corresponding to the degradation products of 1 and 3, exerted arrhythmogenic effect due to a reduction of coronary flow. No alterations in electrical and contractile activities were in fact recorded after perfusion of the isolated papillary muscle with 4. Taxine A (6) and the taxane alcohol 7, corresponding to the terpenoid core of 3 had no significant cardiac effect. Our results suggest that the poisonous properties of the yew tree are probably due to the combined activity of alkaloids of the Winterstein acid type and their corresponding cinnamtes, which can reduce both the excitability and the coronary flow of the heart.

Alkaloids↗

PubMed1992

Aging- and training-induced alterations in collagen characteristics of rat left ventricle and papillary muscle.

We evaluated the single and interactive effects of aging and exercise training on selected parameters of myocardial interstitium in both the left ventricle (LV) and LV papillary muscle of female Fischer 344 specific pathogen-free rats. Ten weeks of treadmill running resulted in significant LV hypertrophy as well as elevated plantaris muscle citrate synthase activity in both young adult (5-mo-old) and senescent (23-mo-old) trained animals (YT, young trained; OT, old trained) compared with age-matched sedentary controls (YC, young control; OC, old control). Proline and hydroxyproline pools were significantly higher (both P less than 0.05) in 23-mo-old vs. 5-mo-old papillary muscles. Degree of maturation (nonreducible cross-linking) of LV collagen was evaluated by measurement of hydroxylysylpyridinoline concentration ([HP]). In a comparison of YC with OC rats, ventricular [HP] increased approximately fivefold from 0.059 +/- 0.007 to 0.285 +/- 0.018 (SE) mol HP/mol collagen (P less than 0.001). Whereas training had no effect on ventricular [HP] in young adult rats, it significantly reduced LV collagen cross-linking in OT rats (0.131 +/- 0.027) so that HP values in this group were less than one-half of those observed in OC rats. Because both collagen concentration and degree of cross-linking are thought to affect muscle stiffness characteristics, we conclude that the observed changes should be considered in any explanation for aging- and training-induced alterations in LV and papillary muscle contractile indexes.

Aging↗

PubMed1989

[Effects of 3,6-dimethamidodibenzopyriodonium citrate (I-65) on action potentials and contractions in guinea pig papillary muscles].

Synchronous recordings of action potentials and contractile force in isolated guinea pig papillary muscles administered 3,6-dimethamidodibenzopyriodonium citrate (I-65) 30 mumol/L showed excitation-contraction uncoupling, ie, the contractile force was markedly depressed although the Vmax and amplitudes of the action potentials were unaffected. At the same concentration, I-65 shortened the duration of the action potentials at 50% and 90% repolarization. However, I-65 at lower concentrations (1-10 mumol/L) decreased Vmax and the amplitude of the slow action potentials which were elicited by isoprenaline in papillary muscles were rendered partially depolarized by KCl 25 mmol/L Tyrode solution. These effects were partially reversed by elevation of the concentration of Ca2+ from 2.7 to 5.4 mmol/L. I-65 also suppressed the abnormal automaticity elicited by BaCl2 and DAD and triggered activity induced by ouabain. The results suggest that I-65 may be a calcium channel blocker.

Action Potentials↗

PubMed1993

Extensive cryoablation of the left ventricular posterior papillary muscle and subjacent ventricular wall. Impact on mitral valve function and hemodynamics.

Ventricular tachycardias that originate from the inferior left ventricular wall may necessitate transmural ablation involving the posterior papillary muscle of the mitral valve. The effect on mitral valve function and hemodynamics of extensive cryoablation of the left ventricular posterior papillary muscle and subjacent ventricular wall was studied in 16 dogs. Two sham experiments were done. All dogs were studied preoperatively and postoperatively by pulsed Doppler and two-dimensional echocardiography. Left ventricular angiographic and hemodynamic studies were performed preoperatively in six treated dogs and two control dogs and in all dogs at the end of follow-up (1, 3, or 6 months). Postmortem studies were performed in all dogs. The cumulative probability of freedom from mitral regurgitation at 2 months was 0.43 +/- 0.14. Thereafter no new cases of mitral regurgitation could be demonstrated. The angiographic degree of mitral regurgitation was mild in five and moderate in two dogs and did not increase from 3 to 6 months. One dog with acute severe mitral regurgitation died early of heart failure. A significant increase in left ventricular end-diastolic and mean pulmonary capillary wedge pressure of 9.4 +/- 2.5 mm Hg and 6.4 +/- 2.6 mm Hg, respectively, was found in treated dogs at 3 months. These results suggest that extensive cryoablation of the left ventricular posterior papillary muscle and subjacent ventricular wall can be accomplished with an acceptable risk of mild to moderate mitral regurgitation, and without serious detrimental effect on left ventricular function. Retraction is probably the main mechanism of mitral regurgitation.

Angiography↗

PubMed1989

[Effects of 2-[p-(dimethylamino) styryl] pyridine methiodide on action potentials of depolarized papillary muscle cells of guinea pig].

Effects of 2-[p-(dimethylamino) styryl] pyridine methiodide (DSPM), nifedipine (Nif), CaCl2 and isoprenaline (Iso) on action potentials (AP) of guinea pig papillary muscle cells depolarized by high K+ (15.4 mmol/L) were studied by microelectrode technique. DSPM 45 mumols/L decreased the Vmaxf and Vmaxs of phasee O of the AP by 14 and 26%, respectively. APD90 was lengthened by 7%, amplitude of action potentials (APA) was decreased by 3%. The effects of CaCl2 on Vmaxs of phase 0 of the AP of depolarized papillary muscle cells were abolished by DSPM 45 mumols/L, but the effects of Iso were not antagonized. Effects of DSPM on Vmaxs of the AP of depolarized papillary muscle cells and the influence of DSPM to the action of CaCl2 and Iso were similar to those of Nif. It further suggests that DSPM may be a calcium antagonist.

Action Potentials↗

PubMed1995

The length dependence of work production in rat papillary muscles in vitro.

The influence of length on work production was investigated for rat papillary muscles using the work loop technique. Active and passive length-force relationships were first determined under isometric conditions and the length for maximum force production (Lmax) was derived. Starting from different lengths within the physiological range, a series of work loops was generated using the stimulation phase shift, strain amplitude and cycle frequency previously found to be optimal for power output at 37 degrees C. The relationship between muscle length and net work was used to determine the length at which work output was maximal (Lopt). In order to examine the dynamic passive properties of the muscles, unstimulated muscles were subjected to the same regime of sinusoidal oscillation as used for the active loops. From the hysteresis loops, lengthening work (work done to extend the passive muscle), passive shortening work (work returned during shortening) and net energy loss (hysteresis) could be measured. The decline in net work production at lengths greater than 95% Lmax could largely be attributed to the rapid and non-linear increase in muscle stiffness and the increase in net energy loss over this range of lengths. The physiological significance of the length-work relationship is considered and the mechanical properties of active and passive papillary muscles are discussed with reference to sarcomere length and cardiac muscle ultrastructure.

Animals↗

PubMed1991

Presynaptic beta-adrenoceptors in guinea pig papillary muscle: evidence for adrenaline-mediated positive feedback on noradrenergic transmission.

Guinea pig papillary muscles were preincubated in the presence of 5 x 10(-9) mol/L unlabeled noradrenaline or adrenaline then incubated with (3H)-noradrenaline and superfused. Electrical field stimulation with 180 pulses delivered at 1 or 3 Hz was used to induce overflow of radioactivity. Comparison of the effects of preexposure of the tissue to adrenaline or noradrenaline revealed that adrenaline incubation caused an enhancement of stimulation-evoked overflow of (3H)noradrenaline and a reduction of the effect of exogenously added isoprenaline. Furthermore, the selective beta 2-adrenoceptor antagonist ICI 118,551 (10(-7) mol/L), but not the selective beta 1-adrenoceptor antagonist ICI 89,406 (10(-7) mol/L), reduced electrically evoked overflow of (3H)noradrenaline in tissue preincubated with adrenaline but not in tissue preincubated with noradrenaline. The overflow-reducing effect of ICI 118.551 occurred at stimulation with 3 Hz but not at stimulation with 1 Hz. The present results support the hypothesis that noradrenergic transmission in guinea pig papillary muscle is facilitated via beta 2-adrenoceptors, and that adrenaline may serve as transmitter in this positive feedback mechanism after its incorporation into sympathetic nerves.

Adrenergic beta-Antagonists↗

PubMed1983

Studies on mechanisms of diltiazem-induced protection of the ischemic myocardium: selective myocardial depressant action of diltiazem on an ischemic isolated blood-perfused canine papillary muscle preparation.

The effect of diltiazem on the contractile and vascular responses to 2 min of total occlusion and reperfusion was investigated in isolated blood-perfused canine papillary muscle preparations. Diltiazem, in doses (3 and 10 micrograms/min) that increased coronary blood flow but did not change developed tension and maximum rate of tension development (dT/dt) in papillary muscle before occlusion, attenuated tension development between 40 and 120 sec of ischemia. At-60 sec postocclusion, developed tension was at 36 +/- 4, 37 +/- 5 and 44 +/- 4% below preocclusion levels for 3, 10 and 100 micrograms/min of diltiazem, respectively (nondiltiazem treated = 24 +/- 3%). The dT/dt increased to 22 +/- 6% above preocclusion value during ischemia in nondiltiazem-treated preparations. This was blocked by diltiazem in a dose-dependent fashion. Propranolol and nitroprusside did not modify the developed tension and the increase in dT/dt of the papillary muscle during occlusion. On reperfusion, an overshoot in developed tension to 22 +/- 4% above preocclusion level was observed. This was significantly reduced by diltiazem and propranolol but not by nitroprusside. Diltiazem inhibited the maximal peak reactive hyperemia response after 2 min of occlusion by 30 to 38%. Both propranolol and nitroprusside did not change this response. The results show that diltiazem selectively depresses the inotropic state of the ischemic myocardium and suggest that a diltiazem-induced reduction in myocardial oxygen consumption during ischemia may contribute to the protection of ischemic myocardium and the reduction in reactive hypermia response in the ischemic heart.

Adenosine↗

PubMedDate not supplied

Positive inotropic action of glyceryl trinitrate as observed in the blood-perfused papillary muscle preparation of the dog heart.

1. The effects of glyceryl trinitrate on the coronary vasculature and on the contractility of the ventricular myocardium were investigated by the use of papillary muscle preparations of the dog, and that on the sino-atrial node activity by the use of sino-atrial node preparations of the dog. The papillary muscle preparation was cross-circulated through the anterior septal artery and the sino-atrial node preparation through the sinus node artery from a donor dog. The papillary muscles were driven at a rate of 120 beats/min. Drugs were injected close-arterially. 2. Glyceryl trinitrate, in doses of 0-03-100 microgram, produced dose-related increases in blood flow and developed tension. An increase in developed tension caused by 100 microgram of glyceryl trinitrate amounted to about 24% of the basal developed tension. Large doses of glyceryl trinitrate (100-300 microgram) produced a negative inotropic effect after a positive one in some preparations. 3. The positive inotropic effect of glyceryl trinitrate was not modified by propranolol, excluding a possible participation of an adrenergic mechanism. 4. Glyceryl trinitrate in large doses failed to modify the positive inotropic effect of calcium chloride. 5. Glyceryl trinitrate in a wide range of doses (0-03-100 microgram) had virtually no effect on sino-atrial node activity.

Animals↗

PubMed1995

Nitric oxide synthase inhibitor alters papillary muscle force-frequency relationship.

We provide evidence for an immediate effect of NG-monomethyl-L-arginine (L-NMMA) on the force-frequency relationship in isolated hamster papillary muscles. L-NMMA (competitive inhibitor of nitric oxide synthase) reversed the force-frequency relationship (staircase effect) in isolated hamster papillary muscles from negative to positive (P < .01; ANOVA; n = 6). The addition of L-arginine (substrate for nitric oxide synthase) blocked the L-NMMA effect (P < .01; ANOVA; n = 6). The addition of the nitric oxide (NO) donor, sodium nitroprusside (NTP), significantly increased the level of cGMP in the tissue bath (P < .01; test; n = 6) and reversed the positive inotropic effect of L-NMMA on staircase (P < .01; ANOVA; n = 6). The addition of 8-Br-cGMP to the bath resulted in a concentration-dependent decrease in tension generated by the papillary muscles (n = 6). Methylene blue (known inhibitor of cGMP) mimicked the effect of L-NMMA on staircase (P < .01; ANOVA; n = 6). L-NMMA also significantly blunted the negative inotropic effect of ryanodine (SR calcium release channel regulator) (P < .01; ANOVA; n = 6). The positive inotropic effect of Bay K 8644 (sarcolemmal, L-type calcium channel regulator) was not affected by L-NMMA (P = NS; ANOVA; n = 6). L-NMMA had no effect on either [3H]ryanodine or [3H]PN200-110 (sarcolemmal, L-type calcium channel regulator) binding to cardiac membranes. These findings support a cGMP-dependent role for endogenous NO in myocardial E-C coupling.

Amino Acid Oxidoreductases↗

PubMed1989

Tetrodotoxin-sensitive component in action potential plateau of guinea pig Purkinje fibers: comparison with the papillary muscle.

1. The effects of tetrodotoxin on action potentials of isolated guinea pig purkinje fibers were examined and compared the findings with those obtained in the ventricular papillary muscle, by use of conventional microelectrode techniques. 2. Tetrodotoxin (5 x 10(-7)-10(-5) M) decreased the amplitude, overshoot, and maximum upstroke velocity of action potentials of the Purkinje fibers, and shortened the duration of action potential at all levels of repolarization concentration- and stimulus cycle length-dependently. 3. The longer the stimulus cycle length, the greater the shortening by the drug of the action potential duration. 4. In particular, the plateau potential of the Purkinje fibers exposed to tetrodotoxin was remarkably depressed, and which occurred even in case of blockade of K+ conductance, using tetraethylammonium. 5. On the other hand, a high concentration (10(-5) M) of tetrodotoxin did not significantly affect the papillary muscle action potentials. 6. These findings suggest that there is a tetrodotoxin-sensitive component of Na+ current in plateau voltage range of the Purkinje fibers, but little in the papillary muscle, and that the component plays an important role to maintain the plateau of Purkinje fibers action potential.

Action Potentials↗