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PubMed1981

Perturbation measurements of papillary muscle elasticity.

Small step-length perturbations (less than 0.5% Lmax) have been applied to rabbit papillary muscle for the purpose of measuring muscle stiffness at rest and during isometric twitch-force development. These stiffness-force measurements were fitted to four mechanical analogs to evaluate whether any of the models adequately predict the mechanical properties of papillary muscle. Stiffness-force relations have been measured at varied initial muscle lengths so that a broad range of applicability of an analog could be evaluated. This study shows that none of the four experimentally definable analogs predicts the stiffness-force responses of the muscle over a physiological range of initial muscle lengths. A two-segment nonhomogeneous analog has the same stiffness-force characteristics as a six-parameter lumped model but cannot be differentiated from the lumped model without a measurement of segmental variations. It is concluded that the passive elastic elements of papillary muscle cannot be controlled only by the manipulation of total muscle length so as to deduce cross-bridge mechanical properties from whole-muscle measurements.

Animals↗

PubMed1987

The effect of myoglobin-facilitated oxygen transport on the basal metabolism of papillary muscle.

A mathematical model of oxygen diffusion into cylindrical papillary muscles is presented. The model partitions total oxygen flux into its simple and myoglobin-facilitated components. The model includes variable sigmoidal, exponential, or hyperbolic functions relating oxygen partial pressure to both fractional myoglobin saturation and rate of oxygen consumption. The behavior of the model was explored for a variety of saturation- and consumption-concentration relations. Facilitation of oxygen transport by myoglobin was considerable as indexed both by the elevation of oxygen partial pressure on the longitudinal axis of the muscle and by the fraction of total oxygen flux at the muscle center contributed by oxymyoglobin. Despite its facilitation of oxygen flux at the muscle center, myoglobin made only a negligible contribution to the total oxygen consumption averaged over the muscle cross-section. Hence the presence of myoglobin fails to explain either the experimentally determined basal metabolism-muscle radius relation or the stretch effect observed in isolated papillary muscle.

Animals↗

PubMed1992

Different patterns of protein kinase C redistribution mediated by alpha 1-adrenoceptor stimulation and phorbol ester in rat isolated left ventricular papillary muscle.

1. In rat left ventricular papillary muscle, phenylephrine, an alpha 1-adrenoceptor agonist, had a staurosporine-sensitive positive inotropic effect and increased the particulate-associated protein kinase C (PKC) activity without significant changes in total PKC activity or in cytosolic Ca2+/phospholipid-independent kinase (PKI) activity. 2. A PKC stimulant, phorbol 12,13-dibutyrate (PDBu), decreased contractility and slightly increased PKC activity in the particulate fractions, with a marked decrease and increase in total PKC and PKI activities, respectively. 3. The PDBu-induced negative inotropic response was attenuated by two protease inhibitors, leupeptine and a microbial peptide isolated from Aspergillus japonicus (E-64), which are known to inhibit the conversion of particulate-associated PKC to PKI. 4. Such differences in the patterns of PKC redistribution, i.e. marked increases in particulate PKC and cytosolic PKI activities caused by phenylephrine and PDBu, respectively, may account for the opposite inotropic effects of PKC stimulation by an alpha 1-agonist and a phorbol ester.

Adrenergic alpha-Agonists↗

PubMed1999

Hybrid logistic characterization of isometric twitch force curve of isolated ferret right ventricular papillary muscle.

We previously found that the isovolumic pressure curve of the left ventricle and the isometric twitch force curve of the right ventricular in situ papillary muscle, both of the blood-perfused canine heart, were precisely fitted by our newly proposed hybrid logistic function. This function describes the difference between the two S-shaped logistic functions for the rising and falling components: A/[1+exp{-(4B/A)(t-C)}]-D/[1+exp{-(4E/D)(t-F)}]+G. This function characterizes comprehensively both ventricular and in situ papillary muscle contraction and relaxation. In the present study, we hypothesized that this function could also characterize the force curve of the most popular, standard-type, isolated and Tyrode-superfused papillary muscle preparation. To test this hypothesis, we investigated how precisely the hybrid logistic function could fit 112 isometric twitch force curves observed in eight isolated and Tyrode-superfused ferret right ventricular papillary muscles at different muscle lengths and extracellular Ca2+ concentrations. We always obtained a precise curve fitting with a correlation coefficient above 0.9987. This fitting was much more precise than sinusoidal and polynomial exponential function curve fittings. These results supported the present hypothesis. We conclude that our hybrid logistic function reasonably characterizes the force curve of the isolated myocardial preparation. This result broadens the generality of the hybrid logistic characterization of ventricular isovolumic pressure and myocardial isometric twitch force generation. The hybrid logistic characterization seems to be an integrative expression of contractile processes in myocardial twitch contraction.

Animals↗

PubMed1992

Influences of changes in calcium concentration and verapamil on the cardiac depressant effect of ethanol in cat papillary muscle.

1. In isolated cat heart papillary muscle electrically driven at a constant rate the depressant effects of increasing concentrations of ethanol on peak tension developed (PTD) was studied in Ringer-Locke solution with different calcium concentrations and with the addition of verapamil. 2. Ethanol induced a concentration dependent decrease in PTD that was significantly greater for each concentration of ethanol in hypocalcic medium (1.1 mM) than in normocalcic medium (2.2 mM). 3. In normocalcic (2.2 mM) medium, verapamil (5.1 x 10(-4) mM) plus ethanol (48.6 and 97.2 mM) produced a decrease in PTD to values significantly greater than those obtained by the addition of ethanol and verapamil alone. Therefore a potentiation of the effects of ethanol by verapamil was observed when both drugs act simultaneously. 4. In hypercalcic medium (4.4 mM), verapamil plus ethanol (48.6 and 97.2 mM) produced a slight decrease in PTD that was significantly less than that observed in normocalcic and hypocalcic mediums. 5. In hypocalcic medium (1.1 mM) verapamil plus ethanol (48.6 and 97.2 mM) produced a decrease in PTD that was of the same relative magnitude (%) as that observed in normocalcic medium. However no potentiation of the combined effects of verapamil plus ethanol was observed in hypocalcic medium.

Animals↗

PubMed1996

Mechanism of negative lusitropic effect of alpha 1-adrenoceptor stimulation in cat papillary muscles.

Experiments were performed in cat papillary muscles to explore the mechanisms by which alpha 1-adrenoceptor stimulation affects myocardial relaxation. Phenylephrine (PE; 10 microM) + atenolol (1 microM; n = 8 experiments) produced a negative lusitropic effect, i.e., a prolongation of half-relaxation time (t1/2; time to 50% relaxation) by 30 +/- 10% (P < 0.05) and a proportionally smaller increase in maximal velocity of relaxation (-T) than in maximal velocity of contraction (+T), which significantly increased the ratio +T/-T. A similar increase in contractility, produced by increasing calcium, failed to significantly change t1/2 and +T/-T. PE-induced negative lusitropic effect was significantly inhibited by two protein kinase C (PKC) inhibitors, staurosporine (0.1 microM) and chelerythrine (10 microM). PE also increased intracellular pH by 0.18 +/- 0.05 pH units (P < 0.05, n = 4), as measured by the fluorescent dye 2'-7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Intracellular alkalosis and the negative lusitropic effect of PE were prevented by the Na+/H+ exchanger inhibitor ethylisopropylamiloride (10 microM). No significant changes in calcium myofilament sensitivity and maximal tension were detected in trabeculae treated with PE either before or after chemical skinning. These results indicate that a Na+/H+ exchanger-induced intracellular alkalosis, possibly mediated by PKC activation, may fully account for the negative lusitropism of alpha 1-adrenoceptor stimulation.

Actin Cytoskeleton↗

PubMed1991

Cardiac cell membrane repolarization is required for onset of mechanical restitution in papillary muscle.

In 10 voltage clamped ferret papillary muscles at 37 degrees C (single sucrose gap), the duration of resting (diastolic, holding) potential was varied in order to define the mechanical restitution process. Following a period of steady state voltage clamp depolarizations to +20 mV, a single test depolarization clamp of 200 or 500 ms duration was introduced. Then, the following period at resting (holding) potential was varied. All the mechanical restitution curves for the 500 ms clamps were delayed by 300 ms compared with the 200 ms clamps. When mechanical restitution was plotted as the relationship between contractile force and test electrical diastolic interval, all processes started from zero interval (i.e. the time of repolarization). Variation of diastolic holding potential between -70 mV and -40 mV did not affect the starting time, but the final force values at full restitution were approached faster and were higher for -70 mV than for -40 mV. There was an inverse relationship between force and second inward current during mechanical restitution after an initial phase of restitution of current. Mechanical restitution is postulated to be due to passage of contractile calcium with time from an uptake to a release compartment within the sarcoplasmic reticulum. Thus the rise of contractile force with increasing test cycle duration should have been independent of whether a 200 or 500 ms depolarization was used. In order to accommodate the discrepancy, we postulate either that (1) sarcoplasmic reticulum calcium release channels require sarcolemmal repolarization to begin to be reactivated or (2) that trigger calcium (calcium induced calcium release from the sarcoplasmic reticulum) is derived from the sarcolemma.

Animals↗

PubMed1975

Effects of extracellular calcium and sodium on depolarization-induced automaticity in guinea pig papillary muscle.

Regenerative discharge of action potentials is induced in mammalian papillary muscles by passage of small depolarizing currents. In this paper, the effects of various extracellular calcium and sodium concentrations and of tetrodotoxin on this phenomenon were studied in guinea pig papillary muscles in a sucrose gap chamber. Phase 4 diastolic depolarization was found to be associated with an increase in membrane resistance. The slope of phase 4 depolarization was decreased by reductions in extracellular calcium or sodium concentration. The range of maximum diastolic potentials and the thresholds from which regenerative potentials arose were reduced, especially at the positive limit of potentials, by a reduction in either ion. It was concluded that both calcium and sodium influence diastolic depolarization and participate in the regenerative action potentials of depolarization-induced ventricular automaticity.

Action Potentials↗

PubMed1986

The effects of the cardiotonic dihydropyridine derivatives Bay k 8644 and H160/51 on post-rest adaptation of guinea-pig papillary muscles.

In isolated guinea-pig papillary muscle, the effect of the two dihydropyridine derivatives Bay k 8644 (0.03-10 mumol/l) and H160/51 (0.1-3 mumol/l) on transmembrane action potentials and force of contraction were investigated at regular stimulation (1 Hz) and after a period of rest (10 min). The following results were obtained: At regular stimulation of the preparations, Bay k 8644 and H160/51 enhanced force of contraction without affecting time-to-peak tension. The time required for relaxation and the action potential duration were prolonged. These effects were transient with exposure to high concentrations of Bay k 8644 (greater than 3 mumol/l). The amplitude of the post-rest contraction thought to depend entirely on transmembrane calcium influx was small under control conditions and increased because of prolongation in time-to-peak tension in the presence of either dihydropyridine derivative. Isoprenaline (30 nmol/l) - as opposed to Bay k 8644 and H160/51 - increased the rate of force development of post-rest contractions. Bay k 8644 and H160/51 prolonged the duration of the first action potential after 10 min of rest. In the course of adaptation to steady state stimulation this prolongation transiently increased further resulting in a biphasic pattern which was attenuated by addition of nifedipine. With isoprenaline the biphasic pattern changed into a monotonous adaptation to pre-rest control. Our results show that the small enhancement of the post-rest contraction in the presence of Bay k 8644 or H160/51 is due to prolonged action potential duration after rest, whereas isoprenaline enhances the intensity of post-rest activation.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1978

Transient force responses in blood-perfused papillary muscle after step changes in load.

In in situ canine papillary muscles, we studied transient responses in peak isometric force at control length, after contraction was suddenly switched from isotonic contractions at various forces and isometric contractions at different lengths. Peak isometric force rapidly decreased after isotonic contractions at relatively low forces and isometric contractions at shorter lengths. In contrast, peak isometric force rapidly increased after isotonic contractions at relatively high forces and isometric contractions at longer lengths. There was no transient response when the preceding isotonic force was about half of the present peak isometric force. Magnitude and direction of the transient force response depended on magnitude and direction of the change in the mean muscle force level produced by the sudden switch of loading conditions. Transient force responses were accompanied by simultaneous changes in time to peak isometric force in the same direction. We proposed that, in the blood-perfused papillary muscle, a sudden change in the mean muscle force causes an abrupt change in coronary flow supply-demand relation which in turn causes a transient change in contractile force.

Animals↗

PubMed1976

The effects of batrachotoxin on cat papillary muscle.

The effects of batrachotoxin (BTX) upon the contraction and transmembrane potential of cat right ventricular papillary muscles were studied in vitro at 37 degrees C. BTX (2.0 x 10(-9) M) increased isometric contractile force by about 50% from control force, decreased the potential difference across the cell membrane to approximate -50 mV and produced spontaneous contractions of the papillary muscles. Each BTX-induced spontaneous contraction was accompanied by a spontaneous action potential which was generated when an oscillation in membrane potential reached threshold level. Spontaneous activity ovvurred only in muscles which were previously stimulated electrically. The positive inotropic effect of BTX was accompanied by an increase in the rate of force development. Papillary muscles from cats pretreated with reserpine did not differ from normal muscles in their responses to BTX treatment. Tetrodotoxin (2.0 x 10(-7) M) antagonized the effects of BTX, a finding which suggests that the actions of BTX are mediated by a selective increase in membrane permeability to sodium ions. The resultant BTX-elicited increase in the intracellular sodium ion concentration may increase the force of contraction through an augmentation of calcium influx via the sodium-calcium exchange system.

Action Potentials↗

PubMed2005

Nifedipine enhances cGMP production through the activation of soluble guanylyl cyclase in rat ventricular papillary muscle.

It is known that nifedipine, an L-type calcium channel blocker, increases cGMP production, which partially contributes to the relaxation of vascular smooth muscle. The aim of our investigation was to clarify whether or not nifedipine regulates cGMP production, which has a physiological role in cardiac muscle. To measure contractile responses and tissue cGMP levels, left ventricular papillary muscles prepared from male Wistar rats (350-400 g) were mounted in the isolated organ chamber under isometric conditions and electrically paced by means of platinum punctate electrodes (1 Hz, 1 ms duration). In papillary muscle preparation, the negative inotropic effect induced by nifedipine (30 to 300 nM) was significantly inhibited in the presence of ODQ(1H-[1,2,4]oxidazolo[4,3-a]quinoxaline1-one; 10 microM), a soluble guanylyl cyclase inhibitor. Furthermore, nifedipine (100 nM) strongly increased the tissue cGMP level, which was significantly decreased in the presence of ODQ. On the other hand,N(G)-monomethyl-(L)-arginine (100 microM), a nitric oxide synthase inhibitor, did not inhibit either the negative inotropic effect or cGMP production induced by nifedipine. These results indicate that in rat left ventricular papillary muscle, nifedipine augments its negative inotropic effect at least partly through direct activation of cardiac soluble guanylyl cyclase but not nitric oxide synthase.

Animals↗

PubMed1979

Effect of hypoxia on mechanical properties of hyperthyroid cat papillary muscle.

It has been previously established that hyperthyroid myocardium exhibits increased performance under well-oxygenated conditions. To date, it is not known whether hyperthyroid cardiac muscle can maintain this increased performance during hypoxia. The responses of isolated right ventricular papillary muscles from hyperthyroid and euthyroid kittens to hypoxia were compared under isometric conditions at 31 degrees C. Under well-oxygenated conditions, the hyperthyroid cardiac muscle exhibited both an increased contractility and an accelerated rate of relaxation. A similar degree of acute hypoxic stress for 15 min resulted in a greater decrease in contractility in the hyperthyroid compared with the euthyroid papillary muscle as indicated by a greater fall in both peak tension development (2.2 +/- 0.25 from 4.2 +/- 0.2 vs. 0.9 +/- 0.15 from 3.2 +/- 0.4 g/mm2, P less than 0.01) and +dT/dt (12.9 +/- 2.3 from 25 +/- 3 vs. 4.0 +/- 0.6 from 14 +/- 1 g-s-1-mm-2, P less than 0.01). In addition, compared with the euthyroid data, hypoxia resulted in impaired myocardial relaxation in the hyperthyroid cardiac muscle. Thus, the hyperthyroid compared with the euthyroid papillary muscle exhibits both a greater decrease in contractility and an impairment of myocardial relaxation during hypoxia, indicating a greater susceptibility to a given hypoxic stress.

Animals↗

PubMed1986

Direct and indirect effects of ciguatoxin on guinea-pig atria and papillary muscles.

The mode of action of ciguatoxin (CTX) on the isolated atrial and papillary muscle of the guinea-pig heart was investigated using conventional methods for the measurement of mechanical and electrophysiological parameters. CTX induced positive inotropic and positive klinotropic responses in atrial and papillary muscles. Each response consisted of two phases. The initial positive inotropic response developed rapidly and resulted from the previously reported indirect action of CTX. The second phase of positive inotropy developed more slowly and was well maintained at doses of CTX up to 0.15 mouse units/ml in atria and up to 0.8 M.U./ml in papillary muscles. This phase was found to result from a direct action of CTX on the myocardium which was not reversed by washing. Tetrodotoxin (TTX) reversed the positive inotropic effects stemming from the direct action of CTX. The (-) and (+) enantiomers of propranolol were equally effective in inhibiting the direct effect of CTX. These antagonists did not displace CTX from the myocardium. CTX induced a TTX-sensitive depolarization of stimulated or quiescent atrial cells. All the effects of CTX on the atrial action potential were reversed by TTX. It was therefore concluded that CTX opens voltage dependent Na+ channels. CTX bound equally to resting and K+-depolarized Na+ channels but there were indications that electrical stimulation enhanced the rate of CTX binding. CTX overrides the positive staircase effect of increasing stimulation frequency. Na+ channels found in the atria which were particularly sensitive to TTX did not play a prominent role in mediating the CTX effect. CTX appeared to have little effect on the normal Na+ channel inactivation process. CTX did not restore contractions in the K+-depolarized cardiac muscles examined. The sensitivity of CTX action to TTX distinguished it from cardiac glycoside activity. Established mechanisms of Na+/Ca2+ exchange and Ca2+-induced release of Ca2+ can explain the link between CTX-induced increase of intracellular [Na+] and the positive inotropic response.

Action Potentials↗

PubMed1999

Role of nitric oxide and platelet-activating factor in cardiac alterations induced by tumor necrosis factor-alpha in the guinea-pig papillary muscle.

OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine with negative inotropic properties, is implicated in several pathophysiological events. To clarify the mechanism of action of TNF-alpha on myocardium, we investigated the possible role of platelet-activating factor (PAF) and nitric oxide (NO) as secondary mediators of the depressant effect of this cytokine. METHODS: Isometric twitches and intracellular action potentials were recorded from guinea pig papillary muscles. The effects of TNF-alpha (1-10 ng/ml) were studied in controlled conditions and after treatment with 0.5% Triton X-100, to destroy the endocardial endothelium NG-nitro-L-arginine methyl ester (L-NAME), D-NAME (1 mM) and the two different PAF-receptor antagonists WEB 2170 (3 microM) and CV 3988 (5 microM) were used to study the role of NO and PAF in cardiac depression induced by TNF-alpha. To study the role of NO in cardiac alterations induced by PAF, papillary muscles were pretreated with L-NAME or D-NAME and then challenged with PAF (0.1-1 microM). Nitrite production by papillary muscles challenged with TNF-alpha alone. TNF-alpha in the presence of WEB 2170 or CV 3988, or PAF was studied with the Greiss reagent method. PAF production by papillary muscles stimulated by TNF-alpha was studied by a bioassay method. RESULTS: TNF-alpha induced an initial, transient positive inotropic effect, then reduced the contractility and the action potential duration in a concentration-dependent manner. Treatment of papillary muscle with Triton X-100 did not modify the response to TNF-alpha, suggesting that the effect of TNF-alpha is not mediated by endocardial endothelial cells. Pretreatment with indomethacin reduced the negative effect of TNF-alpha, while propranolol abolished the initial increase of contractility. The role of PAF and NO as mediators of TNF-alpha was suggested by: (1) the protective effect of L-NAME, but not of D-NAME, on electrical and mechanical alterations; (2) the stimulatory effect of TNF-alpha on nitrite production; (3) the inhibitory effect of WEB 2170 and CV 3988, on both the electromechanical alterations and the nitrite production; (4) the synthesis of PAF induced by TNF-alpha. L-NAME blocked the negative effect of PAF and PAF enhanced nitrite production by papillary muscle. CONCLUSIONS: The present results suggest that in cardiac muscle: (1) the release of PAF triggered by TNF-alpha may account for the stimulation of NO production; (2) both PAF and NO contribute to the development of the electrical and mechanical alterations induced by TNF-alpha; (3) NO production was down-stream to the synthesis of PAF.

Action Potentials↗

PubMed1987

Calcium channels and excitation-contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle.

Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 microM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.

Action Potentials↗

PubMed1995

[Surgical treatment for complete rupture of anterior papillary muscle after acute myocardial infarction].

A 64-year-old male patient with postinfarction complete anterior papillary muscle rupture and massive mitral regurgitation is presented. The diagnosis was suspected clinically and confirmed by transesophageal echocardiography. One week after the episode of acute myocardial infarction (AMI) the patient had a sudden onset of severe congestive heart failure with pulmonary edema and was transferred to our hospital. The patient underwent an emergency mitral valve replacement with a SJM29M prosthetic valve. Histological examination revealed an acute coagulation necrosis of the anterior papillary muscle without specific inflammatory change. To our knowledge this is the second case with successful surgery for a complete rupture of the anterior papillary muscle following AMI in Japan.

Echocardiography, Transesophageal↗

PubMed1982

Actions of prenalterol, a new cardioselective beta1-agonist, terbutaline and isoprenaline on electrophysiological and mechanical parameters of guinea pig atrial and papillary muscles.

The electrophysiological and mechanical effects of prenalterol on the isolated guinea pig atrial trabeculae and papillary muscles were compared with those of terbutaline and isoprenaline. Isoprenaline was the most potent of the drugs tested on all parameters studied. Prenalterol, on the other hand, failed to induce any changes in the atrial action potentials. The action potential duration was shortened in the atrial trabeculae by terbutaline and isoprenaline. All three substances shortened the action potential in the papillary muscles. In addition, isoprenaline increased the plateau height, and like terbutaline, increased the rate of repolarization during phase 3. Neither prenalterol nor terbutaline changed the effective refractory period in the atrial trabeculae whereas isoprenaline shortened it. All three substances shortened this parameter in the papillary muscles. The developed force and the rate of developed force were increased by all three substances. In addition, the total twitch duration was decreased.

Action Potentials↗