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PubMed1984

Right ventricular papillary muscle electrography. Analysis of the site of surgically induced right bundle branch block using a temporary ventricular pacing electrode.

It is believed that the prognosis of patients with surgically induced right bundle branch block (RBBB) related to correction of congenital heart diseases varies according to the site of block. Thus, it is necessary to differentiate the proximal type from the distal type of RBBB. The main purpose of this study was to develop a practical and precise method for the determination of the site of block. The right ventricular papillary muscle activation time (V-PM) was measured 1 or 2 weeks after surgery by means of a temporary pacing electrode placed on the epicardial surface of the right ventricular anterior papillary muscle. This technique is referred to as "right ventricular papillary muscle electrography (PME)". The presence of a proximal RBBB is diagnosed by the finding of a prolongation of V-PM. The unique characteristics of this newly developed PME are as follows: 1) the appropriate site of electrode placement is selected anatomically during surgery by observations of local systolic concavity, and 2) with a unipolar lead, the local activation time can be measured with sufficient accuracy. The average V-PM was 21.0 +/- 6.3 msec (+/- S.D.) in 64 patients without RBBB and 51.1 +/- 7.5 msec in 13 patients with confirmed proximal RBBB in whom distal RBBB had been excluded in view of the surgical procedures that had been performed. As a result, the criterion for the diagnosis of proximal RBBB was established as a V-PM of longer than or equal to 35 msec. According to this criterion, the incidence of proximal RBBB found in surgically repaired tetralogy of Fallot (TF), membranous ventricular septal defect (VSD (2] and supracristal ventricular septal defect (VSD (1] were 46% (11/24), 33% (15/45) and 11% (2/18), respectively. Distal RBBB was observed only in TF, where the incidence was 17% (4/24).

Bundle-Branch Block↗
PubMed1997

A three-component force vector cell for in vitro quantification of the force exerted by the papillary muscle on the left ventricular wall.

Recent clinical studies indicate that functional mitral regurgitation, which is a common complication in patients who suffer from ischemic heart disease, is related to an increase in the tethering forces acting on the mitral valve leaflets. Alterations in the valvular assembly, displacement of the papillary muscles or dilatation of the mitral valve annulus can disrupt the normal force balance on the mitral leaflets and result in an abnormal coaptation geometry with incomplete mitral leaflet closure. The force balance imposed on the mitral leaflets is created by the coapting forces generated by the transmitral pressure difference and the tethering forces at the leaflet attachments. A unique force vector cell capable of accurately measuring the three-component force vector applied by the papillary muscle on the left-ventricular wall was designed and manufactured to permit quantification of the alteration in the force balance acting on the mitral leaflets, and to allow for the study of the influence of papillary muscle displacement on mitral regurgitation.

Animals↗
PubMed1987

Correlation of force-length area with oxygen consumption in ferret papillary muscle.

The ventricular systolic pressure-volume area correlates well with myocardial oxygen consumption. However, in isolated muscle preparations, there are experimental data based on both mechanical and energetic measurements that suggest that the pressure-volume area concept may not obtain. In the present study, force-length area, the analog of pressure-volume area for a linear muscle, was examined in the ferret papillary muscle preparation under a wide range of loading conditions. There were two major findings: first, force-length area is closely correlated with oxygen consumption (r = 0.94-0.98); this correlation is better than those for such other indexes as peak force and force-time integral. Furthermore, this relation of oxygen consumption with force-length area is independent of the mode of contraction (isometric or shortening), while the relations with the other indexes are not. Second, quick release imposed after end-systole during isometric contraction was found to curtail oxygen consumption. The first finding, the optimal correlation of force-length area with oxygen consumption, suggests both that the correlation of pressure-volume area with oxygen consumption on the ventricular level arises from a basic property of cardiac muscle and that force-length area may be the best mechanical index to use in calculating regional oxygen consumption for a ventricular segment. The second finding, however, suggests that the time-varying elastance model, on which the concepts of pressure-volume area and force-length area are based, may not provide a complete description of the mechanical basis of cardiac muscle energetics, especially during the isometric contraction.

Animals↗
PubMed1992

Acute inotropic response of rabbit papillary muscle to triiodothyronine.

The effects of triiodothyronine (T3) on the force frequency responses of isometrically contracting rabbit papillary muscles were studied in the presence of d-glucose, pyruvate or butyrate. The stimulation frequency was varied from 0.1 to 0.5 Hz, and the maximum developed tension and its maximum (Tmx) and minimum (Tmn) time derivative were measured. T3 concentrations ranged from 0.1 to 4.0 ng/ml. The addition of T3 resulted in a substrate-dependent increase in twitch tension; with the largest increases being: d-glucose 118 +/- 7%, pyruvate 143 +/- 6%, butyrate 123 +/- 11%; Tmx:d-glucose 121 +/- 8%, pyruvate 157 +/- 5%, butyrate 138 +/- 12%, and Tmn:d-glucose 150 +/- 10%, pyruvate 159 +/- 6%, butyrate 163 +/- 14%. All three measures of contractility showed a dose-dependent increase reaching a maximum value at a T3 concentration between 1 and 2 ng/ml. These data show that T3 induces an inotropic response in rabbit papillary muscles which is manifested within, approximately 30 min, and that the greatest increase is seen in Tmn.

Animals↗
PubMed1995

[Successful valvuloplasty for isolated tricuspid regurgitation due to traumatic ruptured papillary muscle].

A 44-year-old man suffered from an traffic accident on May 27, 1994. He was transferred to a hospital because of emergent operation for a laceration of liver, right-sided hemothorax and pneumothorax. After surgical treatment for these lesions, he was doing well. However, systolic murmur appeared from August, 1994. By echocardiography and cardiac catheterization, he was diagnosed of isolated tricuspid regurgitation due to traumatic ruptured papillary muscle. Because right heart failure was progressive, an operation was recommended. At operation, annular dilatation of tricuspid valve and ruptured papillary muscle of anterior leaflet were found. And the ruptured end of right ventricular aspect was recognized. Therefore, we performed tricuspid valvuloplasty and annuloplasty. Postoperative course was uneventful. And residual regurgitation was not detected by right ventriculography. Especially, in patients with tricuspid regurgitation due to ruptured papillary muscle, symptoms usually begin soon after trauma. Therefore, an operation should be recommended promptly in the presence of right heart failure not relieved by medical treatment. And an earlier operation could increase the feasibility of tricuspid valvuloplaty, and the possibility of maintaining sinus rhythm.

Adult↗
PubMed1982

Analysis of mechanical alternans in rabbit papillary muscle.

Isometric force and action potentials were recorded in rabbit papillary muscles. It was found that the monophasic decline of the contractile potentiation that was recorded after an extrasystole (ES) was replaced by transient mechanical alternans (TMA) when temperature and calcium concentration of the perfusion medium had been lowered (from 37 degrees to 27 degrees C and from 2.0 to 0.5 mM, respectively). TMA in response to ES was also seen when the preparation was exposed to 2mM 4-aminopyridine. Furthermore, TMA could be induced by a shortening step during activity. Mechanical restitution curves were recorded by relating max. rate of force development of a test contraction to the duration of the preceding stimulus interval. It was found that the alternating contractions during TMA were associated with shifts of the mechanical restitution curve along the force axis. The duration of the action potential was inversely related to force development during TMA. It is proposed that TMA is due to a reduced damping of a regulatory feedback system between inotropic state and intake of activator calcium during the action potential. The following sequence of events are suggested: The abbreviated action potential accompanying a potentiated contraction is associated with reduced intake of activator calcium. This leads to depression of the subsequent contraction. The latter contraction is associated with increased calcium intake due to prolongation of the action potential. This will lead to potentiation of the next beat and the sequence is repeated. It is proposed that recirculation of calcium between heart beats will act as a damping factor of this system.

Action Potentials↗
PubMed2001

Inotropic response of rabbit ventricular myocytes to endothelin-1: difference from isolated papillary muscles.

Endothelin-1 (ET-1) increased cell shortening and Ca2+ transients over the concentration of 3 x 10(-11) M to 10(-9) M with EC50 of 8.3 x 10(-11) M in rabbit single ventricular myocytes. Thus ET-1 was approximately 60 times more potent in single myocytes than in papillary muscles (EC50 = 5.1 x 10(-9) M) of the same species. In single myocytes, ET-1 at 10(-8) M elicited an inhibitory response that counteracted the facilitatory response: the concentration-response curve (CRC) for ET-1 was bell shaped. The ET(A)-receptor antagonist BQ-485 shifted CRC for ET-1 to the right in parallel; however, the facilitatory response to 10(-8) M ET-1 was markedly enhanced by BQ-485 and also by the ET(B) antagonist BQ-788. The ET(A)/ET(B) antagonist TAK-044 abolished the ET-1-induced response. These findings indicate that the response to ET-1 of single myocytes is different from that of papillary muscles in concentration dependence, characteristics of the response, and susceptibility to ET-receptor antagonists. Anomalous pharmacological characteristics of ET-1-induced response in rabbit papillary muscles may be due to integrated regulatory mechanisms that may involve also various types of noncardiac cell in ventricular myocardium.

Animals↗
PubMed1972

Effects of perivascular nerve stimulation on the contraction and automaticity of the blood-perfused canine papillary muscle.

1. Effects of ventricular perivascular nerve stimulation (p.n.s.) on the ventricular contractility and idioventricular rate were investigated with the blood-perfused papillary muscle of the canine right ventricle.2. Perivascular nerve stimulation of supramaximal voltage and 1 msec pulse-duration caused a definite positive inotropic response at a frequency of 1 Hz, which gradually reached a maximum at 15 to 20 Hz when the papillary muscle was electrically driven at 120 beats/min at a constant temperature of 38-39 degrees C. The frequency-response curve was sigmoid.3. The spontaneous regular idioventricular rate of 46+/-4 beats/min was accelerated to at most 60+/-4 beats/min (n=11) by p.n.s. The stimulus frequency-response relations between chronotropic and inotropic responses to p.n.s. were almost the same.4. Tetrodotoxin blocked completely the responses to p.n.s. while it had little or no effect on the inotropic response to exogenous noradrenaline.5. Positive inotropic responses to p.n.s. were diminished by beta-adrenoceptor blocking agents (alprenolol, propranolol and pindolol) and were enhanced during infusion of cocaine.6. In reserpine- or guanethidine-pretreated muscles, p.n.s. as well as field stimulation produced negative inotropic responses, which were enhanced by physostigmine and were blocked by atropine.7. Hexamethonium enhanced slightly the positive inotropic responses to p.n.s. as well as field stimulation.8. It was concluded that the perivascular nerves of the coronary artery of the canine ventricle are mainly composed of postganglionic adrenergic fibres but there are also pre- and postganglionic cholinergic nerve fibres.

Alprenolol↗
PubMedDate not supplied

Analysis of the positive inotropic effect of ibopamine in the blood-perfused canine papillary muscle.

The positive inotropic effect of ibopamine, an orally active dopamine analogue, was examined in an isolated canine papillary muscle perfused with blood of a donor dog through the anterior septal artery (ASA). Administered intraduodenally (25 mg/kg) in the donor dog, ibopamine increased the left ventricular dP/dtmax as well as the contractile force of the isolated papillary muscle. Injected into the ASA (10 micrograms) it had only a slight positive inotropic effect, which was greatly enhanced by preincubation of the drug in plasma. Addition of physostigmine to the plasma prevented this enhancement. Propranolol (0.2 mg/kg i.v.) shifted the dose-response curves for the positive inotropic effect of plasma-dissolved (PD) ibopamine (0.3-10 micrograms), norepinephrine (NE; 1-100 ng), and deoxyepinephrine (Epinine; 0.3-10 micrograms) to the right. At 3 micrograms/min cocaine enhanced the response to NE, but enhanced only slightly the responses to Epinine and PD ibopamine; at 10 micrograms/ml it enhanced the response to NE, but depressed slightly the responses to Epinine and PD ibopamine. The positive inotropic effect of intraduodenally administered ibopamine may be caused by active metabolite(s), possibly epinine, from its hydrolysis by esterases, and may be mediated by both direct and indirect stimulation of beta-adrenoceptors in the canine heart.

Animals↗
PubMed1981

Effect of impromidine (SK&F 92676) on the isolated papillary muscle of the guinea-pig.

Impromidine was found to have a positive inotropic effect on the isolated papillary muscle from the guinea-pig. The dose-response curve to impromidine was shifted to the right by cimetidine and ranitidine. Impromidine was 35 times more potent than histamine but with a maximal response of only 81% that obtained with histamine. This difference, which was statistically significant (P < 0.005), suggested that impromidine acts as a partial agonist at the histamine H2-receptors of the papillary muscle as has been observed in other tissues.

Animals↗
PubMed1996

Negative inotropic action of denbufylline through interfering with the calcium channel independently of its PDE IV inhibitory activity in guinea pig ventricle papillary muscles.

The inotropic actions of xanthine derivatives with long alkyl chains were investigated in guinea pig ventricular papillary muscle. A potent and nonselective phosphodiesterase (PDE) inhibitor, 3-isobutyl-1-methylxanthine, elicited a positive inotropy and inhibited the negative inotropic effects of calcium channel inhibitors, as did a selective PDE III inhibitor, amrinone, and these effects were canceled by a protein kinase inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89). However, 1,3-di-n-butyl-7-(2'oxopropyl)xanthine (denbufylline) and 1-n-butyl-3-n-propylxanthine (XT-044), which have potent and selective PDE IV-inhibitory activities, showed negative inotropic actions that became more potent in the presence of H-89. Denbufylline abolished the late restoration phase induced by ryanodine. This xanthine derivative attenuated the effects of both the calcium channel acting agents Bay K 8644 and verapamil, without interaction with caffeine and dihydropyridine calcium channel inhibitors, and denbufylline had little direct influence on the specific binding of [(3)H]azidopine and [(3)H]desmethoxyverapamil to cardiac membranes. A nonxanthine PDE IV inhibitor, Ro 20-1724, did not affect the inotropic actions of calcium channel inhibitors. The attenuation by denbufylline or XT-044 of the negative inotropic action of verapamil was not influenced by treatment with H-89. These results suggest that in the ventricular papillary muscle, these xanthine derivatives elicit negative inotropy by acting on a verapamil-sensitive site of the calcium channel without involving their PDE-inhibitory activity.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

[Negative inotropic effect of 3,6-dimethamidodibenzopyriodonium citrate (I-65) on guinea pig papillary muscles].

The effects of 3,6-dimethamidodibenzopyriodonium citrate (I-65) on the contractile response of electrically paced guinea pig papillary muscles in vitro were studied. I-65 (0.1-300 mumol/L) decreased the contractile force and inhibited isoprenaline-induced restoration of the contractile response in papillary muscles rendered inexcitable by KCl 22 mmol/L. Both effects were concentration-dependent, and the IC50 were 36.0 and 7.3 mumol/L, respectively. I-65 antagonized the positive inotropic effects of Iso and CaCl2 in a non-competitive manner. Like verapamil, I-65 had a frequency-dependent negative inotropic effect, and delayed the recovery of post-rest potentiation. It is concluded that the negative inotropic effect of I-65 results not only from the reduction of Ca2+-influx through the sarcolemmal membrane, but also from the inhibition of Ca2+ translocation in the sarcoplasmic reticulum.

Animals↗
PubMed1990

Negative inotropic effects of amiodarone on isolated guinea pig papillary muscle.

STUDY OBJECTIVE: The aim of the study was to investigate the inotropic effects on isolated papillary muscle of acute and chronic exposure to amiodarone. DESIGN: Papillary muscles were obtained from untreated and amiodarone pretreated guinea pigs, and tension recording and conventional glass microelectrode techniques were used to assess the effects of amiodarone. SUBJECTS: Guinea pigs of either sex weighing 300-500 g were used: 65 untreated and 18 amiodarone pretreated (20 mg.kg-1.d-1 for 3 1/2 weeks). MEASUREMENTS AND RESULTS: Acute amiodarone exposure (4.4 X 10(-6)-1.1 X 10(-3) mol.litre-1) caused a concentration dependent negative inotropic effect, which was also frequency dependent (0.1-5 Hz), with greater effect at higher stimulation frequencies. Time to peak tension and resting tension increased, while rate of development and relaxation of twitch contraction were slower. Amiodarone caused a dose dependent depression or abolition of slow response action potentials and of contraction in both untreated and amiodarone pretreated specimens. In amiodarone pretreated muscle, contractile forces did not differ significantly from control preparations. Chronic exposure to amiodarone attenuated the negative inotropic effects of acute amiodarone superfusion. CONCLUSIONS: The negative inotropic action of amiodarone may reflect a decrease in Na+ influx via Na+ channels and/or Ca2+ influx via Ca2+ channels, and/or an impairment of Ca2+ sequestration, alone or in combination. The differences in contractile response in relation to acute and chronic amiodarone exposure may be relevant to clinical actions of amiodarone.

Action Potentials↗
PubMed1969

Rat heart papillary muscles: action potentials and mechanical response to paired stimuli.

Electrical reexcitation of rat papillary muscle after a short interval (50 to 80 milliseconds) results in action potentials with no significant mechanical counterpart. The mechanical response recovers as the interval is increased beyond 80 milliseconds. The rate of recovery is slowed at low external calcium levels. It appears that the coupling mechanism passes through a refractory stage owing to the depletion of an intracellular "releasable calcium" fraction.

Action Potentials↗
PubMed1988

Actions of flunarizine dihydrochloride on the electrical activity of isolated guinea-pig papillary muscle and rabbit sino-atrial node.

Effects of flunarizine on electrophysiological properties of isolated guinea-pig papillary muscles and rabbit sino-atrial nodes were examined using conventional microelectrode and double-microelectrode voltage clamp methods. Although flunarizine did not affect the maximum rate of rise of the action potential (Vmax) in fast response fibers, the compound depressed the slow action potentials of K+-depolarized papillary muscle (at above 10 microM) and reduced the automaticity of sino-atrial node (at above 3 microM). In voltage clamp experiments, flunarizine selectively suppressed the slow inward current of sino-atrial node specimens. It is concluded that relatively high concentrations of flunarizine directly modify the electrical activity of isolated mammalian myocardium via a suppression of Ca2+ influx through the cell membrane.

Action Potentials↗
PubMed1996

Subaortic stenosis caused by anomalous papillary muscle of the mitral valve.

We report on a rare case of subaortic stenosis caused by an anomalous posteromedial papillary muscle inserting directly into the anterior mitral leaflet, which had muscular extension to the subaortic region. Resection of the muscular extension alone was ineffective. A second operation including entire resection of the anomalous papillary muscle and mitral valve replacement resulted in successful relief of the obstruction. Microscopic findings of the resected tissue were compatible with those of hypertrophic cardiomyopathy.

Aortic Valve Stenosis↗
PubMed1980

Comparison of the alpha-adrenergic agonists, phenylephrine and methoxamine in rabbit papillary muscles.

The positive inotropic effects of the alpha-adrenergic agonists, phenylephrine and methoxamine were compared in isolated rabbit papillary muscles. Phenylephrine in the presence of 10(-7)M propranolol produced a greater response than methoxamine. Antagonism by phentolamine was competitive for phenylephrine and apparently, noncompetitive for methoxamine. Based upon observed maximum following frequencies, 10(-4)M methoxamine had a greater cardiac depressant effect than 10(-4) phenylephrine. It was suggested that phenylephrine with a beta-adrenergic antagonist possessed advantages over methoxamine as an agonist for studying cardiac alpha-adrenergic receptors in rabbit papillary muscles.

Animals↗