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PubMed1987

Electrical constants of arterially perfused rabbit papillary muscle.

1. Right ventricular rabbit papillary muscles were arterially perfused with a mixture of Tyrode solution, bovine erythrocytes, dextran and albumin. In the recording chamber, they were surrounded by a H2O-saturated atmosphere of O2 and CO2 which served as an electrical insulator. 2. Conduction velocity and passive electrical properties were determined from intra- and extracellular potentials measured during excitation and during flow of subthreshold current. 3. The propagation of the action potential was linear along the muscle at a velocity of 55.6 cm/s. The extracellular wave-front voltage was 51.5 mV. 4. The following values for passive cable properties were obtained: (i) a ratio of extra- to intracellular longitudinal resistance of 1.2; (ii) an extracellular specific resistance (Ro) of 63 omega cm; (iii) an intracellular specific resistance (Ri) of 166 omega cm; (iv) a space constant lambda of 0.357 mm; (v) a membrane time constant tau of 2.57 ms. The space constant lambda* recalculated for zero extracellular resistance was 0.528 mm. 5. Arresting perfusion with drop of perfusion pressure was associated with an immediate increase of the extracellular longitudinal resistance by 35% and a decrease of conduction velocity by 13%. 6. The present results demonstrate the important contribution of the extracellular resistance to electrotonic interaction and propagation in densely packed myocardial tissue. Moreover, changes in perfusion pressure are associated with changes in extracellular resistance, probably as a consequence of changes in intravascular volume.

Action Potentials↗

PubMed1982

Post-rest adaptation of electrical and mechanical activity in the isolated guinea-pig papillary muscle.

In guinea-pig papillary muscle the time course of the changes in contractile force and action potential duration (APD) were studied after periods of rest of variable duration. After a long period of rest, the force of contraction adapted to pre-rest control values in a monophasic manner whereas the time-course of the APD was clearly biphasic. The post-rest adaptation of the APD could be described mathematically by a simple model, which considers the action potential duration during steady state as the sum of a resting value (APDR) plus a lengthening effect of activation (LEA) minus a shortening effect of activation (SEA). LEA and SEA are assumed to occur immediately, with each excitation and to decay continuously. During repetitive stimulation, both effects will accumulate. Using the constants found for the post-rest adaptation of the APD, the steady-state frequency-dependence of the APD could also be described with this model.

Action Potentials↗

PubMed2005

Alpha1-adrenoceptor-mediated negative inotropic effect caused by intracellular ionic activities in guinea-pig papillary muscle.

In guinea-pig papillary muscle, phenylephrine (PE), an agonist of alpha1-adrenoceptor (alpha1-AR), led to a transient negative inotropic effect (NIE) and a subsequent sustained positive inotropic effect (PIE). To clarify the ionic mechanisms underlying the NIE, we measured the [Na+]i or [pH]i by ion-selective microelectrodes. PE produced a decrease in the intracellular Na+ concentration ([Na+]i) and an increase in intracellular pH ([pH]i). During the phase of NIE, PE produced only a (-) change of [Na+]i (Delta[Na+]i). With a decrease in extracellular Na+ or an increase in extracellular Ca2+, the PE-induced NIE was attenuated and PE produced (+)Delta[Na+]i. The PE-induced NIE and (-)Delta[Na+]i were definitely strengthened by lowering the bath temperature or increasing the stimulation frequency. 2-(2,6-di-methoxyphenoxyethyl)amino-methyl-1,4-benzidioxane HCl, an antagonist of alpha1A-AR, completely abolished the PE-induced NIE and (-)Delta[Na+]i. Phorbol 12,13-dibutyrate, an activator of protein kinase C (PKC), decreased the baseline [Na+]i and twitch force and increased the baseline [pH]i in mimicry of PE. Pretreatment with 1-5(isoquinolinesulphonyl)-2-methylpiperazine, an inhibitor of PKC, abolished the PE-induced NIE and (-)Delta[Na+]i. During pretreatment with benzamil, an inhibitor of Na+/Ca2+ exchange, we found that the PE-induced NIE and (-)Delta[Na+]i were reversibly abolished. Our results indicate the PE-induced NIE may be elicited upon the activation of Na+/Ca2+ exchange which can be attributed to the (-)Delta[Na+]i. (-)Delta[Na+]i is mediated through a PKC-dependent pathway via an activation of alpha1A-AR subtype and its effect could be strengthened remarkably at high [Na+]i and [Ca2+]i values.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1987

[Ultrasonic diagnosis of papillary muscle dysfunction in patients with acute myocardial infarct].

A study of 123 patients with acute myocardial infarction demonstrated the potentials of combined use of sectoral scanning and Doppler echocardiography in the diagnosis of the papillary muscle dysfunction syndrome. Two basic pathogenetic mechanisms of papillary muscle dysfunction associated with acute myocardial infarction are identified: direct involvement of the papillary muscles and papillary muscle dysfunction developing in cases of marked left-ventricular dilatation associated with acute aneurysm of the heart. Two-dimensional impulse Doppler echocardiography is found to be a more sensitive method, as compared to sectoral scanning, in the diagnosis of mitral lesions in patients with acute myocardial infarction.

Cardiomyopathies↗

PubMed1991

Activated human polymorphonuclear leucocytes reduce rabbit papillary muscle function: role of the CD18 glycoprotein adhesion complex.

STUDY OBJECTIVE: The aim was to determine if human polymorphonuclear leucocytes activated by human recombinant C5a (hrC5a) reduce the contractile function of the isolated papillary muscle and if this response depends upon the functional integrity of the CD18 glycoprotein adhesion complex. DESIGN: Human neutrophils with or without pretreatment with monoclonal antibodies to the CD18 adhesion complex were added to organ baths containing isolated papillary muscles of the rabbit and activated with hrC5a. Changes in papillary muscle function were measured. EXPERIMENTAL MATERIAL: 52 right ventricular papillary muscles isolated from rabbit and neutrophils isolated from human whole blood were used. MEASUREMENTS AND MAIN RESULTS: Neither neutrophils nor hrC5a alone reduced papillary muscle function, but activation of neutrophils with hrC5a provoked reduction in myocardial contractility. This correlated with the degree of neutrophil stimulation, assessed by cell aggregation. Pretreatment of neutrophils with antibodies to the CD18 adhesion complex significantly attenuated the neutrophil induced contractile impairment. CONCLUSIONS: Activated human neutrophils can impair contractile function of papillary muscles, which is dependent upon adhesion of the leucocytes to the muscle via the CD18 complex.

Animals↗

PubMed1984

Purkinje and ventricular activation sequences of canine papillary muscle. Effects of quinidine and calcium on the Purkinje-ventricular conduction delay.

We have studied in vitro preparations of canine right and left papillary muscles to determine the excitation sequences of the Purkinje and ventricular cells, using both monopolar surface electrodes and intracellular microelectrodes. Our results show, for right papillary muscles, that the Purkinje layer covers the basal part of the muscle, and that activation from the right bundle branch propagates over all of the Purkinje layer, but directly activates the underlying ventricular layer only at specific junctional sites. Left papillary muscles have attachments to both apical and basal Purkinje strands and the Purkinje layer covers the entire muscle, but, as for right papillary muscles, activation from the Purkinje layer to the ventricular layer occurs only at basal junctional sites. Antidromic conduction in papillary muscles (propagation from the ventricular layer to the Purkinje layer) can occur at regions other than the specific sites through which the Purkinje layer activates the ventricular layer. At the identified junctional sites, the Purkinje cell action potential duration is significantly shorter than in the free-running strand, but it remains longer than that of the ventricular cells. The time delay at the junctional sites is increased by quinidine, increased calcium concentration, and increased pacing frequency.

Action Potentials↗

PubMed1994

Autonomic modulation of action potential and tension in guinea pig papillary muscles.

The effects of alpha 1-adrenoceptor and muscarinic acetylcholine receptor stimulation on action potential and tension were studied in guinea pig papillary muscles obtained from both right and left ventricles. Stimulation of muscarinic acetylcholine receptors with carbachol produced a reduction of the action potential duration and a positive inotropic effect in papillary muscles from both ventricles. Both effects were concentration dependent and atropine sensitive. However, differential responsiveness was found upon alpha 1-adrenoceptor activation in muscles obtained from left and right ventricles. In right side papillary muscles, the alpha 1-adrenoceptor agonist, methoxamine, decreased the action potential duration and produced a positive inotropic effect. In contrast, methoxamine decreased the action potential duration but failed to produce a positive inotropic effect in left side papillary muscles. All methoxamine effects were antagonized by prazosin. Responses to maximum concentration of carbachol and methoxamine on the action potential duration and contractility were additive in right side papillary muscles. Phorbol 12,13-dibutyrate (PDB), a direct protein kinase C activator, also decreased the action potential duration in a manner that was additive to both carbachol and methoxamine. However, PDB reversed the positive inotropic effect of carbachol and methoxamine. The methoxamine-induced shortening of the action potential duration was prevented by pretreatment with indomethacin and nordihydroguaiaretic acid, blockers of arachidonic acid metabolism, but not by the protein kinase C antagonist, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7).(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2001

[A case of emergency surgery for acute mitral regurgitation due to complete papillary muscle rupture as a severe form of reperfusion injury: report of a case].

Complete rupture of a papillary muscle following acute myocardial infarction is a severe complication associate with acute left ventricular failure and pulmonary edema. Since the introduction of acute percutaneous transluminal coronary angioplasty (PTCA) in the management of acute myocardial infarction, the frequency of this complication has further decreased. We described a patient who had acute mitral regurgitation due to complete rupture of papillary muscle rupture after successful coronary intervention. Transesophageal echocardiography demonstrated severe mitral regurgitation and the ruptured papillary muscle. At operation, posteriol papillary muscle was found to be totally ruptured. Mitral valve replacement was performed. Postoperative course was uneventful, with 2 days of IABP and 5 days of ventilator support.

Acute Disease↗

PubMed1996

Enhanced regional deformation at the anterior papillary muscle insertion site after chordal transsection.

BACKGROUND: Clinical and experimental studies of mitral valve replacement have shown a depression of ventricular function after chordal transsection; most recent studies have proposed that this is secondary to a depression of local function near the papillary muscle insertion site. However, there is no direct experimental evidence for changes in local fiber shortening in the wall of the left ventricle overlying the papillary muscle. Accordingly, we investigated the effect of chordal transsection on left ventricular shape and on three-dimensional regional deformation of the myocardium near the insertion of the anterior papillary muscle. METHODS AND RESULTS: In six open-chest dogs, two sets of three transmural columns of radiopaque markers were implanted in the anterior wall, one set at the tip of the papillary muscle (basal) and one at the site of papillary muscle fiber insertion (apical). A Björk-Shiley mitral valve was placed in the left atrium adjacent to the native valve. Markers were then tracked with biplane cineradiography, and deformation was quantified with the use of finite strain analysis. Chordal transection resulted in reduced left ventricular end-systolic pressure and slowed relaxation. After chordal transsection, outward displacement of the ventricular wall and transverse shearing deformation were observed in the area of the papillary muscle during isovolumic contraction. Circumferential and radial strains during ejection were maintained at our basal site and enhanced on our apical site. CONCLUSIONS: Chordal transsection led to enhanced local shortening and wall thickening and regional strain nonuniformity. These results indicate that chordal transsection induces an unloading of myocardium at the papillary muscle insertion site and that the resulting heterogeneity of regional function is the mechanism for the reduced global function and slowed ventricular relaxation.

Animals↗

PubMed1976

[Direct measurement of papillary muscle dynamics in the intact canine left ventricle during acute coronary occlusion (author's transl)].

UNLABELLED: The functions of the normal and ischemic papillary muscle in the intact canine heart were studied using an ultrasonic transit time method. Miniaturized piezoelectric crystals (1.5-2 mm 0) were implanted during extracorporeal circulation into the root and tip of the anterior and posterior papillary muscle of the left ventricle. RESULTS: 1. Phasic changes of left ventricular geometry during the heart cycle determine the dynamic pattern of papillary muscle movements. 2. The amplitude and velocity of papillary muscle length is directly related to those of myocardial wall segments. 3. Experimental ischemia induces total dysfunction of the papillary muscle within seconds. 4. Despite total muscle dysfunction no mitral insufficiency occured.

Animals↗

PubMed1997

The parachute-like asymmetric mitral valve and its two papillary muscles.

OBJECTIVES: The morphologic features of parachute-like asymmetric mitral valves are described to discriminate this anomaly from parachute mitral valves. BACKGROUND: Mitral valves with unifocal attachment of chords have been called "parachute valves," independent of the number of papillary muscles. Therefore the anomaly involving two papillary muscles has not received separate attention. METHODS: The gross anatomy of 29 mitral valves with focalized attachment of chords was studied. RESULTS: In 28 of the autopsy specimens asymmetric mitral valves with two papillary muscles were present, and one of the muscles was elongated, located higher in the left ventricle with its tip reaching to the anulus, and attached at both its base and lateral side to the left ventricular wall. The valve leaflets could be directly attached to this abnormal muscle that received few chords or, in three hearts, no chords at all, resulting in an oblique and eccentric orifice. Because of the focalized attachment of chords to one of the two papillary muscles, we call this malformation "parachute-like asymmetric mitral valve," We found only one "true parachute mitral valve," that is, one having a single papillary muscle that received all chords. CONCLUSIONS: The morphologic features of asymmetric mitral valves are essentially different from those of true parachute valves. A distinction between these two anomalies will contribute to recognition by the pediatric cardiologist and surgeon.

Adolescent↗

PubMed1989

The inotropic effect of 4-aminopyridine and pH changes in rabbit papillary muscle.

The effects of 4-aminopyridine (4AP), and pH changes have been examined on tension responses and cyclic nucleotide levels in rabbit isolated right ventricular papillary muscles. 4AP augmented papillary muscle contractions in a concentration-dependent manner. However, this positive inotropic action was largely due to an increase in extracellular pH produced by 4AP, rather than an intrinsic activity of the drug. Increases in extracellular pH (from 5 to 9) produced graded and reproducible increases in contractile force which were not blocked by propranolol (1 x 10(-7) M) but were inhibited by verapamil in a concentration-dependent manner. The positive inotropic effects of Ca2+ were enhanced and depressed by alkaline and acidic pH, respectively. Neither 4AP nor alkaline pH significantly changed cyclic AMP concentration in rabbit papillary muscles. The cyclic GMP content, however, was increased by 4AP only and this effect was blocked by atropine. The results suggest that the positive inotropic effect associated with a rise in pH from neutrality may be due to facilitation of translocation of membrane Ca2+ and/or to increase the release of Ca2+ from sources within the cell. They also illustrate that a major component of the inotropic effect of 4AP is a result of an increase in extracellular pH.

4-Aminopyridine↗

PubMed1980

Comparative inotropic response of newborn and adult rabbit papillary muscles to isoproterenol and calcium.

Age-related changes in the response rabbit papillary muscles to isoproterenol and calcium were studied. Newborn rabbit papillary muscles were not only less sensitive to the inotropic effect of isoproterenol and calcium, but also produced significantly less maximal inotropic tension to these agents in comparison to the adult. The decreased response of newborn papillary to isoproterenol appears to be due to a combination of (a) decreased ability of papillary muscle to respond to calcium and (b) immaturity of isoproterenol-sensitive contractile mechanism. Differences in myocardial norepinephrine content do not appear to play an important role in the age-related difference in the response to isoproterenol and calcium.

Age Factors↗

PubMed1998

Development of the papillary muscles of the mitral valve: morphogenetic background of parachute-like asymmetric mitral valves and other mitral valve anomalies.

OBJECTIVES: To understand papillary muscle malformations, such as in parachute mitral valves or parachute-like asymmetric mitral valves, we studied the development of papillary muscles. METHODS: Normal human hearts at between 5 and 19 weeks of development were studied with immunohistochemistry, three-dimensional reconstructions, and gross inspection. Scanning electron microscopy was used to study human and rat hearts. RESULTS: In embryonic hearts a prominent horseshoe-shaped myocardial ridge runs from the anterior wall through the apex to the posterior wall of the left ventricle. In the atrioventricular region this ridge is continuous with atrial myocardium and covered with cushion tissue. The anterior and posterior parts of the trabecular ridge enlarge and loosen their connections with the atrial myocardium. Their lateral sides gradually delaminate from the left ventricular wall, and the continuity between the two parts is incorporated in the apical trabecular network. In this way the anterior and posterior parts of the ridge transform into the anterolateral and the posteromedial papillary muscles, respectively. Simultaneously, the cushions remodel into valve leaflets and chordae. Only the chordal part of the cushions remains attached to the developing papillary muscles. CONCLUSIONS: Disturbed delamination of the anterior or posterior part of the trabecular ridge from the ventricular wall, combined with underdevelopment of chordae, seems to be the cause of asymmetric mitral valves. Parachute valves, however, develop when the connection between the posterior and anterior part of the ridge condenses to form one single papillary muscle. Thus parachute valves and parachute-like asymmetric mitral valves originate in different ways.

Adult↗

PubMed1977

Rupture of ventricular septum or papillary muscle complicating myocardial infarction.

Ninety-eight specimens with rupture of some portion of the left ventricle complicating acute myocardial infarction from atherosclerotic coronary disease were studied. In 90, a single structure (so-called isolated rupture) had ruptured as follows: free wall of left ventricle, 52 cases; ventricular septum, 18 cases; a papillary muscle, 20 cases. In eight cases, two structures had ruptured, the most common combination being rupture of ventricular septum and left ventricular wal. Inferolateral location of underlying infarction was the common situation in ruptured papillary muscle, while anteroseptal myocardial infarction was more common in rupture of the ventricular septum. Transmural infarction underlay each case of ruptured ventricular septum, while in ruptured papillary muscle 11 of 20 cases showed subendocardial infarction. There was no association between the type of papillary muscle rupture and the type of infarct. Clinically, collapse of the circulation was common in cases of ruptured ventricular septum and ruptured papillary muscle. Death within one week after rupture was usual when the papillary muscle was involved totally or when the ventricular septum was involved. With partial rupture of a papillary muscle, longer survival (months) was observed in two of ten cases.

Aged↗

PubMed1986

Effects of halothane on transmembrane potentials, Ca2+ transients, and papillary muscle tension in the cat.

The effects of halothane on cat papillary muscle were studied in vitro at different pacing rates (60, 75, 100, and 150 beats/min). Simultaneous measurements of transmembrane potentials, intracellular Ca2+ transients, and isometric tension were made before and after introduction of 1 and 2 minimal alveolar concentration halothane. Anesthetic concentrations in the superfusion bath were measured using a gas chromatography procedure. The Ca2+-sensitive photoprotein, aequorin, was microinjected into papillary muscle cells. Aequorin light emission is a function of free intracellular [Ca2+] [( Ca2+]i). The most prominent effects of halothane were a dose-dependent decrease in the contractile force and a decrease in [Ca2+]i, at all pacing rates. The negative inotropic effect of halothane was associated with only small changes in the papillary muscle action potential duration. Increasing the extracellular [Ca2+] produced an increase in [Ca2+]i and counteracted the negative inotropic effects of halothane. Addition of the Ca2+ channel blocker, verapamil, and halothane, produced an additive decrease in [Ca2+]i compared with the control.

Action Potentials↗

PubMed1989

[Effect of anesthesia and/or decapitation on the mechanical behavior of papillary muscles isolated from the left ventricle of the rat].

The mechanical performance of isometrically contracting papillary muscle was studied in rats sacrificed by decapitation or anesthetized with sodium pentobarbital or chloralose before decapitation. The purpose was to evaluate which maneuver would be the more adequate to ve used, when performance of papillary muscle mechanics must be evaluated later. The data suggest that either anesthetic agents used in this experiment and/or decapitation have the same effects on isolated muscle performance in the three groups. The results may be a consequence of the time elapsed between animal decapitation and the recording of cardiac parameters: this fact would attenuate the many factors that could promote mechanical performance dysfunction or isolated papillary muscles.

Analysis of Variance↗

PubMed2001

Improved in vitro quantification of the force exerted by the papillary muscle on the left ventricular wall: three-dimensional force vector measurement system.

Recent developments indicate that the forces acting on the papillary muscles can be a measure of the severity of mitral valve regurgitation. Pathological conditions, such as ischemic heart disease, cause changes in the geometry of the left ventricle and the mitral valve annulus, often resulting in displacement of the papillary muscles relative to the annulus. This can lead to increased tension in the chordae tendineae. This increased tension is transferred to the leaflets, and can disturb the coaptation pattern of the mitral valve. The force balance on the individual components governs the function of the mitral valve. The ability to measure changes in the force distribution from normal to pathological conditions may give insight into the mechanisms of mitral valve insufficiency. A unique in vitro model has been developed that allows quantification of the papillary muscle spatial position and quantification of the three-dimensional force vector applied to the left ventricular wall by the papillary muscles. This system allows for the quantification of the global force exerted on the posterior left ventricular wall from the papillary muscles during simulation of normal and diseased conditions.

Animals↗