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PubMedDate not supplied

[Pathology of the papillary muscles].

Anatomoclinical findings in 21 cases of papillary muscle (PM) damage found in 4,000 consecutive autopsies are reviewed. Mitral PM muscles were involved in 17 cases, the posteromedial muscle in 11 patients, in 8 of these with necrosis (N) in 3 with fibrosis (F), in 2 with rupture. The mitral antero-lateral (MAL) was involved in 4 cases, by myocardial infarction (MI), fibrosis, hemorrhage and infectious endocarditis (IE). Both mitral PM were involved in two patients (MI and endomyocardial fibrosis). Tricuspid PM involvement was found in 4 cases. In two because of MI and the two remaining with fibrosis. In the 12 cases with MI microscopic examination showed, PM necrosis of variable magnitude: in the 7 cases with F, there was increased interstitial tissue by connective tissue; in the case with IE there was severe inflammatory reaction with microabscess formation and in one case, a small central longitudinal artery was damaged, a finding not previously described. Mitral PM infarction caused regurgitant murmurs, increase in heart size, heart failure and death from acute pulmonary edema or serious arrhythmias. There was no radiological evidence of left atrial enlargement. ECG findings were not useful in the diagnosis. Based on this anatomoclinical experience considerations are made about other diagnostic and surgical methods.

Humans↗
PubMed1990

Rupture of both left ventricular papillary muscles following acute myocardial infarction.

A 77-year-old woman collapsed shortly after arrival at the emergency department and attempts at resuscitation were unsuccessful. Autopsy revealed an evolving recent transmural myocardial infarct in the posterolateral free wall of the left ventricle with rupture of both papillary muscles. No well documented description of post infarction dual papillary muscle rupture was found in the literature.

Aged↗
PubMed1992

Treatment of severe mitral regurgitation caused by ischemic papillary muscle dysfunction: indications for coronary angioplasty.

The aim of this study was to evaluate the prognosis and functional outcome of mitral regurgitation caused by ischemic papillary muscle dysfunction with respect to treatment, and to determine the role of coronary angioplasty in this context. Thirty patients with severe ischemic mitral regurgitation were followed up for 33 +/- 3 months. Thirteen patients were treated medically (group I) and 17 patients underwent surgery or angioplasty (group II). The 3-year survival was 59.5% (45.6% in group I and 70.2% in group II). Angioplasty was only used in paroxysmal mitral regurgitation caused by papillary muscle ischemia. This technique resulted in spectacular immediate results in three patients with pulmonary edema caused by mitral regurgitation during myocardial ischemia. Surgical correction of mitral regurgitation should be considered without delay if angioplasty is not feasible or if the regurgitation is permanent or severe. Widening the indications of surgery or angioplasty should result in an improvement of the prognosis of these high-risk patients.

Acute Disease↗
PubMedDate not supplied

Inotropic effects of ethanol on the isolated papillary muscle of the diabetic rat.

The present study was designed to characterize the inotropic effects of ethanol (ETOH) on diabetic rat heart. Left-ventricular papillary muscles, from normal and diabetic (streptozotocin, 50 mg/kg IV; 6 weeks) rats, were superfused with Tyrode's solution at 30 oC while driven at 0.5 Hz. Developed tension, time-to-peak tension (TPT), time-to-90% relaxation (RT90), maximum rate of tension developed (+VT) and maximum rate of tension fall (-VT) were determined in the absence and presence of clinically relevant concentrations of ETOH (80-240 mg/dl, i.e., 1.7-5.2 mM). Ethanol decreased developed tension, TPT, RT90, and VT in papillary muscles from both groups. Ethanol 80 mg/dl reduced tension, +VT and -VT in preparations from diabetic animals. However, this concentration had no effect on normal muscles. An intermediate concentration of ETOH (120 mg/dl), decreased tension and +VT in preparations from both groups, whereas a higher dose (240 mg/dl) decreased tension, TPT, RT90, VT, and -VT, and induced spontaneous contractures in both groups. The negative inotropic effects of ethanol were generally concentration-dependent and the diabetic myocardium maybe more sensitive to inotropic effects of clinically relevant concentrations of ETOH. Ethanol-induced diminution in contractile tension in normal and diabetic myocardium is associated with reduced contraction and relaxation velocity as well as their respective duration.

Animals↗
PubMed1973

Influence of previous mechanical events on the contractility of isolated cat papillary muscle.

1. The influence of previous mechanical events on myocardial contractility has been investigated in the cat papillary muscle preparation.2. When a muscle that had been producing a stable response under isometric conditions was allowed to shorten isotonically, its ability to do so increased in successive beats until it reached a steady level, which represented a potentiated state compared with that seen in the first isotonic beat and in the preceding stable isometric contractions.3. The increase in tension development in the first isometric beat after a period of isotonic beating was used as an index of the degree of potentiation. It was found to be well correlated with the changes in other parameters that could have been used for this purpose.4. The main determinants of the degree of potentiation produced by a period of isotonic beating were:(a) the amount by which the muscle shortened. This was inversely related to the force opposing shortening (i.e. the isotonic load);(b) the number of isotonic beats. There was some potentiation (about 10%) after a single isotonic beat, but the number of beats required for maximal potentiation (up to 25%) depended on the frequency of stimulation; about 8 beats were required at 24 min(-1).5. An isotonic release during the rise of tension in an isometric response was even more effective in potentiating the next isometric beat than an afterloaded contraction against the same load. Isotonic releases at later times had a diminishing influence on tension development in the next isometric beat.6. In the absence of stimulation, the potentiated state produced by a period of isotonic beating decayed with a half-time of about 50 sec. When the muscle was stimulated it disappeared sooner, and its rate of decay depended on the frequency of stimulation; at 24 min(-1) about 8 beats were required to restore contractility to its previous steady level.7. The characteristics of the decay of the potentiated state were closely similar to those of the potentiated states that can be produced by various electrical interventions, and the possibility that all of these might have the same underlying mechanism is discussed.8. Attention is drawn to the practical implications of this phenomenon in the design of experiments in which the muscle contracts under changing mechanical conditions.

Animals↗
PubMed1998

Effects of sex hormones on action potential and contraction of guinea pig papillary muscle.

AIM: To study the effects of sex hormones, estradiol (Est), progesterone (Pro) and testosterone (Tes) on the action potential (AP) and contraction of guinea pig papillary muscle. METHODS: Using conventional glass microelectrode and mechanical recording of myocardial contraction. RESULTS: Est slowed down the maximal rate of rise of phase 0 (Vmax) of AP at low concentration (1 mumol.L-1). At 10 mumol.L-1 and above, Est also prolonged AP duration (APD50 and APD90), effective refractory period (ERP) and decreased the maximal isometric tension (Pmax) and velocity of tension development (dT/dt) of contraction. Tes (100 mumol.L-1 - 1 mmol.L-1) prolonged APD90 and ERP with decreased Pmax and dT/dt. But Pro (1 mumol.L-1 - 1 mmol.L-1) had no effects on both AP and contraction. CONCLUSION: Est prolonged AP and depressed contraction of guinea pig papillary muscle.

Action Potentials↗
PubMed1993

Induction by endogenous noradrenaline of an alpha 1-adrenoceptor-mediated positive inotropic effect in rabbit papillary muscles.

1. The possible involvement of alpha 1-adrenoceptors in the inotropic and electrophysiological responses to endogenous noradrenaline released by tyramine was examined in rabbit papillary muscles. 2. A concentration-dependent positive inotropic effect was produced by tyramine. This effect of tyramine was not observed in muscles from rabbits pretreated with reserpine. 3. The positive inotropic effect of tyramine was greatly inhibited by propranolol, but not altered by prazosin. However, when beta-adrenoceptors were blocked by pretreatment with propranolol, tyramine still produced a positive inotropic effect, an effect which was antagonized by prazosin. 4. Tyramine caused a decrease in action potential duration (APD) and an increase in action potential amplitude in a concentration-dependent manner. Isoprenaline also produced the same electrophysiological effects. These electrophysiological effects of both agents were inhibited by propranolol. 5. When beta-adrenoceptors were blocked by propranolol, the observed prazosin-sensitive positive inotropic effect of tyramine was not accompanied by any change in APD. In contrast, APD was markedly prolonged by alpha 1-adrenoceptor stimulation with phenylephrine in the presence of propranolol, in association with the positive inotropic effect. 6. It is concluded that in rabbit papillary muscles, endogenous noradrenaline causes a positive inotropic effect predominantly mediated by beta-adrenoceptors, but can still evoke a positive inotropic effect through alpha 1-adrenoceptors when beta-adrenoceptor stimulation is eliminated. This suggests that the alpha 1-adrenoceptor-mediated positive intropic mechanism(s) may be masked by simultaneous activation of beta-adrenoceptors. In addition, this study indicates that APD prolongation is not involved in the alpha 1-adrenoceptor-mediated inotropic responses to endogenous noradrenaline.

Action Potentials↗
PubMed1977

Assessment of the selectivity of OPC-2009, a new beta2-adrenoceptor stimulatn, by the use of the blood-perfused trachea in situ and of the isolated blood-perfused papillary muscle of the dog.

1 The potency and selectivity of 5-(1-hydroxy-2-isopropylamino)butyl-8-hydroxy carbostyril hydrochloride hemihydrate (OPC-2009), a new beta(2)-adrenoceptor stimulant, was compared with those of isoprenaline, trimetoquinol and salbutamol by the use of blood-perfused tracheal preparations in situ and of blood-perfused papillary muscle preparations of the dog. All drugs were injected intra-arterially.2 All the four drugs decreased tracheal intraluminal pressure (tracheal relaxation) and increased tracheal blood flow in a dose-dependent manner. The four drugs produced a dose-dependent increase in developed tension of papillary muscles. In both preparations the duration of action of isoprenaline and salbutamol was short, whereas that of OPC-2009 and trimetoquinol was long. These effects were antagonized by propranolol.3 Dose-response curves to the four drugs for tracheal relaxation were almost parallel. OPC-2009 was 2.4 times more potent, and trimetoquinol and salbutamol were 2.2 and 6.2 times less potent than isoprenaline in causing tracheal relaxation.4 Dose-response curves to the four drugs for tracheal vasodilatation were also parallel. OPC-2009, trimetoquinol and salbutamol were 3.9, 6.7 and 23 times less potent than isoprenaline.5 Slopes of the dose-response curves to the four drugs for increased developed tension were not parallel; that of OPC-2009 was the least steep, whereas that of isoprenaline was the steepest. Trimetoquinol, salbutamol and OPC-2009 were about 18, 570 and 2400 times less potent than isoprenaline.6 Selectivity calculated from relative potencies indicate that OPC-2009 was about 6000 times, salbutamol about 92 times and trimetoquinol about 8.2 times more selective than isoprenaline for tracheal smooth muscle as compared to ventricular muscle.7 The high potency and selectivity of OPC-2009 for tracheal smooth muscle and its long duration of action suggest its potential usefulness for treatment of bronchial asthma.8 The present results are also compatible with the concept that beta(1)-adrenoceptors in cardiac muscle and beta(2)-adrenoceptors in tracheal and vascular smooth muscle can be distinguished. Furthermore, the results revealed that the beta-adrenoceptors mediating tracheal relaxation and vasodilatation may also be different.

Adrenergic beta-Agonists↗
PubMed1990

Preservation of all chordae tendineae and papillary muscle during mitral valve replacement with a tilting disc valve.

Mitral valve replacement was performed in 21 patients using a surgical technique that preserves the entire papillary muscle and chordal apparatus. With this technique, the anterior mitral leaflet is split from the center of the free edge toward the annulus. Bilateral incisions are made from the proximal end of this split to the two mitral commissures, detaching the anterior leaflet from the annulus. These two halves of the leaflet, with all chordae intact (corresponding to the anterolateral and posteromedial papillary muscles), are judiciously trimmed to remove areas of leaflet untethered by chordae tendineae and (when necessary) fibrous thickening; then swung posteriorly and sutured to the posterior mitral annulus using mattress sutures with pledgets. This surgical technique is expected to favor the preservation of left ventricular function and avoid occurrence of irreversible left ventricular dilation/dysfunction, and has been used successfully for calcific and degenerative etiologies, using both tilting disc valves and porcine bioprostheses. It is especially useful in the implantation of tilting disc and bileaflet mechanical prostheses because anterior subvalvular chordae tissue may interfere with the disc excursion and relocated to the posterior leaflet annulus.

Adolescent↗
PubMed1994

Class I and III antiarrhythmic actions of prazosin in guinea-pig papillary muscles.

1. The electrophysiological effects of prazosin, a highly specific alpha 1-adrenoceptor antagonist, on transmembrane action potential characteristics were studied in guinea-pig papillary muscles. 2. At concentrations between 10(-6) M and 10(-5) M, prazosin produced a concentration-dependent decrease in the maximum upstroke velocity (Vmax) and a progressive lengthening of the action potential duration at 50% (APD50) and 90% (APD90) of repolarization. The prolongation of the APD50 and APD90 values was independent of the frequency of stimulation. The prolongation of the ADP90 was accompanied by a parallel lengthening of the effective refractory period (ERP) and thus, the ERP/APD90 ratio remained unaltered at all drug concentrations tested. 3. In the presence of prazosin, 5 x 10(-6) M, the percentage of Vmax block increased with the frequency of stimulation, the inhibitory effect being more marked at fast driving rates (frequency-dependent Vmax block). At 3 Hz, the onset kinetics of the frequency-dependent Vmax block was better fitted by a biexponential function, the K values of the fast (K1) and slow components (K2) being 0.254 +/- 0.037 AP-1 and 0.045 +/- 0.010 AP-1, respectively. However, prazosin did not produce tonic Vmax block. 4. The recovery time constant (tau re) from the frequency-dependent Vmax block was prolonged from 19.6 +/- 2.5 ms to 24.4 +/- 5.5 s. This result indicated that prazosin can be considered as a slow kinetics Na channel blocker. 5. Prazosin, 5 x 10(-6) M, shifted the membrane responsiveness curve in a hyperpolarizing direction, which indicated that the blockade of sodium channels increased at less negative potentials (voltage-dependent Vmax block). 6. It is concluded that in guinea-pig papillary muscles, prazosin inhibited the Vmax and lengthened the duration of the action potentials, thus exhibiting both class I and class III antiarrhythmic actions,respectively, that were possibly unrelated to blockade of myocardial alpha l-adrenoceptors.

Action Potentials↗
PubMed1975

Ultrastructral effects of in virto experimentation on right ventricular papillary muscle from cats in hypovolemic shock (38487).

The present data demonstrate for the first time that repeated stimulation (2-3 hr in an oxygenated perfusate) of right ventricular papillary muscles from cats subjected to hypovolemic shock does not alter the ultrastructure of the shock lesions. Neither does the in vitro experimentation cause functional impairment as determined by the measured isometric twitch tension. The data also indicate that electron microscopy is important to the evaluation of papillary muscles from cats subjected to shock.

Animals↗
PubMedDate not supplied

Electropharmacological effects of a new dihydropyridine analog on isolated guinea pig papillary muscles and Purkinje fibers.

The effects of a new dihydropyridine, FR-34235, were compared with those of the dihydropyridine, nifedipine, and verapamil on the normal fast action potentials (APs), slow APs, and contractions of guinea pig papillary muscles and Purkinje fibers. FR-34235 (10(-6) M) blocked the contractions of papillary muscles superfused with normal Tyrode solution within 10-12 min. Maximal upstroke velocity (+Vmax) and overshoot of the fast APs were not affected, whereas the AP durations at 50 and 90% repolarization (APD50 and APD90) were shortened. The effects of FR-34235 on the fast APs and contractions were reversed within 10 min on washout. To determine the effects of the calcium antagonists on slow APs, the fast Na+ channels were inactivated by partial depolarization (to approximately -45 mV) by elevated [K]0, and isoproterenol (10(-6) M) or histamine (10(-5) M) was used to induce slow APs on stimulation. Nifedipine (10(-7) M) and verapamil (2 X 10(-6) M) completely blocked the slow APs. FR-34235 depressed (3 X 10(-8) M) and blocked (10(-7) M) the slow APs in a frequency-dependent manner. The effects were reversed by elevated [Ca]0 or washout of the drug. The contractions accompanying the slow APs were depressed and blocked in parallel with the depression of +Vmax. In guinea pig Purkinje fibers, FR-34235 had no significant effect on the fast AP parameters but produced a marked depression of automaticity. FR-34235 also blocked the slow APs of the Purkinje fibers in a frequency-dependent manner; all drug effects were reversed within 10 min on washout.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1989

[Effect of myocardial alpha 1-adrenoceptor stimulation on the guinea-pig ventricular papillary muscle].

The alpha-adrenoceptor agonist phenylephrine (5.0 x 10(-6) mol/L) was used to stimulate myocardial alpha-adrenoceptors of the guinea-pig ventricular papillary muscle, and changes of transmembrane action potential and contractile force of the muscle were observed. The alpha 1-adrenoceptor blocker prazosin (5.0 x 10(-7) mol/L) and the alpha 2-adrenoceptor blocker yohimbine (5.0 x 10(-7) mol/L) were used to determine which subtype of alpha-adrenoceptor is responsible for the effects. The beta-adrenoceptor blocker propranolol (1.0 x 10(-6) mol/L) was used throughout the experiment. The results show that the myocardial alpha 1-adrenoceptor stimulation (1) increases the contractile force of the guinea-pig ventricular papillary muscle, (2) prolongs the time to peak contractile force while the duration of relaxation is not altered, (3) prolongs the fast response action potential duration, and (4) increases the maximal rate of depolarization during the phase 0 of the slow response action potential. It is suggested that the electrophysiological and positive inotropic effects of myocardial alpha 1-adrenoceptor stimulation might be due to the activation of the slow inward current and an increase in Ca2+ influx.

Action Potentials↗
PubMed1995

Delayed papillary muscle rupture following mild chest trauma.

A case of delayed papillary muscle rupture is reported, which developed 24 hours following a mild chest trauma. Transthoracic echocardiography established the diagnosis; immediate mitral valve replacement was carried out. The postoperative course was uneventful.

Accidental Falls↗
PubMed1990

Inotropic and lusitropic effects of chlorpromazine on rat left ventricular papillary muscle.

The in vitro effects of chlorpromazine on rat cardiac papillary muscle were tested at 10(-6), 10(-5) and 10(-4) M. Mechanical parameters were determined from the contraction and relaxation phases under isotonic and isometric conditions in order to assess contraction, relaxation, contraction-relaxation coupling and load sensitivity of relaxation. The peak power output Emax was determined from the force-velocity relationship. At 10(-6) M, a slight positive inotropic effect was observed, probably related to modifications in cross-bridges kinetics. Negative inotropic effects were observed with 10(-5) and 10(-4) M chlorpromazine. At 10(-5) M, shortening of the isometric relaxation and decrease in R2 = (+dF.dt-1max)/(-dF.dt-1max) suggest that chlorpromazine also diminishes myofilament Ca++ sensitivity. Emax was increased at 10(-6) M (19 +/- 5%, P less than .05), but decreased at 10(-5) M (-28 +/- 10%, P less than .05) and 10(-4) M (-82 +/- 2%, P less than .05). Modifications in the force-velocity relationship at 10(-4) M indicated that lowering myocardial performance by chlorpromazine was associated with a low muscle efficiency from a thermoenergetic point of view. At all concentrations, chlorpromazine impaired the isotonic relaxation and load sensitivity of relaxation. At 10(-4) M, muscle contracture and slowed isometric relaxation were probably due to "calcium overload." These results showed that chlorpromazine finely modulates intrinsic cardiac energetics and mechanics by acting on the sarcoplasmic reticulum, myofilament Ca++ sensitivity and cross-bridges kinetics, according to the level of load and chlorpromazine concentration used.

Animals↗
PubMed2000

Effects of intermittent hypoxia on action potential and contraction in non-ischemic and ischemic rat papillary muscle.

Although it has been reported that intermittent hypoxia had the anti-arrhythmia effect, little is known about the effects on the action potential (AP) and contraction of papillary muscle, as well as the mechanism of anti-arrhythmia. The purpose of present study is to observe the effects of intermittent hypoxia on action potential and contraction of papillary muscle in rat left ventricle simultaneously using conventional intracellular microelectrode and contraction recording. The effects of intermittent hypoxia on AP and contraction during ischemic solution perfusion were also investigated. After exposed to intermittent hypoxia (six hours daily) for 42 days (IH42), duration (APD20) of 20%, 50% (APD50) and 90% (APD90) repolarization of AP prolonged significantly compared with animals in control (Con). Effective refractory period (ERP) in IH42 also prolonged significantly. Perfused with mimic ischemic solution, the changes of electric and mechanical activities in IH42 and in 28 days exposure to intermittent hypoxia (IH28) were much smaller than that in Con and IH14. The result of the study suggested that intermittent hypoxia prolonged the APD and ERP, offered the resistance against the ischemic damage on myocardium, which may be the electrophysiological basis of the anti-arrhythmia of intermittent hypoxia.

Action Potentials↗
PubMed1990

Electrophysiological effects of AFD-21 and AFD-19, new antiarrhythmic compounds on papillary muscles and single ventricular myocytes isolated from guinea-pig hearts.

1. The effects of AFD-21, a newly synthesized antiarrhythmic compound, and AFD-19, its active metabolite, on transmembrane action potentials were examined in right ventricular papillary muscles and single ventricular myocytes isolated from guinea-pig hearts. 2. In papillary muscles, AFD-21 10(-5) M caused a slight prolongation of action potential duration (APD), while AFD-19 above 10(-6) M shortened APD in a dose-dependent manner. 3. Both AFD-21 and AFD-19 above 10(-6) M caused a significant and dose-dependent decrease in the maximum upstroke velocity (Vmax) of the action potential without affecting the resting membrane potential. 4. In the presence of AFD-21 or AFD-19, trains of stimuli at rates greater than or equal to 0.2 Hz led to an exponential decline in Vmax. This use-dependent block was enhanced at higher stimulation frequencies. A time constant for the recovery of Vmax from the use-dependent block was 2.9 s for AFD-21 and 3.6s for AFD-19. 5. The curves relating membrane potential and Vmax were shifted by AFD-21 (10(-5) M), or AFD-19 (10(-5) M) to the direction of more negative potentials by 5.3 mV and 5.1 mV respectively. 6. In single ventricular myocytes treated with AFD-21 (10(-5) M) or AFD-19 (10(-5) M), Vmax of test action potentials preceded by conditioning clamp pulses to 0 mV was decreased progressively as the clamp pulse duration was prolonged. 7. These findings suggest that both AFD-21 and AFD-19 have use- and voltage-dependent inhibitory action on the sodium channel by binding to the channel during its inactivated state, and that the unbinding rate is comparable to that of Class I antiarrhythmic drugs with intermediate kinetics.

Action Potentials↗