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PubMed1986

The anaerobic heart: succinate formation and mechanical performance of cat papillary muscle.

Quiescent or paced, isometrically contracting right ventricular papillary muscles of cat heart were incubated under oxygenated or hypoxic (Po2 less than 10 Torr) conditions in order to investigate lactate and succinate formation. Both compounds were produced and released into the incubation medium during oxygen deficiency. Mechanical performance stimulated synthesis of both compounds under hypoxic as well as oxygenated conditions. Pacing led to the accumulation of large amounts of glutamine both under oxygenated and hypoxic conditions. Hypoxia resulted in a marked depletion of high-energy phosphates and concomitantly mechanical performance was impaired, i.e. developed tension fell rapidly and relaxation rate decreased. Supplying hypoxic, contracting muscles with aspartate (2 mM) resulted in maintenance of muscular function to some extent and led to augmented release of succinate and lactate. The data indicate that anaerobic succinate formation is correlated to the energy requiring processes of the myocardium. Maintenance of myocardial function by the supply of amino acids may be related to their conversion into succinate and to the stimulation of glycolysis.

Alanine↗

PubMed1975

[Effect of D20 on contractility and excitation contraction coupling in the rat papillary muscle].

D2O decreases the isometric contraction force of papillary muscles from the left ventricle of rats. This effect can be compensated only partially by increasing the calcium content in the perfusion solution. Differences in the effect of D2O under different calcium concentrations point also to an action site other than at the contractile proteins. The enlargement of the restitution of contraction 300 msec after the basic beat, the diminution of the postextrasystolic tiation and the disappearance of postextrasystolic depressions because of high calcium potencontent in the bathing solution make it more probable that the action site lies in cell compartments which may be involved into the supply of activator calcium. The increasing occurrence of aftercontractions alredy at slightly enhanced extracellular calcium is in good agreement with this fact.

Animals↗

PubMed1984

[A study on prolapse of the mitral valve in autopsy-proved papillary muscle dysfunction].

Echocardiographic studies have recently documented high incidence of mitral valve prolapse in cases with papillary muscle dysfunction (PMD). However, any pathologic evidence has not been yet described. To evaluate the incidence and the degree of morphologic prolapse of the mitral valve, we examined 76 cases of mitral regurgitation which were pathologically proved to have PMD among 3,000 consecutive autopsy cases over 60 years of age. The morphologic evidence of "mitral valve prolapse" was defined as overshooting of the mitral leaflet into the left atrium beyond the degree of normal hooding. Papillary muscle dysfunction was classified into three types; Type A due to old myocardial infarction, Type B due to acute myocardial infarction, and Type C induced by other factors such as cardiomyopathies. The following results were obtained: Morphologic "mitral valve prolapse" was found in 19 among the 76 cases (25%) of PMD, but marked "prolapse" was found in only one case. The incidence of morphologic "prolapse" did not show any difference among the types of PMD (cf. Fig. 1). The site of "prolapse" was mainly in the region of posteromedial commissure of the mitral valve. Echocardiographic study of 39 cases with PMD showed mitral valve prolapse in only two cases who belonged to the eight cases having morphologic "mitral valve prolapse". This study suggests that prolapse formation of the mitral valve secondary to PMD can be differentiated morphologically from those following primary myxomatous degeneration of the mitral leaflets as observed in cases with MVP.

Aged↗

PubMed2000

Coronary arteriovenous fistula with papillary muscle rupture.

We describe a patient who had a coronary arteriovenous fistula (CAVF) and whose mitral valve papillary muscle ruptured from chronic ischemia due to a coronary steal phenomenon. He was treated surgically with ligation of the CAVF (left circumflex to coronary sinus), coronary artery bypass grafting, and mitral valve replacement. This is the first report of papillary muscle rupture related to CAVF.

Arteriovenous Fistula↗

PubMed1980

[Effect of the pacing interval and extrasystole on amplitude and damping of diastolic oscillations in the rabbit papillary muscle].

Diastolic mechanical oscillations of right ventricular rabbit papillary muscles investigated at 15 degrees C in the perfusion chamber were analysed using a relaxation model with 6 parameters. From this analysis follows that the first diastolic oscillation amplitude plotted against the driving interval ("interval amplitude curve" of the first diastolic oscillation) shows tow maxima thus differing from the shape of the interval strength curve of the preceding driven contraction. It is concluded that the amplitude of diastolic oscillations is less determined by the Ca-amount released from the sarcoplasmic reticulum during the action potential than by the frequency of processes which effect the Ca release and the Ca-sequestration. The damping ratio varies within the range of tested driving intervals (0.36 to 10 s). After an extrasystole damping ratio and period of diastolic oscillation are diminished compared with the values after regularly driven contractions.

Animals↗

PubMed1986

Interaction of halothane and verapamil in isolated papillary muscle.

The combined depressant effects of verapamil and halothane on myocardial contractility were studied using isolated papillary muscle from the rabbit. Verapamil alone (0.5 microM) significantly decreased peak developed tension (PDT) by 15 +/- 2%, time to peak tension (TPT) by 10 +/- 1%, and maximum rate of increase of tension (+dT/dt) by 5 +/- 1%, but not maximum rate of decrease of tension (-dT/dt). Halothane alone (0.8%) significantly decreased PDT by 56 +/- 2%, TPT by 11 +/- 2%, +dT/dt by 53 +/- 2%, and -dT/dt by 56 +/- 2%. During the exposure period, the combination of verapamil and halothane together produced a simple additive effect (no significant interaction effect by two-way analysis of variance), with PDT decreased by 68 +/- 2%, TPT by 20 +/- 3%, +dT/dt by 62 +/- 2%, and -dT/dt by 65 +/- 2%. The reversibility of halothane-induced depression was also studied. Peak developed tension showed complete reversibility 30 min after discontinuing halothane. In the presence of verapamil, however, the reversibility of halothane-induced depression was not complete, and significant residual depression of PDT (19 +/- 3%) was observed. We conclude that the acute depressant effect of verapamil plus halothane in isolated papillary muscle is additive, but reversibility of halothane-induced depression may be impaired or prolonged in the presence of verapamil.

Animals↗

PubMedDate not supplied

Effects of vanadate ions on action potentials and tension development in papillary muscles and cultured heart muscle cells.

In isolated and electrically driven (1/s) papillary muscles peak tension and, to a slighter degree, resting tension increased through treatment with Na3VO4 in concentrations higher than 10(-4)M. The positive inotropic effect was found to be transient. With vanadate, the resting membrane potential became more negative and rate of rise and overshoot of the action potential increased. Positivity and duration of the action potential plateau was markedly lessened by vanadate. These vanadate-induced changes of the electrical activity were not transient and hardly recovered during washout. Single cardiac cells in culture showed increased beat frequency when treated with vanadate ions in excess of 10(-4)M. This increase was fast but transient and led to cessation of spontaneous discharge. Simultaneously with the initial increase of beat frequency, maximum of rate of rise, diastolic potential and overshoot of the action potential also increased. Cells inactivated by vanadate (5 X 10(-4)M and higher concentrations) were relaxed in diastole and could be excited by intracellular stimulation.

Action Potentials↗

PubMed1982

Electrical decoupling by Sr action potentials in guinea-pig papillary muscle.

The membrane constants of guinea-pig papillary muscle have been derived by cable analysis, utilizing a single sucrose gap and micro-electrode recordings. In Na-free 20 mmol/l Sr Tyrode, the longitudinal resistance (ri) was increased by 210% from the control value after the passage of ten action potentials (APs) and by 457% after twenty APs but this increase in ri was reversibly abolished by perfusing with Na-containing solutions. ri was not affected by stimulation in Na-containing 20 mmol/l Sr Tyrode. Concomitant with the increase in ri, the conduction velocity of Sr APs was decreased from the control level of 8.6 to 3.1 cm/s after about twenty evoked Sr APs. The twitches elicited in the Na-free Sr Tyrode were large but the relaxation time was comparatively slow (20-30s), whereas those elicited in the Na-containing Sr Tyrode had a large amplitude and relaxation occurred within a few seconds. It is suggested that the increase in ri is due to junctional decoupling, produced either directly, by an intracellular accumulation of Sr2+, or indirectly by an increase in intracellular H+.

Action Potentials↗

PubMed2001

Repair of anterior leaflet prolapse by papillary muscle repositioning: a new surgical option.

BACKGROUND: Although mitral valve repair is considered the gold standard for treating mitral regurgitation, anterior leaflet prolapse may still remain a challenging problem. This challenge is even greater for posterior commissural prolapse. We have used papillary muscle repositioning to treat anterior leaflet prolapse and suggest it as an alternative technique for all other methods previously described. METHODS: From 1989 to 1999 we performed 253 mitral valve repairs, among which 132 involved anterior leaflet prolapse. In this population there were two groups: group I (n = 92) treated with papillary muscle repositioning and group II (n = 40) treated with chordal shortening. There was no statistical difference between the two groups concerning age, functional class, and left ventricular function. Etiology was similar in both groups, a degenerative process being predominant. At echocardiography, regurgitation was graded 3.4/4 in both groups. There was no statistical difference concerning preoperative ejection fraction, end-systolic and end-diastolic left ventricular diameter. RESULTS: There were one in-hospital death in group I and two deaths in group II not related to mitral valve repair. Mean follow up is 36.4 +/- 29.2 months in group I and 70.5 +/- 9.5 months in group II. No patient was lost to follow-up. Mean regurgitation at follow-up was 0.75 +/- 0.67 in group I and 0.8 +/- 0.8 in group II (p = not significant). There was no statistical difference between the two groups concerning postoperative ejection fraction, end-systolic and end-diastolic left ventricular diameter. There was no late cardiac death in either group and there were no thromboembolic events. Actuarial survival rate is 98.9% and 96.3% in group I and 92.5% and 88.1% in group II at 3 and 8 years, respectively. CONCLUSIONS: Therefore, we conclude that papillary muscle repositioning is a safe technique that provides excellent results at mid-term follow-up and facilitates treatment of anterior leaflet prolapse.

Aged↗

PubMed1981

Intracellular chloride activity in rabbit papillary muscle: effect of ouabain.

Intracellular chloride activity (aiCl) and membrane potential (Vm) were measured in rabbit papillary muscle under in vitro conditions. The cellular chloride concentration (Cli) was estimated from measurements of total water content, extracellular space, and total chloride concentration. The effects of therapeutic (10(-8) M) and toxic (10(-6) M) concentrations of ouabain on these parameters were tested. The chloride-sensitive microelectrodes were of the liquid-ion exchanger type. Selectivity for HCO-3 was taken into account in the calculation of aiCl. In 11 control experiments made with two different protocols aiCl was determined in subendocardial and in deeper cells. The mean membrane potentials were -78.7 and -78.0 mV and the mean cytoplasmic chloride activities were 17.5 and 17.7 mM, respectively. The chloride equilibrium potentials were -43.5 and -43.2 mV. These results indicated that chloride is not passively distributed in rabbit papillary muscle. Ouabain (10(-8) M) did not change Vm or aiCl. At a toxic concentration of ouabain, Vm fell to -68.0 mV in superficial cells and to -67.8 mV in deeper cells, but aiCl remained unchanged . These results suggested that under in vitro conditions intracellular chloride is distributed within more than one cellular compartment.

Animals↗

PubMed1969

Membrane characteristics of the canine papillary muscle fiber.

Passive and active responses to intracellular and extracellular stimulation were studied in the canine papillary muscle. The electrotonic potential produced by extracellular polarization with the partition chamber method fitted the time course and the spatial decay expected from the cable theory (the time constant, 3.3 msec; the space constant, 1.2 mm). Contrariwise, spatial decay of the electrotonic potentials produced by intracellular polarization was very short and did not fit the decay curve expected for a simple cable, although only a small difference of time course in the electrotonic potentials produced by intracellular and extracellular polarizations was observed. A similar time course might result from the fact that when current flow results from intracellular polarization, the input resistance is less dependent on the membrane resistance. The foot of the propagated action potential rose exponentially with a time constant of 1.1 msec and a conduction velocity of 0.68 m/sec. The membrane capacity was calculated from the time constant of the foot potential and the conduction velocity to be 0.76 microF/cm(2). The responses of the papillary muscle membrane to intracellular stimulation differed from those to extracellular stimulation applied with the partition method in the following ways: higher threshold potential, shorter latency for the active response, linearity of the current-voltage relationship, and no reduction in the membrane resistance at the crest of the action potential during current flow.

Action Potentials↗

PubMed1985

The relative sensitization by acidosis of five calcium blockers in cat papillary muscles.

We have previously reported that the negative inotropic effects of both verapamil and nifedipine on cat papillary muscles are enhanced as pH is lowered from 7.4 to 6.8 and 6.0. These studies have now been extended to compare the relative sensitization by acidosis of verapamil, nifedipine, lidoflazine, perhexilene and diltiazem. Developed tension was recorded in cat papillary muscles and the calcium concentration was adjusted over the range 2 to 10 mM. At pH 7.4, addition of all five drugs moved the dose response curve to the right with pA2 values from 4.82 (lidoflazine) to 9.94 (nifedipine). At pH 6.0, there was eight-fold sensitization by acidosis for verapamil, but four, three, and two-fold sensitization for nifedipine, lidoflazine and perhexilene. Diltiazem, however, was not sensitized by acidosis. The differential effects of acidosis on the negative inotropic properties of the five drugs may reflect their ancillary properties opposite gating of the calcium channel, local anaesthesia, intracellular calcium movement or Na+/Ca2+ exchange, but also suggest that diltiazem may have the property of inhibiting the effects of low pH on cell membranes.

Acidosis↗

PubMed1980

[The influence of adrenaline on the effects of halothane and enflurane on the myocardium. Papillary muscle of the cat (author's transl)].

In this paper the influence of epinephrine on the isolated papillary muscle has been investigated with respect to the myocardial effects of enflurane and halothane. The contractile properties have been described under isotonic conditions by the parameters "muscle length change", "velocity of shortening and under isometric conditions by the parameters "peak tension" and "maximum rate of tension development". The studies led to the following results: 1. Halothane and enflurane cause a dose-dependent decrease of the contractile properties of the cat papillary muscle. Averaged for all parameters the mycocardial depressant effect of halothane is 2.6 times higher than that of enflurane, referring to equal concentrations. 2. Epinephrine has a positive inotropic effect which is most pronounced under isotonic mode of contraction for "velocity of shortening" and during isometric conditions for "maximum rate of tension development". 3. The positive inotropic effect of epinephrine is partially neutralized by halothane and enflurane. There is, however, evidence that the relative decrease of contractility due to halothane and enflurane is diminished by epinephrine. This finding shows that the myocardial effects of inhalation anaesthetics are overestimated in in-vitro-experiments (because of the lack of exogenous epinephrine) in contrast to experiments with intact animals. As this finding is referring to both halothane and enflurane, there is no specific difference to be found concerning the myocardial effects in comparative studies, including both in-vitro and in-vivo conditions.

Animals↗

PubMed1993

Effects of bupivacaine on contraction and membrane potential in isolated canine papillary muscles.

The effects of bupivacaine on myocardial contraction and membrane potential were examined in isolated canine right ventricular papillary muscles. Bupivacaine (10(-6) to 10(-4) mol/l) produced a dose-dependent and reversible decrease in the electrically induced contractile response of canine right ventricular papillary muscles. The inhibitory effects of bupivacaine on contraction were more pronounced at high stimulation frequencies (2 and 3 Hz) than at low frequency (< 1 Hz). The resting membrane potential was not affected by bupivacaine. The maximal upstroke velocity of the action potential was reduced by 10(-6) mol/l bupivacaine (74 +/- 28% of control), and these effects were also dose dependent. At 10(-4) mol/l, bupivacaine blocked fast action potentials in normal Tyrode's solution. Furthermore, bupivacaine (10(-4) and 10(-3) mol/l) decreased both slow action potential duration and associated contractions in high-K+ (26 mmol/l) Tyrode's solution in the presence of isoproterenol. Our results suggest that low concentrations of bupivacaine depress contraction mainly due to an Na+ channel block, whereas at higher concentration, this local anesthetic may block Ca2+ channels.

Action Potentials↗

PubMed1982

Effects of harmala alkaloids on transmembrane potentials of guinea-pig papillary muscles.

1 The significance of the presence of a methoxy group in the 7 position of the indole nucleus of harmala alkaloids in terms of their effects on the action potential of cardiac muscle was analysed. Guinea-pig papillary muscles were superfused with Tyrode solution at 30 degrees C and exposed to harmine or its analogue harmane, in which the methoxy group has been removed from the molecule. 2 Harmine 2 x 10(-5) M enhanced the amplitude of the action potential (AAP) of normal fibres and of slow responses elicited by noradrenaline in fibres depolarized by 21.6 mM K+-Tyrode. The effect of harmine on AAP occurred in the absence of any change in membrane resting potential or maximum velocity of the upstroke and it was abolished by propranolol. Harmane 2 x 10(-5) M did not have any effect on normal action potentials and slow responses. 3 Higher concentrations of the two analogues depressed both AAP and the maximum velocity of the upstroke of the action potential, without affecting the duration of the action potential. 4 It is concluded that: (a) removal of the methoxy group from harmine (1) abolishes the catechol-mediated stimulatory effect of a low concentration of the drug on the slow component of the upstroke of the action potential, and (2) does not modify the depressant effect of a high concentration of the drug. (b) The two analogues, harmine and harmane, do not affect the duration of the action potential of ventricular muscle.

Action Potentials↗

PubMed1986

[Mitral insufficiency, excluding ruptured papillary muscles, in the acute phase of posterior primary infarction. Anatomical study].

Mitral regurgitation (MR) was demonstrated by water testing valve closure in 23 out 46 cases of patients dying in the 8 days following primary posterior wall infarction due to occlusion of the right coronary or left circumflex arteries (normal valves and chordae; no chronic fibrosis of the papillary muscle). MR was less common with right coronary artery occlusion (14 out of 32; 44%) than with left circumflex occlusion (9 out of 14; 64%). Two anatomical conditions seem to be necessary (all cases but one) for MR to occur: ischaemic necrosis of all or nearly all of the posterior papillary muscle and its base of implantation on the posterior wall. These valvular leaks are usually mild (papillary muscle rupture was excluded) and do not seem to play a major role in the haemodynamic deterioration of these patients, the majority of whom die of irreducible cardiac failure caused by extensive myocardial destruction. The mechanism of the majority of these MR was systolic eversion of the posterior part of the posterior leaflet in the left atrium (6 cases) of the posterior juxtacommissural part of both leaflets (13 cases), of the posterior part of the anterior leaflet (3 cases). Ischaemic destruction of the posterior papillary muscular system and its base of mural implantation (anatomical criteria that we retained) correlated with the occluded artery.

Aged↗

PubMedDate not supplied

Effects of 17 beta-estradiol on early afterdepolarizations and L-type Ca2+ currents induced by endothelin-1 in guinea pig papillary muscles and ventricular myocytes.

By use of standard microelectrodes and whole cell patch clamp, the effects of 17 beta-estradiol on early afterdepolarizations (EADs) and increase of L-type Ca2+ currents (L-Ica) induced by endothelin-1 (ET-1) were studied in guinea pig ventricular papillary muscles and myocytes. The results indicated that superfusion with ET-1 for 30 min resulted in a marked prolongation of the action potential duration (APD) and caused stable EADs leading to triggered activity occurring at the plateau of the action potentials in isolated guinea pig ventricular papillary muscles. With the addition of 17 beta-estradiol (30 mumol/l), APD was shortened and EADs were decreased. In the patch clamp study, ET-1 induced an increase of mean peak L-Ica from 534.46 +/- 46.23 to 1003.15 +/- 39.12 (pA) with the peak voltage-current curve shifting to the left. When 17 beta-estradiol (30 mumol/l) was added, the L-Ica was decreased by up to 33.32% (p < 0.01) with the peak voltage-current curve shifting to the right. In contrast to the steady-state inactivation curve, ET-1 shifted the steady-state activation curve in the depolarization direction. However, with the addition of 17 beta-estradiol, the deviation of the steady-state activation and inactivation curves caused by ET-1 was suppressed. In conclusion, 17 beta-estradiol appears to attenuate the prolongation of APD and reduce EADs induced by ET-1 in guinea pig papillary muscles by its inhibitory effect on L-Ica.

Action Potentials↗

PubMed2003

Acute mitral regurgitation due to total rupture in the anterior papillary muscle after acute myocardial infarction successfully treated by emergency surgery.

A 68-year-old female was admitted for sudden onset of chest pain. She received a successful percutaneus coronary intervension for total occlusion in the diagonal artery, but continued to develop progressive heart failure. A chest X-ray showed right pulmonary edema without cardiomegaly, and an echocardiogram revealed massive mitral regurgitation with prolapse in the anterior mitral leaflet due to a rupture in the papillary muscle. An emergency operation was conducted using routine cardiopulmonary bypass. There was complete rupture in the anterior papillary muscle. Mitral valve replacement with posterior mitral leaflet preservation was performed using a size 25 mm Carbomedics prosthetic valve. The postoperative course was uneventful, and she was discharged on postoperative day 29 in New York Heart Association class I. Postoperative pathological findings showed necrosis in the papillary muscle with inflammatory changes. Early diagnosis, prompt medical stabilization, and aggressive surgical intervention are essential to save such a group of patient.

Acute Disease↗