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PubMed2003

Role of the Na+-H+ exchanger (NHE1) in heart muscle function during transient acidosis. A study in papillary muscles from rat and guinea pig hearts.

The sodium-hydrogen exchanger (NHE) helps the cell to recover from intracellular acidosis. In this study, we have investigated the effect of HOE 642 (a specific NHE1 blocker) on papillary muscles from rats and guinea pigs during transient acidosis and PKC activation by recording developed force (DF), action potential characteristics, and electrical conductance (stimulus-response interval). Two protocols were used, with or without HOE 642 (10(-5) mol/L): papillary muscle was exposed (i) for 15 min to a glucose-free, nonoxygenated HEPES buffer containing lactate (20 mmol/L) (pH 6.8) followed by 15 min recovery or (ii) to a PKC activator (phorbolmyristate acetate (PMA) (10(-9) mol/L)) for 30 min. The DF after acidification remained significantly decreased in the NHE-blocked papillary muscles. During recovery from acidosis, papillary muscles exposed to HOE 642 remained at a higher electrical resistance. The present study shows that post-acidotic continued depression of DF and change in tissue electrophysiological properties might occur as a result of blocking the NHE. During infarct development, the tissue-protecting effect of NHE blockade has been well documented. When acidosis or reduced contractile function is present, however, blocking NHE by HOE 642 might not improve the situation.

Acidosis↗
PubMed1986

Resection of scarred papillary muscles improves outcome after surgery for ventricular tachycardia.

Papillary muscle scarring is encountered frequently during operations for sustained ventricular tachycardia (VT). Indications for excision of the papillary muscle scar and mitral valve replacement (MVR) are controversial. The findings in 46 consecutive patients undergoing operative electrophysiologic map-directed endocardial resections for VT were reviewed. There was papillary muscle scarring in 15 patients (average age: 59 years; sex: 11 male, 4 female; average ejection fraction: 31 +/- 14%). Eleven patients had a VT with the site of origin on a scarred papillary muscle; four had another VT site of origin. Six patients underwent papillary muscle scar resection (5 with MVR); six underwent papillary muscle cryotherapy (-60 C X 2 min); and three had neither papillary muscle resection nor MVR. All six patients with papillary muscle resection +/- MVR are alive and free of arrhythmia after 14.3 +/- 7.6 months of follow-up. Five of six patients treated by papillary muscle cryotherapy alone manifested spontaneous (4 patients) or inducible (1 patient) VT during early postoperative evaluation. Two of the three patients with untreated papillary muscle scarring developed late complications requiring reoperation. One patient developed mitral regurgitation requiring MVR 5 months later. The other developed a previously undocumented VT 2 years after operation. Significant papillary muscle scarring visualized at the time of operation for arrhythmia is an indication for resection of the scar and the papillary muscle, even if this necessitates MVR. In this series, attempts to preserve the papillary muscle, by incomplete resection of the scar or by cryotherapy, resulted in a high failure rate owing to recurrent VT or mitral regurgitation.

Aged↗
PubMed1984

A Ca2+-dependent mechanism for the positive inotropic response to an increase in afterload in cat papillary muscle.

In cat papillary muscles, under control conditions (1.25 mmol/L Ca2+ bathing solution, 25 degrees C), increasing the afterload by switching from isotonic to isometric contraction elicited a positive inotropic response. Halving the bath [Ca2+] resulted in a percentagewise similar or greater positive inotropic response to increased afterload, while doubling the bath [Ca2+] reduced and caffeine abolished or reversed this response, indicating [Ca2+]i predictably influences it. Since it was markedly reduced by verapamil and unaffected by propranolol, the positive inotropic response to increased afterload was concluded to be largely due to increased Ca2+ influx, unrelated to catecholamine release, caused by increased mean muscle length over time owing to the changing from isotonic to isometric contraction. While at 25 degrees C, increasing the afterload caused a positive inotropic response at 12 to 48 stimulations/min, at 37 degrees C and at similar frequencies, a negative inotropic response occurred. This reversed to a positive inotropic response at 86 stimulations/min, well below the normal cat heart rate, suggesting an increased afterload would cause a positive inotropic response via this mechanism in vivo, as observed for years in intact mammalian hearts. Similarities between positive inotropic responses to increased afterload in isolated cardiac muscle, isolated hearts, and intact animals indicate all may be examples of the same phenomenon (Anrep effect).

Animals↗
PubMed1994

Dissimilar action of two cyclic adenosine-monophosphate analogues on the sodium current in intact rat papillary muscle.

In intact papillary muscles from rat we have found with the loose-patch-clamp technique an increase of the fast cardiac sodium current (INa+) by isoproterenol (ISO). In this study we have tested two membrane permeable analogues of the intracellular second messenger cyclic adenosine-monophosphate (cAMP) to investigate the intracellular pathway: 8-Br-cAMP (50 microM) and the newer developed Sp-5,6-Dichloro-1-beta-D-ribofuranosylbenzimidazole- 3',5'-cyclic-monophosphorothioate (5,6-DCl-cBiMPS, 20 microM). The availability of INa+ was determined with test pulses to +/- 0 mV every 3.5 seconds after 2.5-second conditioning between -130 mV and -50 mV and a holding potential at the resting potential of the cell under examination, and after wash-in of either compound. The peak currents were fit to a Boltzmann equation, and expressed by the maximal attainable current INa+,max, the mid-point potential V1/2, and a steepness parameter alpha. Values are given by mean +/- SEM. 8-Br-cAMP showed a significant shift of the availability curve in the hyperpolarized direction (V1/2 = -82 +/- 2 mV vs -86 +/- 2 mV, n = 5, P < 0.05) with only minor changes of INa+,max and alpha. In contrast, 5,6-DCl-cBiMPS had no significant effect on V1/2 but increased INa+,max by 8% +/- 2% versus control (n = 5, P < 0.05). In an intact muscle preparation we have found that 5,6-DCl-cBiMPS has a similar effect as that observed with the beta-adrenergic agonist ISO (100 nM), whereas 8-Br-cAMP exhibited a dissimilar action.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1995

The clinical utility of transesophageal echocardiography in ischemic papillary muscle rupture.

Ischemic papillary muscle rupture is a potentially lethal complication of myocardial infarction. Acute mitral regurgitation, shock with pulmonary edema, may ensue as its result. Transthoracic echocardiography is the initial noninvasive tool used to confirm the diagnosis. Transesophageal echocardiography has overcome some of the limitations of transthoracic imaging, permitting timely surgical management of these critically ill patients.

Aged↗
PubMed1992

External ATP antagonizes the effect of potassium channel openers in guinea-pig ventricular papillary muscle.

Right ventricular papillary muscles of the guinea-pig heart were electrically stimulated. Cromakalim 10-100 microM and Ro 31-6930 3 microM depressed the contractile force and shortened the duration of action potentials. Glibenclamide 0.3-3 microM, ATP 100 microM and alpha, beta-methylene ATP (alpha, beta-meATP) 30 microM antagonized these effects. Suramin 300 microM failed to reverse the alpha, beta-meATP-evoked antagonism of the action of cromakalim. It is concluded that both intra- and extracellular ATP may interfere with potassium channel openers and that extracellular ATP does not act via the known P2-purinoceptor subtypes.

Action Potentials↗
PubMed1994

Magnetic stimulation of ferret papillary muscle.

1. Ferret papillary muscles were magnetically stimulated by the discharge of a capacitor through an inductance. 2. An induced current density of 39 mA cm-2 averaged over 280 microseconds (= 11 microC cm-2) corresponded to threshold. 3. A short galvanic current pulse was found to have a comparable charge threshold. 4. The time-varying magnetic field or the magnetically induced electrical field did not result in excitation unless current was allowed to flow. 5. Threshold conditions could be reached by adding subthreshold magnetically induced current to subthreshold galvanic current. A suprathreshold galvanic current could be prevented from exciting by simultaneously applying induced current of opposite direction. 6. It is concluded that outward current through the membrane capacity is the stimulus, independent of the origin of the current.

Animals↗
PubMed1996

Transesophageal echocardiographic assessment of papillary muscle rupture.

BACKGROUND: In some patients with papillary muscle rupture, the ruptured head may not prolapse into the left atrium, which makes diagnosis by transthoracic or transesophageal echocardiography difficult. METHODS AND RESULTS: In an attempt to find additional or more definite diagnostic echocardiographic features, we analyzed intraoperative transesophageal echocardiograms of 21 consecutive patients with papillary muscle rupture (20 involved the left ventricle and 1 involved the right ventricle) confirmed at surgery. In 7 (35%) of 20 patients with left ventricular papillary muscle rupture, the ruptured head was not seen to prolapse into the left atrium. In these patients, examination of the left ventricle proved most useful. Abnormal, large-amplitude erratic motion (1 to 5 cm in 17 patients; 0.5 cm in 1 patient) of a large echo density in the left ventricle consistent with the ruptured head was noted in 18 (90%) of these 20 patients. This included all 7 patients with non-prolapse of the ruptured papillary muscle head into the left atrium. Less prominent erratic motion or flutter of the papillary muscle still attached to the left ventricular wall was also noted but was less sensitive in the diagnosis of papillary muscle rupture. The single patient with right ventricular papillary muscle rupture showed erratic motion as well as prolapse of the ruptured head into the right atrium. CONCLUSIONS: Transesophageal echocardiographic examination of the left ventricle is useful in the diagnosis of papillary muscle rupture, especially in those patients in whom the ruptured head does not prolapse into the left atrium. The left ventricle should be scrutinized thoroughly during transesophageal echocardiographic examination for erratic papillary muscle motion in all patients with suspected rupture.

Adult↗
PubMed2006

Pentoxifylline improves reoxygenation-induced contractile recovery through a nitric oxide-dependent mechanism in rat papillary muscles.

In this study, the protective effect of pentoxifylline against hypoxia-reoxygenation injury and the possible involvement of nitric oxide (NO)-mediated pathways in this protection were investigated in isolated rat papillary muscles. Papillary muscles were excised and isolated in Krebs-Henseleit solution aerated with 95% O2 and 5% CO2. Hypoxia was simulated by substituting O2 with argon. Three sets of experiments, testing 30, 60, and 90 min of hypoxia, were performed. The effects of different pentoxifylline concentrations on papillary muscle contractile parameters and responsiveness to isoproterenol were assessed. To investigate the role of NO, N(omega)-nitro-L-arginine methyl ester was added before pentoxifylline treatment. Pentoxifylline did not show any inotropic effect on papillary muscles. Hypoxia caused a profound depression of contractile parameters, which was not affected by pentoxifylline treatment. Reoxygenation resulted in significant partial recovery of contractile parameters after 30 and 60 but not 90 min of hypoxia. In experiments with 30 and 60 min of hypoxia, reoxygenation-induced contractile recovery and responsiveness to isoproterenol were improved by pentoxifylline in a concentration-dependent fashion. These functional improvements were completely blocked by N(omega)-nitro-L-arginine methyl ester pretreatment. No improvement was observed in 90-min hypoxia experiment. In conclusion, pentoxifylline improved contractile recovery during reoxygenation and postreoxygenation responsiveness to beta-adrenergic stimulation through the NO-dependent mechanism.

Adrenergic beta-Agonists↗
PubMed1985

Inotropic effect of different albumin solutions on isolated papillary muscle.

We used a papillary muscle assay to study the inotropic effect of albumin solution. Unlike specially prepared citrate-free solutions, commercial preparations produced a negative inotropic effect. This is because their high citrate concentrations bound much of the calcium, so that little ionized calcium was available for physiologic processes. Citrate-free albumin did not show any inotropic effect on isolated papillary muscle. The amount of albumin normally used for resuscitation should not have enough citrate to depress ionized plasma calcium. Our experiments showed no evidence for primary myocardial depressant action of a commercial albumin preparation.

Albumins↗
PubMed2005

Remarks on the morphology of the papillary muscles of the right ventricle.

In addition to the papillary muscles of right ventricle referred to in anatomical nomenclature, namely the anterior, posterior and septal, we have distinguished the "conal papillary muscle" and the "papillary muscle of the posterior angle of the right ventricle". The conal papillary muscle was described by Luschka in the 17(th) century as the most constant of the septal papillary muscles. We have distinguished the muscles of the posterior angle of the right ventricle as muscles which would not be clearly classified as either septal or posterior muscles. Moreover, the muscles of the posterior angle of the right ventricle are probably associated with the transfer of the papillary muscles from the septum to the posterior wall of the right ventricle during phylogenetic evolution. Some researchers have classified them with the septal papillary muscles, while others have assigned them to the posterior group. The morphology of the muscles was classified using earlier categories for the posterior papillary muscles only. We have adopted the concept of multi-apical and multi-segmental muscles.

Classification↗
PubMed1984

A mechanical model of mitral insufficiency using canine papillary muscle preparation.

A canine papillary muscle is loaded to mimic the load of the myocardium in the wall of the left ventricle with atrio-ventricular valvular insufficiency. This mechanical model which simulates the atrio-ventricular valvular regurgitation is based on two simple assumptions. The assumptions arranged for the papillary muscle experiment are as follows: 1) the force that the myocardium encounters during muscle shortening is proportional to the muscle shortening velocity due to regurgitation through a narrow regurgitant orifice; and 2) the myocardium exerts a constant force while the aortic valve is open. The muscle shortening except the isotonic phase is ascribed solely to regurgitation since the aortic valve is closed during these phases. In the combined antegrade/retrograde ejection phase, which is characterized by a constant muscle force, the shortening velocity due to regurgitation is constant because of the assumed functional relation between the muscle force and shortening velocity. The amount of shortening assigned to regurgitation in this phase is given by the product of the velocity at the beginning point of the isotonic phase and the duration of this phase. The present in-vitro studies offer an alternative explanation for decrease in the regurgitant fraction as total load was reduced at a constant preload. The regurgitant fraction decreased as preload was increased at a constant total load in the present study. The regurgitant fraction also decreased by either isoproterenol or CaCl2 administration via the coronary artery.

Animals↗
PubMed1976

Effects of derivatives of cyclic amp and cyclic gmp on contraction force of cat papillary muscles.

Right ventricular kitten papillary muscles were incubated with dibutyryl adenosine 3',5'-monophosphate (dbcAMP) at varying concentrations as low as 1 X 10(-4)M. A positive inotropic effect was observed with all concentrations of dbcAMP. Concomitant administration of 5 X 10(-4)M monobutyryl guanosine 3',5'-monophosphate (mbcGMP) and 1-2 X 10(-4)M dbcAMP prevented the inotropic response observed when dbcAMP was used alone. When higher doses of dbcAMP were used (5 X 10(-4) M, 10 X 10(-4) M), there was no significant difference in the inotropic response seen between control tissues and papillary muscles pretreated with mbcGMP.

Animals↗
PubMed1994

Enhancement of the positive inotropic effect mediated by alpha 1-adrenoceptors in pertussis toxin-treated rabbit papillary muscles.

1. In rabbit papillary muscles, pretreatment with pertussis toxin (PTX) significantly increased the positive inotropic response to isoprenaline and abolished the inhibitory action of carbachol on the isoprenaline response. 2. Phenylephrine in the presence of propranolol produced a positive inotropic effect and prolonged action potential duration through activation of alpha 1-adrenoceptors. Both of the effects of phenylephrine were significantly enhanced by PTX pretreatment. 3. Accumulation of [3H]inositol monophosphate (IP1) in papillary muscles prelabeled with myo-[3H]inositol was increased by phenylephrine in a concentration-dependent manner, which was antagonized by prazosin. Although PTX pretreatment significantly elevated the basal level of [3H]IP1 formation, the phenylephrine-induced increase in [3H]IP1 formation was unaffected. 4. It is concluded that the cardiac responses to alpha 1-adrenoceptor stimulation studied in these experiments are not transduced by a PTX sensitive G protein (Gi). However, the positive inotropic effect and prolongation of action potential duration mediated by alpha 1-adrenoceptor may be negatively regulated by Gi.

Action Potentials↗
PubMed1997

Alpha 1-adrenoceptor subtype involved in the positive and negative inotropic responses to phenylephrine in rat papillary muscle.

1. In rat papillary muscle, stimulation of alpha 1-adrenoceptors results in a biphasic inotropic response: a transient negative inotropic phase and a subsequent sustained positive inotropic phase. This study was designed to determine whether the positive and negative inotropic effects in this tissue are mediated by different alpha 1-adrenoceptor subtypes. 2. After treatment with the tumor-promoting compound, phorbol 12, 13-dibutyrate, phenylephrine (in the presence of propranolol) produced only a positive inotropic effect. The selective alpha 1A-adrenoceptor antagonist, WB4101, significantly inhibited the positive inotropic effect. In contrast, inactivation of alpha 1B-adrenoceptors with chloroethylclonidine (CEC) did not alter the positive effect. 3. In the presence of the Ca2+ channel antagonist, nifedipine, phenylephrine induced only a sustained negative inotropic effect. The negative inotropic effect was significantly attenuated by WB4101, but was not affected by CEC. 4. We conclude that both the positive and negative inotropic responses of rat papillary muscle to phenylephrine are mediated exclusively by the WB4101-sensitive but CEC-resistant alpha 1-adrenoceptor subtype. The alpha 1-adrenoceptor subtype with such a property may correspond to the alpha 1A-subtype.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed2004

Papillary muscle rupture following acute myocardial infarction.

OBJECTIVES: Papillary muscle rupture following acute myocardial infarction (AMI), which rarely occurs, leads to catastrophic outcomes. We reviewed 6 patients who were diagnosed as having papillary muscle rupture. SUBJECTS AND METHODS: Between February 1986 and September 2002, 6 consecutive patients underwent mitral valve replacement (MVR) for acute mitral regurgitation due to postinfarction papillary muscle rupture (4 men and 2 women, mean age 67 years). Preoperatively, all were in New York Heart Association (NYHA) class IV. All patients had intraaortic balloon pumping, and one needed additional percutaneous cardiopulmonary support. Operations were performed within 1 to 19 days (mean 6.8) after the onset of AMI, and within 24 hours after papillary muscle rupture. Complete ruptures were found in 5 of 6 patients. Four patients had posterior papillary rupture and 2 patients anterior. All patients underwent MVR to preserve the posterior mitral leaflet. Concomitant coronary artery bypass grafting was performed in 5 of 6 patients (mean 1.6 grafts per person) and pulmonary venous isolation for atrial fibrillation in one patient. RESULTS: The cardiopulmonary bypass time ranged from 178 to 325 minutes (mean 236), and the aortic cross clamp time from 123 to 196 minutes (mean 155). Two patients died of low cardiac output syndrome. Of 4 operative survivors, 3 patients were in NYHA class I and one in class II. The mean follow-up term was 21 months. One patient with the pulmonary venous isolation has been in sinus rhythm. All survivors have been doing well without any valve related complications. CONCLUSION: Six patients underwent MVR for the papillary muscle rupture following AMI and the perioperative mortality rate was 33%. All survivors have been well with no cardiac events. We propose that in papillary muscle rupture following AMI emergent surgery should be undertaken as soon as possible, and that concomitant surgery should be performed as thoroughly as possible.

Aged↗
PubMed2003

Successful surgical treatment of mitral regurgitation for complete rupture of the anterior papillary muscle after acute myocardial infarction.

Papillary muscle rupture complicating acute myocardial infarction leads to mitral regurgitation and is associated with significant mortality. We experienced a case involving massive mitral regurgitation caused by complete anterior papillary muscle rupture following acute lateral myocardial infarction. A 75-year-old woman developed heart failure shortly after her admission, and the diagnosis was confirmed by echocardiography and cardiac catheterization. Under intra-aortic balloon pumping, the patient underwent emergency mitral valve replacement and coronary revascularization. Her postoperative course was uneventful, and she was discharged on the 40th postoperative day. We believe that prompt surgical treatment should be performed even in stable patients with ischemic mitral regurgitation, given that deterioration may be sudden and unpredictable especially in cases involving complete papillary muscle rupture.

Aged↗
PubMed2005

The comparative investigation of morphology of papillary muscles of left ventricle in different species.

The papillary muscles of the heart are conical projections into the respective chamber of myocardium covered by endocardium. Functionally, the papillary muscles are important part of the respective valve complex. They prevent the cusps of a valve from being everted when the ventricle contracts. Our study was conducted on papillary muscles in left ventricle of 135 normal adult hearts (20 humans, 25 dogs, 60 sheep and 30 goats). The length (L), width (W), head number (HN), angle with ventricular wall (A degrees ), distance with annulus (AnD) and apex (ApD), and the shapes of the anterior and posterior papillary muscles were observed. The tendinous chords (CTN) attached to each papillary muscle were counted at their origin. The values of both anterior and posterior papillary muscles were not statistically significant (p > 0.05) in measurements of L, W, HN, A degrees and AnD of all species, but those of CTN and ApD were significant (p < 0.05) between human and animal hearts, while the difference was not significant (p > 0.05) between sheep and goat hearts. Knowledge of morphology of papillary muscles in different species will be of much use to clinical investigators in their studies.

Adult↗