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PubMed2001

Cleft posterior mitral valve leaflet associated with counterclockwise papillary muscle malrotation.

Isolated clefting of the posterior mitral valve leaflet is an uncommon congenital malformation. We report a case of cleft posterior mitral valve leaflet with counterclockwise papillary muscle malrotation. Similar abnormalities in papillary muscle position have been described in association with atrioventricular septal defect but have not been previously reported accompanying isolated clefting of the posterior mitral valve leaflet.

Aged↗
PubMed1999

Tight coupling between the rate of rise of Ca2+ transient and peak twitch contraction in guinea-pig papillary muscle.

We evaluated the relationship between cytoplasmic Ca2+ concentration ([Ca2+]i) and force in guinea-pig papillary muscles loaded with a fluorescent Ca2+ indicator, fura-PE3. In the absence of ryanodine, [Ca2+]i transient and force were altered by changing extracellular Ca2+ concentration and stimulation frequency, and also by adding methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyri dine-5-carboxylate (Bay K 8644) or ouabain. Under these conditions, the peak force correlated linearly with the maximal rate of rise of [Ca2+]i (gamma = 0.948) more than the peak [Ca2+]i transient (gamma = 0.737). Ryanodine inhibited the increase in the maximal rate of rise of [Ca2+]i resulting in abolishment of the correlation between force and the maximal rate of rise of [Ca2+]i. These results suggest that the maximal rate of rise of [Ca2+]i reflects Ca2+ release from the sarcoplasmic reticulum, and this fraction of [Ca2+]i is crucial for determining the amplitude of twitch contractions when the sarcoplasmic reticulum is intact in guinea-pig papillary muscle.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Traumatic papillary muscle dysfunction: attempted mitral-valve repair and eventual prosthetic replacement.

A previously healthy young man sustained a deceleration chest injury. Severe mitral regurgitation was confirmed by Doppler and cardiac catheterisation. The mitral valve and subvalvular apparatus appeared normal at the subsequent surgery. Papillary muscle dysfunction was considered to be the principal cause of the regurgitation. Mitral-valve repair failed to preserve the competence of the valve, leading to successful mitral-valve replacement. Histology of the papillary muscle showed necrosis, confirming the original diagnosis. Post-traumatic papillary muscle dysfunction is concluded to be one of the cause of severe mitral regurgitation. Appropriate treatment is valve replacement rather than attempting conservative management.

Adult↗
PubMed2000

Positive inotropic effects of adrenomedullin on rat papillary muscle.

Adrenomedullin is a peptide recently isolated from pheochromocytoma that has vasorelaxant and long-lasting hypotensive activities. Plasma levels of adrenomedullin are elevated in patients with congestive heart failure, but the effects of adrenomedullin on the cardiac function are unclear. We, thus, investigated the effects of adrenomedullin on the contraction of rat papillary muscles. We measured the isometric tension and cAMP contents of isolated rat papillary muscles. Adrenomedullin exhibited concentration-dependent inotropic effects. Adrenomedullin also significantly increased intracellular contents of cAMP. Addition of the calcitonin gene-related peptide (CGRP) receptor antagonist inhibited both contractile force and cAMP generation of papillary muscles stimulated by adrenomedullin. The adrenomedullin-induced inotropic effect was further increased in the presence of the phosphodiesterase inhibitor, 3-isobutyl-1-methyl-xanthine (IBMX), while the effect was significantly suppressed by KT5720 and Rp-8-bromoadenosine-3',5'-cyclic monophosphorothioate (Rp-8-Br-cAMPS), protein kinase A inhibitors. These results indicate that adrenomedullin has positive inotropic effects on the heart, at least partially through a cAMP-dependent pathway.

Adrenomedullin↗
PubMed1999

Long term results of mitral valve repair: posterior papillary muscle repositioning versus chordal shortening.

OBJECTIVE: Mitral valve repair is considered as the gold standard to treat mitral regurgitation. However anterior leaflet prolapse in the posterior paramedial and paracommissural area remains a challenging problem. Indeed several elongated chordae may arise from a single posterior papillary muscle head which does not allow safe separate chordal shortening (CS). We therefore suggest use of papillary muscle repositioning in such cases. METHODS: In a cohort of 180 mitral valve repair performed between 1989 and May 1998, we have retrospectively studied 100 consecutive patients who underwent anterior leaflet repair in the posterior paramedial and paracommissural area. Group I (n = 60) had posterior papillary muscle repositioning (PPMR) and group II (n = 40) had CS. There was no statistical difference between the two groups concerning age, functional class and left ventricular function. Etiology was similar in both groups, degenerative process being predominant. At echocardiogram, 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 no in-hospital deaths in group I and two deaths in group II not related to mitral valve repair. Mean follow up is 26.4 +/- 24.2 months in group I and 46.1 +/- 28.8 months in group II. No patient was lost to follow up. Severe mitral regurgitation was not observed. Mean regurgitation at follow up was 0.8 +/- 0.7 in group I and 0.8 +/- 0.8 in group II (P = n.s.); 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 100% and 94.4% in group I and 92% and 84.4% in group II at 2 and 6 years, respectively. CONCLUSION: This experience shows that PPMR provides as good longterm results as CS to repair anterior leaflet prolapse in posterior paramedial and paracommissural area with lesser morbidity and mortality.

Adult↗
PubMed1994

Electrophysiologic effects of total flavones of Hippophae rhamnoides L on guinea pig papillary muscles and cultured rat myocardial cells.

The effects of total flavones of Hippophae rhamnoides L (TFH) were evaluated using conventional microelectrode technic. After administration of TFH 100-200 mg.L-1, the action potential duration of 50% repolarization (APD50) was shortened both in cultured rat myocardial cells and in guinea pig papillary muscles. The slope of phase 4 of depolarization (SP4) in cultured rat myocardial cells was decreased and the contractile force (CF) in guinea pig papillary muscles was weakened. Arrhythmias evoked by strophantin G in guinea pig papillary muscles were suppressed by TFH 100 mg.L-1. These findings suggested that the influence of TFH on myocardial cells may be resulted mainly from its inhibition of Ca2+ influx and its interference with intracellular Ca2+ reservoir.

Action Potentials↗
PubMed1977

Nonuniform contraction in the isolated cat papillary muscle.

Microspheres infused into the coronary microcirculation were used as markers to define segments within isolated cat papillary muscles. Video recording and analysis provided measurements of the variations of segment lengths as the muscles contracted at lengths of 76-100% Lmax. In all muscles, segments in the center region were found to shorten during muscle isometric contraction while those in the end regions lengthened. Central shortening was typically 10-15%. In the passive state, segment lengths varied directly with muscle length over a broad range characterized by low force. Segments in the center region, however, displayed an abrupt transition to high stiffness at a certain length while end regions continued to stretch. Force-length relationships obtained for the presumably healthy center segment are significantly different from those obtained for the whole muscle. These results suggest that there may be major difficulties with the interpretation of mechanical measurements on papillary muscles unless contractile inhomogeneity is eliminated or taken into account.

Animals↗
PubMed1981

Intracellular Cl activity, Cl binding, and 36Cl efflux in rabbit papillary muscle.

Chloride liquid ion-exchange microelectrodes were used to measure intracellular chloride activity (aCl)i or rabbit papillary muscle in vitro. In HCO3- -- CO2 buffered Ringer (aCl)i was 15.2 +/- 0.6 mM (n = 40) at pH 7.3 and 15.4 +/- 0.3 mM (n = 29) at pH 6.8. In HEPES-buffered Ringer (aCl)i was 24.1 +/- 0.6 mM (n = 21) at pH 7.3 and 20.0 +/- 0.3 mM (n = 17) at pH 6.9. If Cl was distributed passively across the membrane (aCl)i should be about 3 mM. From total muscle Cl analysis and [14C]sorbitol extracellular space measurements we calculate an apparent intracellular Cl concentration of 71 mM. As this estimate is three times larger than the measured free Cl in the cytoplasm we conclude that a significant fraction of muscle Cl must be bound or compartmentalized. Analysis of 36Cl efflux from the papillary muscle indicates the presence of two compartments. The compartment with the slower efflux rate (2.0 X 10(-2) min-1) contains about 25% of the intracellular Cl, which compares with the estimation (21%) of the free intracellular CL fraction obtained from the Cl microelectrode measurements. Our data permit us to conclude that about 37% of the muscle Cl is bound and that it is probably located extracellularly.

Animals↗
PubMed1988

Negative inotropic and arrhythmic effects of high doses of ciguatoxin on guinea-pig atria and papillary muscles.

Ciguatoxin, the toxin present in fish responsible for ciguatera, at doses equal or above the maximum positive inotropic dose in atria (greater than 0.15 mouse units/ml) induced arrhythmias in atria and papillary muscles stimulated at 1 Hz and dose-dependent negative inotropy in atria. Negative inotropy was enhanced by ouabain or by an increase in stimulation to 3 Hz, little affected by procaine or increasing Ringer [Ca2+] and reversed by lidocaine and tetrodotoxin (TTX). Ciguatoxin caused negative inotropy associated with cell depolarisation in 1.2 mM Ca2+-Ringer and additionally caused signs of Ca overload in 3.2 mM Ca2+-Ringer. Ciguatoxin induced transient after-contractions and contracture in atria which were common in 3.2 mM but not 1.2 mM Ca2+-Ringer and which were enhanced by ouabain. TTX and lidocaine abolished after-contractions and contracture while procaine was less effective. Extrasystoles consisting of short bursts of 1-2 extra contractions per sec were seen in atria and papillary muscles within 45 min of ciguatoxin being added. The effect was observed in 3.2 mM but seldom in 1.2 mM Ca2+-Ringer and was absent when low doses of propranolol or TTX were added prior to ciguatoxin. Flutter was observed in a few papillary muscles after ciguatoxin. These results suggest that the toxic effects of ciguatoxin stem from its direct action of opening myocardial Na+ channels. Extrasystoles appeared to result mainly from its effect on neural Na+ channels causing an increased release of noradrenaline from the nerves associated with the myocardium.

Animals↗
PubMed1988

Electromechanical effects of bPTH-(1-34) on rabbit sinus node cells and guinea pig papillary muscles.

The effects of bPTH-(1-34), a synthetic preparation of bovine parathyroid hormone containing the first 34 amino acids, on electromechanical activity of isolated rabbit sinus node cells and guinea pig papillary muscles were examined by microelectrode techniques. In sinus node cells, bPTH-(1-34) (10(-7) M) decreased the cycle length of spontaneous firing (SPCL) accompanied by an increase in the maximum upstroke velocity at phase 0 (dV/dtmax) without affecting the amplitude of the action potential (APA) or the maximum diastolic potential (MDP). All the effects of bPTH-(1-34) on sinus node cells were abolished by verapamil (5 X 10(-7) M), but not by pindolol (2 X 10(-7) M). In constantly driven guinea pig papillary muscles, bPTH-(1-34) caused a positive inotropic effect (+31%). The parameters of the action potential were not significantly affected. This inotropic effect of bPTH-(1-34) was inhibited by pretreatment with verapamil or a low calcium medium (0.12 mM), but was not affected by pindolol. In contrast, ryanodine (2 X 10(-6) M), an inhibitor of internal Ca2+ release, which decreased the contraction with a prolongation of the action potential duration augmented the inotropic effect of bPTH-(1-34). In papillary muscles depolarized by 26 mM [K+]O, bPTH-(1-34) enhanced the slow action potential. In voltage clamp experiments using a single sucrose-gap method, bPTH-(1-34) caused an increase in the peak amplitude of the slow inward current, while it did not affect the outward current.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1997

Effects of melatonin in isolated rat papillary muscle.

Melatonin (N-acetyl-5-methoxytryptamine), the principal hormone of the vertebral pineal gland, elicits several neurobiological effects. However, the effects of melatonin on cardiac muscle are still unknown. The first goal of the study was to investigate the role of melatonin on myocardial contractility in isolated rat papillary muscle using dose-response curves to melatonin, to isoproterenol and calcium either in the presence or in the absence of melatonin (0.3 nM). Response curves to isoproterenol were additionally performed in the presence of melatonin plus the specific receptor antagonist N-acetyltryptamine (10 microM); the adenylate-cyclase stimulator forskolin (10 microM) was also used. Melatonin has no direct inotropic effect in isolated rat papillary muscle but counteracts isoproterenol but not [Ca2+] effects. In fact, the EC50 for isoproterenol was significantly higher in the presence than in the absence of melatonin (p < 0.001). This anti-adrenergic action occurs through an interaction to a specific cardiac receptor. Forskolin-stimulated adenylate cyclase induced an increase of contractile force (+118 +/- 25%) which was reduced in the presence of melatonin (+26 +/- 10%; p < 0.01). In conclusion, we found that melatonin possess anti-adrenergic effect in isolated rat papillary muscle. This phenomenon was abolished in the presence of its receptor antagonist N-acetyl-tryptamine demonstrating that melatonin operates through a specific cardiac receptor. The reduction of contractility increase, induced by forskolin-stimulated adenylate cyclase, shows that melatonin may act through a reduction of cyclic AMP accumulation.

Adenylyl Cyclases↗
PubMed1993

[Early papillary muscle rupture in myocardial infarction, diagnosis with transesophageal echography].

We describe the case of posterior papillary muscle (PPM) rupture with severe mitral regurgitation at the very beginning of an inferior myocardial infarction (MI) in a 79-year-old woman. The diagnosis was made by transesophageal echocardiography (TEE) and confirmed at autopsy. This case confirms the value of TEE in diagnosing PPM rupture and the association of PPM rupture with small posterior myocardial infarction. Moreover the case presents some unusual aspects: the rupture occurred very early; at transthoracic approach, a systolic convergence flow zone was the only sign of mitral regurgitation by color flow mapping; at TEE flail mitral leaflets were absent; in systole, the trunked papillary muscle did not prolapse into the left atrial cavity, but crushed into the atrial side of posterior mitral leaflet, remaining at the atrioventricular level; at autopsy, there was a split PPM with a completely ruptured medial branch. On the atrial side of the posterior mitral leaflet there was an ecchimothic zone, due to the crushing of the PPM.

Aged↗
PubMed1992

Cyclic GMP inhibits the inotropic response to alpha 1-adrenoceptors in the papillary muscle of the ferret.

The physiological role of cyclic GMP in the heart remains controversial. In the present study we investigated the interaction between a number of agents known to increase the level of cyclic GMP in the myocardium and alpha 1-adrenergic stimulation in isolated preparations of cardiac papillary muscle in the ferret. Inotropic responses to the cumulative addition of phenylephrine were measured in papillary muscles of the ferret in the absence and presence of 1 microM sodium nitroprusside, 1 microM atrial natriuretic peptide, 0.1 microM substance P (which stimulates the release of nitric oxide from endocardial endothelium) or 1 microM 8-bromo-cyclic GMP. In parallel experiments using similar preparations, alpha 1-induced hydrolysis of phosphatidylinositol was assessed by measuring changes in the levels of inositol 1,4,5-trisphosphate in response to 10 microM phenylephrine in the absence and presence of the same agents that increase the level of cyclic GMP. Phenylephrine (0.001-10 microM) induced a concentration-dependent positive inotropic effect that was significantly inhibited by each of the agents that increase cyclic GMP. Phenylephrine (10 microM) induced an approximately three-fold rise in the level of inositol trisphosphate in the myocardium, which was likewise significantly inhibited by each of the agents that increase cyclic GMP. These data show that agents that increase the level of cyclic GMP in the myocardium inhibit both the positive inotropic and phosphatidylinositol response to alpha 1-stimulation in isolated preparations of papillary muscle in the ferret.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗