SEARCH · PubMed Health

Results for “Papillary Muscles”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources

PubMed1980

Effect of acetylcholine on membrane currents in guinea-pig papillary muscle.

1. The effect of acetylcholine (ACh) on the membrane current components in guinea-pig papillary muscle was studied by the single sucrose gap voltage clamp method. 2. The slow inward current (is) elicited by various depolarizations from the holding potential of -40 mV was evidently diminished by ACh greater than 5 x 10(-7) M. The amplitude of is, estimated as the difference between the peak of is and the current at 150 msec, was reduced to 56.8 +/- 12.9% (mean +/- S.D., n = 34) by 2 x 10(-8) M-ACh when estimated at the membrane potential where the amplitude was maximal. 3. is was suppressed almost completely by 2 mM-Co2+, is obtained by subtracting the current remaining in 2 mM-Co2+ was also diminished to the same extent by 2 x 10(-6) M-Ach with little change in its time course; the degree of decrease was not dependent on the membrane potential. 4. The time-dependent outward current during the depolarizing pulse was also diminished by 2 x 10(-6) M-Ach. Correspondingly, the positive tail current obtained when the membrane was repolarized to the holding potential of -40 mV after various 1 sec depolarizations was reduced in a proportionate manner to 68.6 +/- 7.3% (n = 10). 5. The time-independent inward rectifying outward current was not affected by 2 x 10(-6) M-Ach. 6. Atropine (10(-6) M) restored is and the time-dependent outward current which had been previously depressed by 2 x 10(-6) M-ACh. 7. ACh may decrease tension development by depressing is, thereby preserving the duration of the action potential with relatively little change, since, different from atrial muscle, ACh does not increase the outward current in mammalian ventricular muscle.

Acetylcholine↗

PubMed1980

Rupture of a papillary muscle of the tricuspid valve in primary pulmonary hypertension.

Rupture of a papillary muscle of the tricuspid valve is a rare occurrence, and nontraumatic rupture is still rarer. We describe a 26-year-old male with primary pulmonary hypertension presenting with severe dyspnea and paroxysmal nocturnal dyspnea following spontaneous rupture of the septal papillary muscle of the tricuspid valve. The clinical diagnosis was confirmed at autopsy.

Adult↗

PubMed1975

Influence of potassium ions and osmolality on the resting membrane potential of rabbit ventricular papillary muscle with estimation of the activity and the activity coefficient of internal potassium.

Resting membrane potentials of rabbit right ventricular papillary muscles were measured in modified Tyrode's solutions that were isotonic (1.0 X T), hypertonic (1.58 X T), or hypotonic (0.76 X T) at eight different concentrations of external potassium, [K]o, ranging from 0.78 to 100 mM. The amount of hyperpolarization produced by exposure to the hypertonic solutions was relatively constant with an average of 4.6 mv at all levels of [K]o except 0.78 and 1.56 mM. This potential change is much less than the 10.6 mv which would be predicted if the papillary muscles behaved as nearly perfect osmometers and the activity coefficient of intracellular potassium (K) remained constant. The amount of depolarization produced by exposure to the 0.76 X T hypotonic solutions averaged 6.8 mv at all levels of [K]o except 0.78 mM; this value is close to the predicted value of 6.9 mv. Variations in the activity and the activity coefficient of intracellular K were introduced to explain these discrepancies. We estimated that the activity of intracellular K in 1.58 X T hypertonic solution was increased 15-23% compared with that in isotonic solution. This change is much less than the 58% that would be predicted if the papillary muscle behaved as a nearly perfect osmometer. We also estimated that the activity of intracellular K in 0.76 X T hypotonic solution fell 22-26%, which is very close to the predicted value of 24%. The activity coefficient of intracellular K appeared to fall in 1.58 X T hypertonic solution to about 0.76 of its value in isotonic solution. This decline in the estimated activity coefficient of intracellular K could not be attributed to an increase in Coulombic attractive and repulsive forces as predicted by the Debye-Hückel equation for a univalent electrolyte.

Animals↗

PubMed1997

The effect of applied mechanical vibration on two different phases of rat papillary muscle relaxation.

Applying external mechanical vibration during the relaxation phase of rat papillary muscle decreases the duration of the first part of the relaxation phase. To elucidate the basic mechanism responsible for this shortening of the relaxation period, we applied a controlled vibration to isolated twitching rat papillary muscles during various phases in the relaxation of a twitch. The first part of the relaxation phase was accelerated when length perturbations were applied in the first part of the relaxation of a twitch, dependent on both amplitude and frequency of the perturbation. When vibrations were applied in the first half of the relaxation, the second phase of relaxation was slightly slower (about 20%), but when no vibrations were applied in the first phase, relaxation could be accelerated by applying vibration in the latter half of the relaxation phase. Thus, in the latter half of relaxation, the acceleration of relaxation depended upon perturbation events earlier during that twitch. This study indicates that vibration-induced acceleration of relaxation is due (at least in part) to an apparent increase in detachment rate of attached cross-bridges from the thin filament without substantial reattachment.

Animals↗

PubMed1993

Diagnosis of papillary muscle rupture after acute myocardial infarction by transthoracic and transesophageal echocardiography.

The sensitivity of transthoracic echocardiography to visualize the structural abnormality of papillary muscle rupture (PMR) after acute myocardial infarction can be anticipated to average about 50%; therefore, we evaluated five patients exhibiting the condition with both transthoracic and transesophageal echocardiography. The use of the two imaging techniques resulted in the fact that no instance of PMR was missed. Using transthoracic echocardiography in two patients and transesophageal echocardiography in four, the ruptured papillary muscle was visualized directly. Mitral insufficiency as an indirect sign was observed in all patients. In one patient the papillary muscle rupture developed in a mitral valve previously affected by endocarditis. All patients underwent mitral valve replacement and coronary artery bypass grafting. The diagnosis was confirmed at surgery in all patients. Four patients died in hospital, the fifth 5 months later. We recommended that transesophageal echocardiography be performed in patients with suspected PMR if transthoracic echocardiography does not provide an unequivocal diagnosis.

Aged↗

PubMed1988

Coiled perimysial fibers of papillary muscle in rat heart: morphology, distribution, and changes in configuration.

The morphology, distribution, and configuration of coiled perimysial fibers of rat heart papillary muscle were studied. Methods included bright-field light microscopy of silver-stained sections, scanning and transmission electron microscopy, and differential interference contrast light microscopy of unfixed and unstained specimens. Coiled fibers, elliptical in cross section, are arranged in a branched network that diverges from the muscle-tendon junction and is continuous throughout the length of the muscle and into the ventricle wall. Most fibers range in diameter from less than 1 micron to 10 micron and are parallel with the long axis of the muscle, although branching is common and oblique orientations are seen. Several myocytes are associated with each coiled perimysial fiber. Constituent fibrils (diameter, 40-50 nm) occur in bundles twisted within the fiber. Small satellite elastic fibers are parallel to the collagen fiber axes. Stereo analysis of the coiled perimysial fibers reveals helical configurations, as opposed to planar waviness, that become less convoluted or even straighten as the resting muscle is stretched. Calculations based on cross-sectional areas of fibers, changes in fiber configurations, and tensile moduli reported for collagen fibers of other tissues show that the potential tensile strength of the network of coiled perimysial fibers is sufficient to contribute significantly to the mechanical properties of papillary muscle. Detailed evaluations of possible roles of the coiled perimysial collagen fiber system as a function of passive stretch and contraction in ventricular wall, as well as in papillary muscle, warrant further study.

Animals↗

PubMed1994

Gene expression of atrial natriuretic peptide in rat papillary muscle. Rapid induction by mechanical loading.

The effect of mechanical stretch on protein synthesis and the expression of the gene for atrial natriuretic peptide (ANP) was examined in electrically paced, isolated papillary muscles from rat heart. Incorporation of [3H]phenylalanine into protein increased only in stretched but not in unloaded muscles. Five hours of stretching increased ANP mRNA levels more than threefold as compared to freshly excised papillary muscles. A drastic fall in ANP mRNA levels was observed in unloaded muscles over this time. These data indicate that papillary muscles similar to other ventricular tissue are capable of activating ANP gene expression in response to increased load. The effect occurs in vitro and does not depend on circulating or nervous factors. The unexpected rapid induction of ANP gene expression in such a particular structure of the heart raises the possibility of local actions of ventricular ANP.

Animals↗

PubMed1988

Electrophysiological studies on the effects of mianserin, a tetracyclic antidepressant agent, on isolated guinea-pig papillary muscle.

We studied the effects of mianserin on the action potentials of papillary muscle from the guinea-pig. Mianserin (above 10 microM) reduced the maximum rate of the rise (Vmax) of the action potential, and shifted the Vmax-Em relationship to more negative potentials. The compound also depressed the slow action potentials of K+-depolarized papillary muscles. It is concluded that relatively high concentrations of mianserin had an inhibitory action on the electrophysiological properties of both the fast- and slow-response fibers of the heart.

Action Potentials↗

PubMed1991

Anomalous insertion of papillary muscle directly into anterior mitral leaflet in hypertrophic cardiomyopathy. Significance in producing left ventricular outflow obstruction.

BACKGROUND: Obstruction to left ventricular outflow in hypertrophic cardiomyopathy (HCM) is usually due to systolic anterior motion of the mitral valve. Occurrence of structural mitral valve abnormalities in HCM and their significance in producing outflow obstruction (even in the absence of typical systolic anterior motion) has not been fully appreciated. METHODS AND RESULTS: Analysis of 78 mitral valves excised from patients with obstructive HCM showed that 10 (13%) had anomalous insertion of one or both left ventricular papillary muscles directly into the anterior mitral leaflet. This malformation was identified by echocardiography, which demonstrated direct continuity between the hypertrophied papillary muscle and mitral leaflet, resulting in a long rigid area of midcavity narrowing that appeared to be solely or largely responsible for outflow obstruction. Basal subaortic pressure gradients were large (70-150 mm Hg). Mitral valve replacement reduced the outflow gradient substantially to 0-15 mm Hg in four patients with postoperative cardiac catheterization. However, two other patients who underwent septal myotomy/myectomy had persistent symptoms and incomplete relief of obstruction (gradients 60 and 70 mm Hg) because of continued midcavity apposition of papillary muscle and ventricular septum. CONCLUSIONS: Anomalous papillary muscle insertion into anterior mitral leaflet represents a mechanism of obstruction to left ventricular outflow in patients with HCM and differs considerably from typical dynamic obstruction caused by mitral valve systolic anterior motion that occurs in many other patients with HCM. Recognition of this malformation emphasizes the diverse morphological expression of HCM and also has important clinical implications for patients requiring operation because the gradient is likely to persist even after adequate myotomy/myectomy; consequently, mitral valve replacement would appear to be the operation of choice in most such patients.

Adult↗

PubMed1998

[A successful valve repair case of isolated tricuspid regurgitation due to traumatic lacerated papillary muscle of the tricuspid valve].

A case of tricuspid valve regurgitation due to a non-penetrating chest trauma was presented. This case involves a 20-year-old man, who was admitted to a nearby hospital because of rib fracture, mandibular fracture, and hemorrhage of the left hemopneumothorax, caused by a traffic accident. Palpitation and chest discomfort were observed at admission time, but there was no follow-up. Tricuspid regurgitation was pointed out during surgery for the mandibular fracture, and he continued follow up treatment at an outpatient clinic. However his palpitation and chest discomfort worsened, and he was admitted to our department 8 month after injury. During surgery to repair the tricuspid valve, a papillary muscle rupture, valve cusp laceration, and anulus dilatation were found. We performed a papillary muscle repair (chorda tendineae reconstruction), valve cusp suture, and annuloplasty. Absence of the left pericardium was observed during the operation. We reported valve repair of traumatic tricuspid regurgitation which with papillary muscle rupture. Due to its rarity and the fact that there has been no reported cases of papillary muscle repair for traumatic tricuspid regurgitation in Japan, we used researched information on the subject.

Adult↗

PubMed1999

[Papillary muscle rupture during stress ECG after myocardial infarct].

The case of a 57 year old patient is reported, who suffered from an acute myocardial infarction with maximum CK and CKMB values of 821 and 84 U/l, respectively. The patient underwent bicycle exercise testing 9 days after a myocardial infarction in 25 W steps every 2 min starting with 50 W. The ergometry was interrupted at 125 W because of ST segment depression of 0.28 mV in V6. Systolic blood pressure dropped to 55 mm Hg, combined with severe angina and shock. Volume substitution and catecholamines did not elevate blood pressure. Immediate M-mode and Doppler echo revealed a "stiletto"-shaped mitral regurgitation profile typical of acute mitral valve insufficiency. The transesophageal echocardiogram showed a distinct mass moving between the left ventricle and left atrium, diagnostic of papillary muscle rupture. Despite of shock, mitral valve replacement was performed successfully. To our knowledge, this is the first report of a papillary muscle rupture during exercise testing after myocardial infarction. Papillary muscle rupture can be induced by exercise. This fateful event may not be predicted by the course of the ergometry. In case of hypotension during exercise, papillary muscle rupture should be considered. The diagnosis is to be established by transesophageal echocardiography.

Echocardiography, Doppler↗

PubMed1995

Quantification of the voltage-response relationship between punctate and field electrical stimulation and the function of isolated rat left atria and papillary muscles.

The effects of varying the electrical stimulation voltage on the noradrenergic tone and systolic and diastolic cardiac function of isolated rat cardiac preparations is unknown. If a wide range of voltages substantially alters the basal noradrerengic tone of isolated cardiac preparations, highly variable responses may complicate the interpretation of the cardiac effects of interventions, such as drugs or toxins. This study was designed to determine whether field or punctate electrode stimulation altered systolic and diastolic cardiac function of isolated rat atrial and ventricular muscle preparations through a beta-adrenergic receptor-mediated mechanism. Isolated left atria and right ventricular papillary muscles from adult Sprague-Dawley rats were stimulated to contract isometrically in Krebs bicarbonate buffer (30 degrees C, pH 7.4, 0.5 Hz). Cardiac muscle function was assessed by determining cardiac contractility (dF/dt), relaxation (80% relaxation time), and muscle stiffness (changes in resting force). Muscles were electrically stimulated to contract using either punctate or field electrodes. Basal values of cardiac function were determined at threshold voltages, and voltage was increased in stepwise fashion, over a wide range, to obtain a voltage response-relation to cardiac function. In left atrial preparations, both punctate and field electrical stimulation caused a 200% increase in cardiac contractility. The greatest changes in contractility occurred at near threshold voltages (less than 5 volts for punctate and 19 volts for field stimulation). The voltage-dependent increases in cardiac contractility were attenuated or abolished by pretreatment with atenolol (10 micromol/L; selective beta 1-antagonist) or reserpine (5 mg/kg i.p., 24 hr before euthanasia). In contrast to left atrial preparations, neither field or punctate electrical stimulation had any effect on the cardiac contractility of papillary muscle preparations. Neither field or punctate electrical stimulation had any effect on cardiac relaxation (80% relaxation time) or muscle stiffness (changes in resting force) of left atrial or papillary muscle preparations. This study demonstrates that punctate and field electrical stimulation can significantly increase cardiac contractility of rat left atrial preparations at near threshold voltages by increasing noradrenergic tone. Thus, control of the voltage range may be required to reduce variation in cardiac function of isolated rat left atrial preparations.

Animals↗

PubMed1982

Reversible alterations in excitation-contraction coupling during myocardial hypertrophy in rat papillary muscle.

To investigate the possible role of an alteration in excitation-contraction coupling in cardiac hypertrophy, we compared simultaneously recorded action potentials along with isometric or isotonic contractions of normal and hypertrophied papillary muscles. Hypertrophy was produced by renal hypertension in rats. Hypertrophied papillary muscles were taken from rats that had been hypertensive for 10 [HBP (10)] or 20 [HBP (20)] weeks. Regression of changes induced by hypertrophy was studied in rats that had been hypertensive for 10 weeks and then made normotensive for 10 weeks by removal of the ischemic kidney. Papillary muscles from age-matched, sham-operated rats [SHAM (10), SHAM (20)] were used as controls. We found that HBP (10) rats had significantly longer action potentials than SHAM (10) rats and that difference in the action potential duration recorded during isotonic and isometric contractions was significantly different from SHAM (10) and HBP (10) rats. Peak developed tension was the same in HBP (10) and SHAM (10) muscles, but the duration of isometric contraction and time-to-peak shortening were longer in HBP (10) muscles. Similarly, whereas the peak tension was the same in HBP (20) and SHAM (20) muscles, the duration of the action potential and isometric contraction, as well as the time-to-peak tension, was longer in HBP (20) muscles. The longer values for action potential duration, isometric contraction, and time-to-peak tension in HBP (20) muscles returned to SHAM values in HBP (R) muscles. The functional relationship between contraction and the action potential time course was assessed by plotting action potential duration against four parameters of contraction: peak developed tension, time-to-peak tension, time-to-half relaxation, and time-to-peak shortening. Statistical analysis of these data showed a significant correlation between action potential duration and all four parameters of contraction in SHAM (10) and SHAM (20) muscles. In contrast, HBP (10) muscles showed a significant correlation between action potential duration and only two contractile parameters, whereas action potential duration did not correlate significantly with any of the contractile parameters in HBP (20) muscles. Remarkably, in HBP (R) preparations a significant correlation was restored between action potential duration and three of the four contractile parameters. The results of this study suggest that reversible cardiac hypertrophy is associated with reversible alterations in excitation-contraction coupling. The reversibility of the mechanical and electrical alterations that accompany hypertrophy suggests, in turn, that cardiac hypertrophy is an adaptive process.

Action Potentials↗

PubMed1991

The effects of thyroid state on sarcomere dynamics of ventricular cells and contraction of papillary muscles in the rat heart.

Diastolic sarcomere length, amplitude of maximal sarcomere shortening, maximal rate of sarcomere shortening, maximal rate of sarcomere re-lengthening, time to peak sarcomere shortening and trans-sarcolemmal ion currents were measured in isolated ventricular cells from euthyroid, hypothyroid and hyperthyroid rats. The data were compared with the developed tension and time to peak tension of papillary muscles. The diastolic sarcomere length was not affected by the changes in thyroid state. Hypothyroidism led to an increased time to peak sarcomere shortening, an increased time to peak tension of the papillary muscle, and a depression of the maximal rates of shortening and elongation of the sarcomeres. Changes in dynamics of the sarcomere and contraction of papillary muscle did not occur in parallel under the influence of hyperthyroidism. In comparison with the euthyroid state, the time to peak tension was shortened and amplitude of shortening of the sarcomere was increased. The time to peak shortening of the sarcomere and developed tension of papillary muscle remained unaltered. In cardiac cells, hypothyroidism was associated with a decreased slow Ca2+ current and hyperthyroidism with an increased slow Ca2+ current. In contrast to euthyroid and hypothyroid cardiac cells, the hyperthyroid cardiomyocytes exhibited a trans-sarcolemmal transient inward current after repolarization. Both hypothyroidism and hyperthyroidism resulted in a depressed potentiation of sarcomere shortening and myocardial developed tension after resting.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Effect of 1-acyl-5,6-dialkoxy-2-alkylthiobenzo[d] imidazoles on the action potential duration and isometric contraction in guinea pig atrium activated by carbachol and in guinea pig heart papillary muscles.

BACKGROUND: Studies have shown that some benzo[d]imidazole derivatives (1-(5,6-dimethoxy-2-methylthio-1H-benzo[d]imidazol-1-yl)-1-ethanone (1), 1-(6-ethylthio-5H[1,31dioxolo[4',5':4,5] benzo[d]imidazol-5-yl)-1-propanone (2), 1-(2-ethylthio-6,7-dihydro-1H[1,4]dioxino [2:3':4,5]benzo[d]imidazol-1-yl)-1-pro-panone (3) and 2,3,9,10-tetrahydro-8H [1,4]dioxino[2' 3":4',5']benzo[4,5]imid-azo[2,1-b][1,3]thiazin-10-one (4)) possess strong cardiotonic activity. The goal of this study was to investigate the effect of compounds 1-4 on the action potential (AP) duration and contractile force in guinea pig atrium activated by carbachol and in guinea pig heart papillary muscles. METHODS: The experiments were carried out on the guinea pig papillary muscles and atrium. Isometric contraction and transmembrane potential were recorded using a force transducer and standard microelectrode technique. RESULTS: Compounds 1-4 exerted a positive inotropic effect in a dose-dependent manner on the electrically driven left atrium and papillary muscles, more pronounced in atrium. In response to 1 micromol/L carbachol the AP duration at a 90 % repolarization in atrium shortened more than 70 %, the isometric contraction decreased to the similar level as well. Compounds 1 and 4 significantly antagonized the shortening of the AP duration induced by carbachol and increased it. Compound 1 abolished the reduction of isometric contraction as well. Derivative 3 significantly lengthened (31 ms) the AP duration at a 90 % repolarization in papillary muscles, while 1 and 4 failed to affect this index. The selective blockade of the rapid component of the delayed rectifier potassium current (Ikr) by dl-sotalol (1 micromol/L) did not show the substantial influence on benzimidazole effects. CONCLUSION: These findings support the hypothesis that the tested benzo[d] imidazole derivatives abolish the influence of carbachol on AP and the isometric contraction by inhibition of acetylcholine-activated potassium current (KACh) in guinea pig atrial myocytes and therefore may be beneficial for the prognosis of patients with advanced heart failure and atrial fibrillation.

Action Potentials↗

PubMed1990

[Mitral valve replacement in post-infarction rupture of the papillary muscle. Apropos of 13 cases surgically treated during the acute phase of infarction].

Between 1983 and 1988, thirteen patients (12 men and 1 women, average age 63 years) were operated in the acute phase of myocardial infarction for papillary muscle rupture (PMR). The rupture involved the posterior papillary muscle in 12 cases. The average left ventricular ejection fraction was 47 +/- 9 per cent (range 34 to 63%). Pulmonary capillary pressures ranged from 76 to 41 mmHg (average 35 mmHg). Eleven patients presented with acute pulmonary oedema and 7 had cardiogenic shock. Coronary arteriography showed triple vessel disease in 3 cases, double vessel disease in 7 cases and single vessel disease in 3 cases. Surgery was carried out on average 2.7 days after the rupture and 10 days after the initial infarct. In addition to mitral valve replacement (N = 13), 11 patients underwent a myocardial revascularisation procedure. The operative mortality was 15 per cent (N = 2). Papillary muscle rupture in the acute phase of myocardial infarction causes cardiac failure which is related more to the mechanical abnormality than to an alteration of left ventricular function. Considering the operative mortality and the natural history of PMR treated medically, the authors recommend early surgery as the only management which can improve the precarious haemodynamic status of patients with this complication.

Aged↗

PubMed1991

Intracellular sodium activity in papillary muscle from diabetic rat hearts.

In quiescent papillary muscles isolated from hearts of rats with streptozotocin-induced diabetes resting intracellular sodium activity (aiNa) was about 56% greater than in muscles from controls. An intracellular acid load induced by the NH4+ method caused a rise in aiNa whose maximum amplitude was similar in both groups of muscles. However, the half-time to maximum amplitude was increased by about 56% in diabetic muscles. These results are consistent with a diabetes-induced decrease in the activity of the sarcolemmal Na(+)-H+ exchange.

Animals↗

PubMed1995

Effects of N6-cyclopentyladenosine on afterdepolarizations and triggered activity induced by isoproterenol in guinea pig papillary muscle.

AIM: To investigate the effects of N6-cyclopentyladenosine (CPA, selective adenosine A1 receptor agonist) on afterdepolarizations and triggered activity induced by isoproterenol (Iso) in guinea pig papillary muscle. METHODS: The stable and reproducible early afterdepolarization (EAD) and delayed afterdepolarization (DAD) of guinea pig papillary muscle were induced by Iso 50 nmol.L-1. The parameters of EAD and DAD were recorded using intracellular microelectrodes. RESULTS: CPA markedly attenuated the development of EAD, DAD, and triggered activity (TA) induced by Iso in guinea pig papillary muscle. The inhibitory effects of CPA on Iso-induced EAD and DAD were antagonized by 8-phenyltheophylline (8-PT) and glibenclamide (Gli). CONCLUSION: ATP-sensitive K+ channels were involved in Iso-induced EAD and DAD, and in the inhibitory effects of CPA on EAD and DAD.

Action Potentials↗