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 397 records · Page 22Linked to original sources

PubMedDate not supplied

Fat diet, osmotic fragility of erythrocytes and inotropic response of rat heart papillary muscle to noradrenaline stimulation: early appearance of the diet effect by lovastatin.

Intake of lovastatin, an inhibitor of endogenous cholesterol synthesis, leads to a compensatory increase in the uptake of cholesterol from plasma (low density lipoprotein endocytosis). The drug might exert effects also by facilitating uptake of fatty acids carried in low density lipoprotein. It has been reported that dietary fat may alter physical properties of erythrocytes as well as adrenergic effects in heart muscle. We have therefore studied osmotic fragility of erythrocytes and inotropic and lusitropic responses of isolated heart papillary muscles taken from rats fed for 3 weeks either a purified high fat diet (olive oil/coconut oil 16 g/6 g/100 g diet), prepared plus and minus lovastatin, or similar diets in which 4 g/100 g diet of the olive oil was replaced by cod liver oil. Three weeks feeding of a high fat diet containing cod liver oil did not affect osmotic fragility of erythrocytes or indices of inotropy or lusitropy in papillary muscles in response to noradrenaline stimulation neither in the absence nor in the presence of lovastatin. In contrast, purified high fat diet lacking cod liver oil increased osmotic fragility in a fraction of the erythrocytes. When lovastatin was added to this diet the osmotic fragility was increased for the whole population of erythrocytes. In this situation the "relaxation-onset index"--an index of early relaxation in the papillary muscles--was shifted to higher concentrations of noradrenaline. Thus, intake of lovastatin may lead to an early appearance of effects of dietary fat on osmotic fragility of erythrocytes and on heart muscle responses to catecholamines. These effects of lovastatin are, however, apparently dependent upon the kind of dietary fat as they are prevented by the presence of cod liver oil.

Animals↗

PubMedDate not supplied

[Papillary muscle dysfunction in acute myocardial infarct: a clinical and Doppler echocardiographic study].

The "papillary muscle dysfunction" concept includes a disrupted sequence of one or more structures of the mitral valve complex and not merely a disturbance of a papillary muscle itself. We studied a group of seventeen patients, 14 men and 3 women (mean age 51 and 39 years, respectively). Acute myocardial infarction was the first evidence of heart disease. In all of them, Doppler and M mode echocardiography were performed and correlation clinical features were done. In addition a tricuspid regurgitation flow patterns was scanned on each patient. Mitral regurgitation was found in 29% of them by Doppler echocardiography and only 17% had a mitral systolic murmur suggestive of this entity. In those patients with mitral regurgitation-flow patterns, the infarct site was similar to those with anterior and inferior infarction and serum CPK-level was greater in these patients than the non-mitral regurgitation flow pattern group. The evidence of tricuspid regurgitation by pulsed-Doppler echocardiography was associated with mitral regurgitation in 80% of patients, mainly those with right ventricular extension of acute myocardial infarction, and with the greatest hemodynamic impairment. It seems likely in this study, that mitral regurgitation was due to valve ring dilation with an increase of left ventricular diameter and a decrease on ventricular systolic function.

Adolescent↗

PubMed1995

Variations in the papillary muscles of the normal mitral valve and their surgical relevance.

A mid-mitral plane passing through the middle of the aortic and mural leaflets divides the chordopapillary support of the mitral valve into anterolateral and posteromedial halves. The papillary muscles of the mitral valve were studied in 100 human autopsy hearts collected at random. The anterolateral papillary support had 1 belly in 67 hearts, 2 in 27, 3 in 4, 4 in 1, and 5 in 1 heart. Likewise, the posteromedial papillary support had 1 muscle belly in 50 hearts, 2 in 36, 3 in 11, and 4 in 3. The single papillary muscles were conical, mammillated, flat topped, grooved, stepped, wavy, arched, sloped or saucerized. When there were two bellies they presented a two tiered, interlinked, parallel, arched, V, Y, or H configuration. Three papillary muscles formed a parallel, interlinked or arched arrangement; or two bellies were interlinked or formed a two tiered arrangement with the third belly separate. When four or five bellies existed, they were parallel or interlinked. In the anterolateral and posteromedial group, the papillary muscle bellies were mostly intraluminal in 14% and 11%, mostly intraluminal with the tip anchored in 19% and 28%, equally sessile and intraluminal in 54.5% and 41.5%, mostly sessile in 12.5% and 19.5%, respectively. In the anterolateral group 19% of papillary muscle bellies arose from the upper third of the ventricle, 79.5% from middle third, and 1.5% from lower third. The corresponding figures for posteromedial group are 6%, 92.5%, and 1.5%, respectively. Four to 22 chordae originated from the anterolateral papillary group, ending in 14 to 72 chordal insertions into the corresponding half of the valve. Likewise, 2 to 18 chordae arose from the posteromedial papillary group ended in 12 to 80 leaflet insertions. The chordae in each group are best considered in toto as a fan. The configuration of the fan is unique in each heart. Imaging techniques need to be refined to outline these variations more precisely. The relevance of chordopapillary variations in rheumatic heart disease, reparative procedures, papillary muscle dysfunction, mitral valve prolapse, mitral valve replacement, and use of mitral valve homograft for mitral/tricuspid replacement is discussed.

Cardiac Surgical Procedures↗

PubMed1983

Papillary muscle rupture complicating acute myocardial infarction: analysis of 17 patients.

The records of 17 patients (10 men and 7 women) with the diagnosis of acute papillary muscle rupture secondary to acute myocardial infarction (AMI) were reviewed to determine the clinical course and pathologic features of this entity. Eight patients underwent operation after papillary muscle rupture had been diagnosed, and 9 had the diagnosis confirmed at autopsy without a prior surgical procedure. The ages were 44 to 80 years (mean 64). The site of AMI was inferolateral in 15 and anterior in 2. The recorded onset of mitral regurgitation ranged from less than 24 hours to 28 days after AMI (mean 6 days). Of the 11 patients presenting with pulmonary congestion alone, 6 remained stable and had subsequent mitral valve replacement and coronary artery bypass graft operation; however, 5 patients' condition initially stabilized with medical therapy and then suddenly deteriorated after a variable period (1 to 60 days), followed by death. Of the 6 patients who presented with systemic hypotension and pulmonary congestion, 4 were treated medically and died; 1 of the 2 who had surgical treatment survived. The extent of the AMI at autopsy was small and was limited to the subendocardium in half of the patients. Significant coronary artery disease was limited to a single vessel in 7 of 14 patients. The unpredictable and rapid clinical deterioration and the limited extent of coronary atherosclerotic disease and infarct size suggest that early surgical repair should be undertaken in patients with papillary muscle rupture after AMI.

Adult↗

PubMed1988

Mitral valve dysfunction following papillary muscle cryoablation.

Cryoablation is recognized as a useful modality for diagnostic mapping, as well as for permanent obliteration of arrhythmogenic foci. This technique has been used to eradicate irritable foci at the base of papillary muscles. We report a case of mitral valve dysfunction requiring valve replacement following cryoablation of the posterior papillary muscle. Based on this experience, we caution against extensive cryoablation of papillary muscle tissue because of the possibility of disrupting mitral valve function.

Cardiomyopathies↗

PubMedDate not supplied

Oxygen dose-response curve of cardiac papillary muscle from fetal and nonpregnant adult sheep exposed to long-term, high-altitude hypoxemia.

OBJECTIVE: We tested the hypothesis that hearts of fetal and nonpregnant adult sheep exposed to long-term hypoxemia would be able to sustain higher contractile function during exposure to acute hypoxia than hearts from normoxic animals. METHODS: Pregnant and nonpregnant sheep were exposed to high altitude (3820 m) for 100 days. Right and left ventricular papillary muscle strips were obtained from fetuses and nonpregnant adults, mounted in an isolated bath system, stimulated electrically and subjected to acute hypoxia in a dose response manner. Measurements were made of maximum tension production (Tmax), maximum rate of tension development (+dT/dtmax), maximum rate of relaxation (-dT/dtmax), time to peak tension, and duration of contraction. Results were compared to papillary muscle from a normoxic group of animals. RESULTS: Baseline values (95% O2 + 5% CO2 bubbled in the bath) of Tmax and +/- dt/dtmax for each ventricle were greater in adults than fetuses in both normoxic and long-term hypoxemic groups. During hypoxia (at 40 and 20% O2) Tmax and +/- dT/dtmax, were all maintained at significantly higher values in papillary muscle from long-term hypoxemic fetuses than in papillary muscle from normoxic fetuses. Duration of contraction and time to peak tension did not differ between the normoxic and hypoxemic groups. In both ventricles of the long-term hypoxemic adult, Tmax and +/- dT/dtmax, as well as duration and time to peak tension, were significantly higher than in normoxic adults, but only at the lowest level of hypoxia (20% O2). CONCLUSIONS: Contrary to the original hypothesis, heart muscle from both fetal and adult sheep that had been exposed to long-term hypoxemia could maintain contractile function better during acute hypoxia. The responsible mechanisms are not clearly understood.

Animals↗

PubMed1986

Comparison of the effects of nifedipine, diltiazem and verapamil on the mechanical activity of rabbit papillary muscles induced by barium chloride.

Isolated rabbit papillary muscles that do not present pacemaker activity under physiological conditions develop a spontaneous activity in the presence of 2 mmol/l BaCl2. Ba-induced contractions were unaffected by high concentrations of the Na antagonist procainamide (10(-5) mol/l). Tetrodotoxin (10(-5) mol/l), a specific blocker of the fast Na current, only slightly increased the amplitude of contractions. In contrast, the calcium entry blockers nifedipine, diltiazem, and verapamil strongly depressed the mechanical activity in a time- and dose-dependent manner. The concentrations that decreased the amplitude and frequency of contractions by 50% were determined. The order of potency was nifedipine much greater than diltiazem greater than or equal to verapamil. Ba-induced automaticity is a particularly useful model on which the potency of calcium entry blockers could be assessed.

Animals↗

PubMed1979

Effects of palytoxin on mechanical and electrical activities of guinea pig papillary muscle.

Effects of palytoxin (PTX) on isolated papillary muscles of guinea pigs were studied in an attempt to elucidate the mechanical and electrical activities. Inotropic effects of PTX above 3 x 10(-9) g/ml; an early positive inotropic effect, slowly developing contracture accompanied by decline in phasic tension, appearance of aftercontractions and arrhythmias at high doses. The positive inotropic effect of PTX was enhanced in high Ca2+ medium but was not modified by propranolol. PTX induced a sustained depolarization and decrease in the amplitude, upstroke velocity and duration of action potential. During development of depolarization, arrhythmias occurred, which lasted for 5--10 min and reappeared 30--60 min after. Oscillatory afterpotential often appeared. Neither reserpine nor practolol prevented the PTX-induced arrhythmia while propranolol prevented it. Tetrodotoxin slowed the development of depolarization due to PTX and inhibited PTX-arrhythmias. In low Na+ medium, PTX exerted fewer effects on resting and action potentials and produced no arrhythmia. The results suggest that PTX-induced depolarization is responsible for the generation of contracture and arrhythmia and that the depolarization is due to the change in membrane Na permeability.

Acrylamides↗

PubMed2002

Surgical relocation of the posterior papillary muscle in chronic ischemic mitral regurgitation.

Mitral annuloplasty is the preferred surgical treatment for chronic ischemic mitral regurgitation. Although this is usually successful, leaflet restriction by apical displacement of the posterior papillary muscle tip may cause residual mitral regurgitation. Ventricular remodeling surgery is an effective procedure for surgical relocation of the posterior papillary muscle tip in the setting of a severely dilated left ventricle. Direct relocation of the posterior papillary muscle may be useful for patients with a minimally dilated left ventricle or regional left ventricular geometric changes causing mitral regurgitation. Such a surgical procedure is described.

Cardiac Surgical Procedures↗

PubMed1989

Effect of calcium overload on the phosphoinositide breakdown in the rat left ventricular papillary muscle.

We investigated the effect of Ca2+ overload on the phospholipase C-catalyzed hydrolysis of phosphoinositides in the rat left ventricular papillary muscle. Ca2+ overload on the papillary muscle was induced by treatment with 0.3 mM ouabain in Ca2+-containing medium following either Ca2+-containing or Ca2+-free superfusion. The phosphoinositide breakdown was evaluated by determining accumulations of [3H]inositol phosphates ([3H]IPs) in the tissues prelabeled with [3H]inositol. Ca2+ repletion following Ca2+-free superfusion resulted in a rapid but small increase in resting tension that was not followed by contracture, nor was it associated with a significant increase in [3H]IPs accumulations. Treatment with ouabain following Ca2+-containing superfusion increased resting tension after a lag period of several minutes and produced contracture associated with an increase in [3H]IPs accumulations. The ouabain induced increases in resting tension, and accumulations of [3H]IPs were significantly potentiated by prior Ca2+-free superfusion instead of Ca2+-containing superfusion. There was a significant positive correlation between increases in resting tension and the phosphoinositide breakdown. The increased resting tension and the accumulations of [3H]IPs were not antagonized by treatments with prazosin plus atropine or indomethacin, but were abolished by superfusion with Ca2+-free buffer solution. Although the enhanced phospholipase C-catalyzed hydrolysis of phosphoinositides appears to be a consequence rather than a cause of increased intracellular Ca2+, such a biochemical change may provoke a positive feedback mechanism to develop the muscle contracture through the putative intracellular messenger action of inositol triphosphate and diacylglycerol.

Animals↗

PubMed2004

Tricuspid valve repair with papillary muscle shortening for severe tricuspid regurgitation in children.

We describe tricuspid valve repair using papillary muscle shortening for severe tricuspid regurgitation due to leaflet prolapse in children combined with De Vega annuloplasty. The papillary muscle was shortened until the prolapsed leaflet was at the same height as the other nonprolapsed leaflets. Although echocardiographic tricuspid regurgitation tends to increase over time, it rarely requires long-term intervention.

Abnormalities, Multiple↗

PubMed1993

Heat produced by rabbit papillary muscle during anoxia and reoxygenation.

Resting heat rate was measured in superfused rabbit papillary muscles at 20 degrees C during 40 minutes of anoxia and subsequent reoxygenation. To reveal the nature of the reactions underlying energy output under such conditions, the data obtained were compared with values predicted from data on chemical change. Before and after the anoxic period, muscles were stimulated at 0.2 Hz, during which time the contraction-related heat rate was measured. During anoxia, muscles were kept at rest or stimulated at 1 Hz. Stimulation was switched off intermittently to determine resting heat rate. Before anoxia, resting heat rate was 8.7 +/- 1.1 (mean +/- SEM) mW.g dry wt-1. During anoxia, it decreased to 38% and 50% of the preanoxic level in resting and stimulated muscles, respectively (P < .05). In resting muscles, heat rate increased with reoxygenation in approximately 10 to 15 minutes to 1.3 times the preanoxic level, whereas this was 3.7 times in stimulated muscles. Resting heat rate returned within 65 (resting muscles) or 150 (stimulated muscles) minutes to the baseline. The ratio of force- and contraction-related heat rate, ie, the economy of contraction, was not different before and after anoxia. We estimated that the heat produced by muscles during anoxia was not different from the heat to be expected from the hydrolysis of creatine phosphate, the breakdown of nucleotides, and the formation of lactate. The overshoot in resting heat during reoxygenation of resting muscles could be accounted for by the resynthesis of the energy store. The much larger overshoot in resting heat of stimulated muscles was due to the contracture. The finding that the economy of contraction was not altered by anoxia and reoxygenation suggests that both sarcoplasmic reticulum Ca(2+)-ATPase and myofibrillar ATPase are depressed by anoxia and that the enhancement of cytosolic calcium transients with reoxygenation, reported in other studies on papillary muscle, results from reduced binding of calcium rather than from enhanced release.

Animals↗

PubMed1996

[Partial rupture progressing to complete rupture of the left ventricular anterior papillary muscle after acute myocardial infarction: a case report].

A 71-year old man presented with partial rupture progressing to complete rupture of the left ventricular anterior papillary muscle after acute anterolateral myocardial infarction. The progressive rupture was demonstrated by transthoracic and transesophageal echocardiography. Transthoracic echocardiography showed exaggerated systolic prolapse of the anterior mitral leaflet with grade III mitral regurgitation and partial disruption of the anterolateral papillary muscle, but transesophageal echocardiography during surgery disclosed the progression of the partial rupture to complete rupture. The flail anterior mitral leaflet with severe mitral regurgitation and the head of the ruptured papillary muscle into the left atrium in systole were confirmed. The patient was treated by coronary artery bypass grafting and mitral valve prosthesis using a St. Jude Medical valve with good outcome.

Aged↗

PubMed2006

Defect in oxidative phosphorylation in LV papillary muscle mitochondria of patients undergoing mitral valve replacement.

Mitochondria play a pivotal role in cellular metabolism, especially in energy production. Myocardial function depends on adenosine triphosphate (ATP) supplied by oxidation of several substrates. In the adult heart, this energy is obtained primarily from fatty acid oxidation through oxidative phosphorylation (OXPHOS). With this in view, we studied OXPHOS, Total-ATPase and cytochrome content in the mitochondria of the left ventricular (LV) papillary muscles in excised mitral valves of patients who underwent mitral valve replacement (MVR). The mitochondrial OXPHOS, cytochrome content and ATPase activity were studied in 70 patients (ranging from 22 to 40 years) operated on for mitral valve disease. Control study includes 25 normal mitral valves removed at necropsy from patients who died of extracardiac causes. In the presence of glutamate and succinate as substrates, the rate of mitochondrial oxygen consumption was significantly lower in LV papillary muscles of pathological mitral valves (P<0.001) by using with and without addition of ADP. The ADP/O ratio indices for glutamate and succinate were not significantly affected. Using glutamate as substrate, respiratory control index was significantly raised (P<0.05) as compared with control. A significant reduction of total cytochrome content and ATPase activity (P<0.001) was noted in LV papillary muscles of patients operated for mitral valve disease. Our results showed that OXPHOS, cytochromes 'a', 'b', 'c+c(1)' and ATP activity are significantly impaired in LV papillary muscles in patients with pathological mitral valve. Cardiac mitochondrial oxygen consumption is a very valuable tool to investigate the regulation of cardiac mitochondrial energy metabolism. There is increasing evidence that mitochondrial diseases, such as mitochondrial cardiomyopathy, valvular disease and some myopathies, can be responsive to treatment with metabolic intermediates such as coenzyme Q(10), thiamine, prednisone, and vitamin therapy.

Adenosine Triphosphatases↗

PubMed1992

5-HT4 receptors, present in piglet atria and sensitive to SDZ 205-557, are absent in papillary muscle.

Putative 5-HT4 receptors were investigated in isolated piglet left atria and papillary muscles. In atrial tissues, 5-hydroxytryptamine (5-HT) was a potent positive inotropic agent with a pD2 of 6.7. Its effects were antagonised in a selective and competitive manner by the 5-HT4 receptor antagonist, SDZ 205-557, with a pA2 of 7.3. In contrast to atrial tissues, piglet papillary muscles were virtually unresponsive to 5-HT 10(-8)-10(-3) M, suggesting that functional cardiac 5-HT4 receptors are not present in ventricular tissue.

4-Aminobenzoic Acid↗

PubMed1962

Effect of reserpine pretreatment on the response of isolated papillary muscle to ephedrine.

Reserpine pretreatment of cats abolished the action of ephedrine to induce spontaneous beating in papillary muscles obtained from these animals. This spontaneous beating was viewed as resulting solely from catechol amine release. The positive inotropic action of ephedrine was diminished but not abolished by reserpine pretreatment. Reserpine reduced the heart rate in vivo, but it did not affect the peak contraction height or the rate of failure of the isolated papillary muscle. The contractile response to adrenaline (0.1 mug/ml.) was not affected by reserpine pretreatment. However, in this concentration adrenaline induced spontaneous beating only after reserpine.

Animals↗

PubMed1975

Studies on the kinetics of (3H)-ouabain uptake and exchange in the isolated papillary muscle of the guinea-pig.

1 The uptake, wash-out and exchange of [3H]-ouabain was studied in isolated, resting, and electrically stimulated papillary muscles of the guinea-pig. 2 At the equilibrium level of uptake, a different tissue/medium ratio was obtained for each of the concentrations used, i.e. 3.4, 1.8 and 0.82 for 1 times 10-minus 7M, 7.7 times 10-minus 7M, and 5 times 10-minus 6M ouabain, respectively. Equilibrium was reached more rapidly at high concentrations of ouabain. 3 The maximum number of binding sites for ouabain was estimated to be 1 times 10-15 binding sites/g wet weight. 4 No difference in [3H]-ouabain uptake could be detected between resting and electrically stimulated papillary muscles. 5 The kinetics of the ouabain uptake, wash-out and exchange are discussed. The results suggest that there is a saturable compartment in papillary muscle which can best be demonstrated if low concentrations of ouabain are used. Because of its small size, the saturable compartment submerges in the process of the filling of the extracellular space at high concentrations (5 times 10-minus 6M).

Animals↗

PubMed1999

Preconditioning prevents the negative inotropic action of phenylephrine in rat isolated stunned papillary muscle.

The aim of the present study was to establish a model of ischemic preconditioning of rat isolated papillary muscle and to investigate its effect on the simulated ischemia-induced disturbances in contractility and responsiveness to isoproterenol and phenylephrine. Experiments were performed in rat left ventricle papillary muscle. The following parameters were measured: force of contraction (Fc), velocity of contraction (+dF/dt), velocity of relaxation (-dF/dt), time to peak contraction (ttp), and relaxation time at the level of 10% of total amplitude (tt10). After 60 min of simulated ischemia induced by the perfusion of isolated tissues with no-substrate solution aerated by 95% N2/5% CO2, all of the measured parameters were markedly decreased. There was not complete recovery of Fc, +dF/dt and -dF/dt after 60 min of reperfusion. Positive inotropic action of isoproterenol does not differ before and after simulated ischemia. In contrast, phenylephrine induces a positive inotropic action in non-treated, but a significant negative one in simulated ischaemia/reperfusion treated preparations. The latter effect of phenylephrine was reversed by chloroethylclonidine (CEC), a selective blocker of alpha1b-adrenoceptor, but not by WB-4101, a selective blocker of alpha1a-adrenoceptor. Ischemic preconditioning of rat isolated cardiac tissue induced by the 5 min perfusion with no-substrate solution, aerated by 95% N2/ 5% CO2, in the presence of fast electrical pacing (BCL shortened from 2000 ms to 700 ms) and 10 min reperfusion, significantly improves a recovery of the contractility and prevents phenylephrine negative inotropic action.

Adrenergic alpha-Antagonists↗