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At least 433 records · Page 24Linked to original sources
PubMed1999

Cyclic AMP but not phosphorylation of phospholamban contributes to the slow inotropic response to stretch in ferret papillary muscle.

cAMP has been suggested to mediate the increased intracellular Ca2+ transient and contraction seen during the slow response to stretch in cardiac muscle. We measured cAMP in ferret papillary muscles stretched from 80-85% to 98% of their length at which maximum active tension is produced (Lmax) for 15 min. cAMP was significantly (P<0. 05) increased by 53% in muscles at the longer length which showed the slow response compared with controls. By contrast, in a population of muscles that were stretched but did not show the slow response, cAMP was not significantly different from that in muscles at the short length. Although cAMP can increase sarcoplasmic reticulum (SR) Ca2+ uptake by phosphorylation of phospholamban, we found no significant effect of stretch on phosphorylation of phospholamban at either Ser16 or Thr17. Further support for the hypothesis that cAMP is a mediator of the slow response was obtained by exposure of some muscles to the cell-permeable cAMP antagonist 8-bromo, adenosine 3',5'-cyclic monophosphorothioate, Rp isomer (Rp-8-Br-cAMPS, (2.5-10 microM). The slow response was reduced by 30% (P<0.05) in the presence of this antagonist. Our results not only provide evidence for the mediation of the slow response to stretch by cAMP, they also suggest that cAMP may rise in an intracellular compartment inaccessible to the SR.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1993

Effects of etomidate on the cardiac papillary muscle of normal hamsters and those with cardiomyopathy.

BACKGROUND: Etomidate has been shown to induce no significant inotropic effect on normal myocardium, but its effects on diseased myocardium remain unknown. METHODS: The effects of etomidate (1 and 5 micrograms/ml) on the intrinsic contractility of left ventricular papillary muscle from normal hamsters and those with cardiomyopathy (strain BIO 82.62, 6 months old) were investigated in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, Ca++ 2.5 mM, stimulation frequency 3/min). RESULTS: The contractility of papillary muscles from hamsters with cardiomyopathy was less than that of controls, as shown by the decrease in maximum shortening velocity (-25%, P < .001), isometric active force (-45%, P < .01), peak power output (-57%, P < .01), and sarcoplasmic reticulum function (P < .01). Etomidate did not induce a significant inotropic effect, as shown by the absence of changes in maximum shortening velocity and active isometric force, except at 5 micrograms/ml in cardiomyopathic hamsters (+8 +/- 10%, P < .05). The effects of etomidate on these inotropic parameters were not different in normal and cardiomyopathic hamsters. Etomidate impaired contraction-relaxation coupling under low load in both groups, suggesting that etomidate decreased sarcoplasmic function. This impairment was less (P < .02) pronounced in cardiomyopathic muscles. The effects of etomidate on contraction-relaxation coupling under heavy load were not different between groups. In both groups, etomidate had no effect on the peak power output and the curvature of the total force-velocity curve, suggesting that it did not modify the muscle myothermal economy. CONCLUSIONS: Etomidate had only a slight effect on the intrinsic mechanical properties of hamster cardiac papillary muscles, and these effects did not depend on the pathophysiologic state of the myocardium. These results may be clinically useful as, unlike etomidate, most anesthetics depress myocardial contractility.

Animals↗
PubMed2001

Isolated acute anterolateral papillary muscle rupture presenting as a sole manifestation of acute myocardial infarction and mimicking mitral valve vegetation.

We present here a case of an acute myocardial infarction presenting solely as rupture of the head of anterolateral papillary muscle of the mitral valve with an echocardiographic appearance of a mitral valve vegetation. A 61-year-old male patient presented to the hospital with cardiogenic shock. Transesophageal echocardiography revealed normal left ventricular global and regional systolic function with the echocardiographic appearance of a large vegetation attached to the anterior mitral valve leaflet and severe mitral regurgitation. Intraoperatively, an infracted and ruptured head of the anterolateral papillary muscle was found with no evidence of vegetations. Papillary muscle rupture is a rare complication of acute myocardial infarction, is usually associated with inferior myocardial infarction and rarely seen as the only clinical and echocardiographic finding. Transesophageal echocardiography is more sensitive than transthoracic echocardiography but misdiagnosis can still occur.

Diagnosis, Differential↗
PubMed1981

Surgical correction of complete rupture of the anterior papillary muscle.

A 59-year-old patient with postinfarction complete rupture of the anterior papillary muscle and massive mitral regurgitation is described. The diagnosis was suspected clinically and confirmed by echocardiography and cardiac catheterization. Two months after the acute episode, the patient underwent a valve-conserving procedure by reattachment of the papillary muscle to the left ventricular wall. The patient is well and asymptomatic 3 years after operation with evidence of good anatomical and functional correction of the mitral valve lesion. This type of repair should be possible in selected patients with this lesion.

Cardiac Catheterization↗
PubMed2005

Papillary muscle dysfunction attenuates ischemic mitral regurgitation in patients with localized basal inferior left ventricular remodeling: insights from tissue Doppler strain imaging.

OBJECTIVES: The purpose of this research was to test whether papillary muscle (PM) dysfunction attenuates ischemic mitral regurgitation (MR) in patients with left ventricular (LV) remodeling of a similar location and extent. BACKGROUND: Papillary muscle dysfunction could attenuate tethering and MR because of PM elongation. However, variability in the associated LV remodeling, which exaggerates tethering, can influence the relationship between PM dysfunction and MR. METHODS: In 40 patients with a previous inferior myocardial infarction but without other lesions, the LV volume, sphericity, PM tethering distance, PM longitudinal systolic strain, and MR fraction were quantified by echocardiography. The patients were divided into two groups: group 1 with significant basal inferoposterior LV bulging but without advanced LV bulging involving other territories, therefore with a similar location and extent of LV remodeling, and group 2 without significant LV bulging. RESULTS: The medial PM tethering distance was significantly correlated with the %MR fraction (r2 = 0.64, p < 0.01), and multiple regression analysis identified an increase in the tethering distance as the only independent determinant of the MR fraction in all subjects and also in group 1. The PM longitudinal systolic strain had no significant relationships with MR fraction in all subjects with variable degrees of LV remodeling, but it had a significant inverse correlation with the MR fraction (r2 = 0.33, p < 0.01) in group 1 with LV remodeling of a similar location and extent, indicating that PM dysfunction is associated with less MR. CONCLUSIONS: Papillary muscle dysfunction, reducing its longitudinal contraction to induce leaflet tethering, attenuates ischemic MR in patients with basal inferior LV remodeling.

Aged↗
PubMed2005

Arginine-glycine-aspartic acid (RGD)-containing peptides inhibit the force production of mouse papillary muscle bundles via alpha 5 beta 1 integrin.

Integrins are considered to be an important mechanosensor in cardiac myocytes. To test whether integrins can influence cardiac contractile function, the force-frequency relationships of mouse papillary muscle bundles were measured in the presence or absence of a synthetic integrin-binding peptide, GRGDNP (gly-arg-gly-asp-asn-pro). Results demonstrate that in the presence of an arginine-glycine-aspartic acid (RGD)-containing synthetic peptide, contractile force was depressed significantly by, 28% at 4 Hz, 37.7% at 5 Hz and 20% at 10 Hz (n = 6, P < 0.01). Treatment of myofibres with either protease-generated fragments of denatured collagen (Type I) or denatured collagen that contain the RGD motif, also reduced force production significantly. An integrin-activating antibody for beta(1) integrin inhibited the force similar to synthetic RGD peptide. Function-blocking integrin antibodies for alpha(5) and beta(1) integrins reversed the effect of the RGD-containing peptide, and alpha(5) integrin also reversed the effect of proteolytic fragments of denatured collagen on contractile force, whereas experiments with function-blocking antibody for beta(3) integrin did not reverse the effect of RGD peptide. Force-[Ca(2)(+)](i) measurements showed that the depressed rate of force generation observed in the presence of the RGD-containing peptide was associated with reduced [Ca(2)(+)](i). Data analyses further demonstrated that force per unit of Ca(2)(+) was reduced, suggesting that the myofilament activation process was altered. In addition, inhibition of PKC enzyme using the selective, cell-permeable inhibitor Ro-32-0432, reversed the activity of RGD peptide on papillary muscle bundles. In conclusion, these data indicate that RGD peptide, acting via alpha(5)beta(1) integrin, depresses the force production from papillary muscle bundles, partly associated with changes in [Ca(2)(+)](i) and the myofilament activation processes, that is modulated by PKCepsilon.

Animals↗
PubMed1978

Influence of thyroid hormone on the positive inotropic effects mediated by alpha- and beta-adrenoceptors in isolated guinea pig atria and rabbit papillary muscles.

Effects of thyroxine treatment for 7--11 days on the positive inotropic effects mediated by alpha- and beta-adrenoceptors were studied in isolated guinea pig atria and rabbit papillary muscles. In guinea pig atria, the thyroxine treatment inhibited the positive inotropic effect of lower concentrations of phenylephrine (PHE), and attenuated the inhibitory effect of phentolamine on the PHE response. The effect of isoproterenol (ISO) was potentiated by the thyroxine treatment. In rabbit papillary muscles, the thyroxine treatment shifted the dose--response curve for PHE to the right and attenuated the inhibitory effect of phentolamine on the PHE response. Propranolol, in both guinea pig atria and rabbit papillary muscles, inhibited the PHE response more effectively in preparations from thyroxine-treated animals than in controls. In guinea peg atria, the attenuation of the PHE response mediated by alpha-adrenoceptors was observed after the thyroxine treatment for only 2 days, whereas the potentiation of the ISO response required the thyroxine treatment for a longer period. It was concluded that the thyroxine treatment attenuated the positive inotropic effect mediated by alpha-adrenoceptors and potentiated that mediated by beta-adrenoceptor-mediated positive inotropic effects due to the thyroxine treatment may be independent of each other.

Animals↗
PubMedDate not supplied

The blood supply of the papillary muscles of the left ventricle in the Hereford cattle.

The blood supply of the Papillary Muscle (PM) of the left ventricle, cranial (PM) and caudal (PM), in Hereford cattle was studied. The results obtained from the dissection of 50 hearts injected with neoprene latex, indicated that the cranial PM is supplied by collateral of the Ramus descendens paraconalis in all cases, alone or together with vessels from the Ramus circumflexus of the Arteria coronaria sinistra. The caudal PM is supplied from arteries coming mainly from the Ramus circumflexus of the A. coronaria sinistra, and also from the Ramus descendens subsinuosus and Ramus descendens paraconalis. When present, the A. diagonalis supplies the cranial PM and in some cases the caudal PM too. Thus this vessel can be termed "artery of the papillary muscle".

Animals↗
PubMed1987

Negative inotropic effects of halothane, enflurane, and isoflurane in papillary muscles from diabetic rats.

Myocardial contractile responses to halothane, enflurane, and isoflurane were studied in papillary muscles isolated from streptozotocin-induced diabetic rats and in those from age-matched control rats. The developed tension in diabetic papillary muscles electrically paced at a constant rate was not different from that in control muscles, but both the time to peak tension and the relaxation time of the isometric contraction were significantly prolonged in diabetic muscles. Halothane, enflurane, and isoflurane all produced negative inotropic effects in both diabetic and control muscles. However, the negative inotropic effects were significantly less in the muscles from diabetic rats than in the muscles from control rats throughout the range of concentrations. In muscles from both the diabetic and control rats, the negative inotropic effects of these anesthetics were accompanied by decreases in the time to peak tension and in relaxation time. The results suggest that the myocardium from the diabetic rat is less sensitive to the negative inotropic action of volatile anesthetics than is the myocardium of normal hearts.

Animals↗
PubMed1996

Excessive papillary muscle traction and dilated mitral annulus in mitral valve prolapse without mitral regurgitation.

This study demonstrated excessive papillary muscle displacement during peak systole but normal mitral annulus function during the cardiac cycle in patients with mitral valve prolapse and no mitral regurgitation. The excessive papillary muscle displacement may play an important role in the pathogenesis of the superior displacement of mitral leaflets in patients with mitral valve prolapse.

Adolescent↗
PubMed1996

[Mitral valve replacement and coronary artery bypass grafting for postinfarction mitral papillary muscle rupture].

A 79-year-old man was admitted to our hospital with heart failure following acute inferior myocardial infarction. An echocardiogram demonstrated severe mitral insufficiency, and coronary arteriography revealed double vesel disease. Following diagnosis of ischemic papillary muscle dysfunction, PTCA was performed, but the mitral insufficiency was not eliminated. Follow-up echocardiography disclosed rupture of the posterior papillary muscle. He underwent surgery on the 30th day after onset of acute myocardial infarction. Partial rupture of the posterior papillary muscle was found at surgery, and mitral valve replacement and single coronary artery bypass to Lcx were performed. His postoperative course was uneventful, and he was discharged on the 46th day after operation.

Aged↗
PubMed1982

[Morphology of 2 cardiomyocyte populations in the papillary muscles of the rat heart].

A light optic and quantitative electron microscope investigation has been performed in order to study papillary muscles in the rat heart. Certain quantitative differences have been revealed in the structure of the conducting and working myocardium. Innervation of the papillary muscles has been characterized. A new type of the conducting cardiomyocytes (IV) has been revealed which had not occurred in the composition of the sinuatrial and atrioventricular ganglia of the atrioventricular (His') bundle and its peduncles, their differences from other three types of the conducting cells revealed before are described. The data obtained are compared to morphological characteristics of the papillary cardiac muscles in other mammalian species.

Animals↗
PubMed1985

A histological study of surgical landmarks for the specialized atrioventricular conduction system, with particular reference to the papillary muscle.

Surgical landmarks of the conduction system were histologically evaluated in 29 cardiac specimens. The distribution of the system was grossly inherent to the type of ventricular septal defect as classified by Soto and coworkers, although it varied individually. The relationship of the right bundle branch (RBB) to the papillary muscles was of surgical interest. In defects unrelated to maldevelopment of the septum of the conus, the RBB passed beneath or slightly anterior to upper accessory papillary muscles (AcPMs) and posterior to the medial papillary muscle (MPM), regardless of the subtype of defect. In defects caused by maldevelopment, such as tetralogy of Fallot, it passed anterior to the MPM. Such data support the hypothesis that the RBB descends beneath or anterior to embryological upper AcPMs, whatever the morphological role may be, because of the supposedly independent developmental origin of the MPM and AcPMs. The relationship between the RBB and upper AcPMs appeared further modified by the attitude of the trabecula septomarginalis. Our improved clinical results have demonstrated that such information offers a gross but practical guide for prevention of conduction disturbances.

Aged↗
PubMed1984

Inotropic effect of amrinone in rabbit papillary muscle: reversal of the myocardial depressant effect of halothane.

In rabbit papillary muscles, the pronounced inotropic effect of amrinone (0.4-0.8 mg/mL) observed at low stimulation frequencies (0.1-0.5 Hz) diminished as the frequency was increased to 1.0-2.0 Hz. Reversal of the negative inotropic effect of halothane (1%) by amrinone (0.8 mg/mL) was similarly dependent on stimulation frequency. The contractile response to paired-pulse stimulation in the presence of amrinone (0.8 mg/mL) was summation rather than postextrasystolic potentiation. Amrinone (0.8 mg/mL) was not effective in reversing the negative inotropic effect of halothane (1%) on potentiated state contraction generated by paired-pulse stimulation. These results suggest that amrinone increases the influx of extracellular Ca2+ across the sarcolemma but not the availability of cellular Ca2+ which accumulates, most likely in sarcoplasmic reticulum, under the condition of potentiation.

Aminopyridines↗
PubMed1979

Papillary muscle rupture in fatal acute myocardial infarction: a potentially treatable form of cardiogenic shock.

Although cardiogenic shock in acute myocardial infarction is usually associated with a critical loss of myocardium, this may not be the case in papillary muscle rupture. During the past 21 years, 13 patients came to autopsy (11 died in cardiogenic shock) with a papillary muscle rupture complicating myocardial infarction. Rupture occurred from 2 to 7 (mean, 4) days after the infarct, and survival after rupture was usually brief (median, 3 days). The infarct involved between 1% and 50% (mean, 19%) of the left ventricle, and in 10 it was less than 25%. In all instances myocardium around the mitral annulus was not infarcted. Because papillary muscle rupture occurred mostly with first infarcts (eight), involved relatively small areas of necrosis, and spared the myocardium surrounding the annulus, early mitral valve replacement should make this cause of fatal acute myocardial infarction one of the most treatable forms of cardiogenic shock.

Acute Disease↗
PubMed1987

Characterization of the class I antiarrhythmic activity of cibenzoline succinate in guinea pig papillary muscle.

The effects of cibenzoline on transmembrane action potentials were examined in guinea pig papillary muscle. Cibenzoline (1-128 microM) did not alter the action potential durations at 50 and 90% of repolarization, the effective refractory period or the ratio of effective refractory period to action potential duration at 90% of repolarization. Likewise, the maximum diastolic potential was virtually unaffected. Cibenzoline depressed the maximum rate of rise of phase 0 (dV/dtmax). This effect was dependent on the rate of stimulation and occurred at a relatively low concentration (2 microM). The onset of use-dependent depression was monoexponential and dependent on the drug concentration, as well as the rate of stimulation. The rate of recovery from use-dependent depression also followed a single exponential time course but was independent of drug concentration and stimulation rate. When cibenzoline and lidocaine were combined in the tissue bath, dV/dtmax recovered with a double exponential time course. The first and second components of this recovery corresponded to the time course observed with lidocaine (first) and cibenzoline (second) alone. Also, the magnitude of the second component was less with the combination than with cibenzoline alone, indicating an interaction between the two drugs. In addition, cibenzoline shifted the curve relating normalized dV/dtmax to membrane potential in the hyperpolarizing direction. Finally, cibenzoline did not alter slow-response action potentials induced by elevated [K]o and isoproterenol. The authors conclude that cibenzoline acts as a class la antiarrhythmic agent in guinea pig papillary muscle.

Action Potentials↗
PubMed1992

Effects of ouabain, DBcAMP, caffeine, and high [Ca2+]o on twitch tension, intracellular Na+ activity, and action potential of guinea pig papillary muscles.

To explore ionic mechanisms of the positive inotropic process in guinea pig ventricular papillary muscles, we simultaneously measured twitch tension, intracellular Na+ activity (aiNa) and action potential at a stimulus rate of 60/min. The aiNa was 5.0 +/- 0.1 mM in the steady state. When the Na-K pump was inhibited by ouabain (1 microM), the twitch tension was increased in proportion to the aiNa, and the action potential was decreased at diastolic state and at duration for 90% of repolarization (APD90). While exposed to caffeine (3 mM), the aiNa kept increasing even when the twitch tension achieved a peak level. Concomitantly, the action potential slightly depolarized at diastolic state with a prolonged APD90. An application of DBcAMP (1 mM) or an increase in [Ca2+]o (from 1.8 to 3.6 mM) enhanced the twitch tension with a fall of aiNa and a shortening of APD90. These results suggest that in guinea pig papillary muscles Na-Ca exchange plays an important role in the regulation of contractile force and membrane potential, and that the Na influx should be balanced by the activation of the sarcolemmal Na-K pump, a negative feedback mechanism, to prevent calcium overload and abnormal pacemaker activity in electrical excitation.

Action Potentials↗