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At least 649 records · Page 36Linked to original sources
PubMed1987

Heat production and oxygen consumption following contraction of isolated rabbit papillary muscle at 20 degrees C.

The time course of oxygen uptake following isometric twitch contractions of isolated rabbit papillary muscles was measured using a polarographic oxygen electrode. Using a diffusion model we eliminated the effect of oxygen storage on the measured time course of oxygen uptake to determine the time constant of mitochondrial "off" kinetics. Two different approaches were followed. In Method 1, two steady-state levels were compared, whereas in Method 2, the time course of mitochondrial "off" kinetics was studied. Using Method 1 we found tau = 20 +/- 8 seconds (n = 7), whereas Method 2 yielded tau = 26 +/- 9 seconds (n = 11). These findings were compared with preliminary measurements of recovery heat production of the same preparation and at the same temperature. Heat produced after a train of 10 twitch contractions appeared to follow a monoexponential time course with a time constant of 24.9 +/- 9.5 seconds (n = 9). These results suggest that aerobic metabolism in isolated rabbit papillary muscle constitutes the only recovery process.

Animals↗
PubMed1981

Visualization of hypertrophied papillary muscle mimicking left ventricular mass on gated blood pool and T1-201 myocardial perfusion imaging.

A sixty-year old man with acute myocardial infarction was incidentally found to have a hypertrophied anterolateral papillary muscle (ALPPM) of the left ventricle on gated blood pool (GBP) and T1-201 myocardial perfusion images. Hypertrophy of the ALPPM was visualized as a movable defect in the lateral basal area on GBP imaging throughout the cardiac cycle and on the TI-201 study as a radionuclide accumulating structure, consistent with the defect in the GBP. A combination of these findings may suggest the presence of a hypertrophied papillary muscle of the left ventricle.

Cardiomyopathies↗
PubMed1987

Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction.

Permanent coronary occlusion produces time-dependent changes in surviving subendocardial cellular properties. We compared the functional alterations in Purkinje (P) and ventricular muscle (VM) activation early (24 hr) and late (4 weeks or greater) after permanent coronary occlusion in an in vitro preparation of canine papillary muscle. High-density extracellular (1 to 2 mm resolution) and selected intracellular recordings were made in five animals early and seven animals late during stimulation of a free-running P strand. Activation patterns of P and VM layers from ischemic and unaffected papillary muscles were compared in the same animal. Average P layer conduction velocity was determined in normal and ischemic regions with the use of a linear array of recording and stimulating electrodes. Purkinje activation was altered little in the early phase of infarction, while healing was associated with a generalized 25% reduction in P layer conduction velocity and localized block and fragmentation of P waveforms. Intracellular recordings at sites of nonsynchronous P activation revealed electrotonic interaction between cell groups. At 24 hr, small groups of VM were present but with abnormal activation patterns in regions of necrosis with fragmented and delayed extracellular waveforms produced by partially uncoupled groups of cells. Local delay and block could be modulated by rate and site of stimulation. After healing, VM activation abruptly stopped at the visual infarct border, marked by a characteristic "end potential." These studies demonstrate important differences in the functional attributes of the P and VM layers studied early and late after coronary occlusion. Alterations in cell-to-cell relationships are likely very important in determining abnormalities of activation in both settings.

Animals↗
PubMed1987

Dynamic stiffness measured in central segment of excised rabbit papillary muscles during barium contracture.

The dynamic mechanical behavior of excised rabbit papillary muscles that had been tonically activated by replacing bathing Ca2+ with Ba2+ was studied. Steady activation was used to visualize the dynamic behavior of cardiac myofilaments more clearly than is possible during twitches, which are complicated by the kinetics of excitation-contraction coupling. To avoid artifacts due to damaged ends of the muscle, the length of a central segment, which was defined by 2 tungsten pins inserted through the muscle, was measured. To test the mechanical behavior of the contractured muscles (at 24 degrees C), the central segment length was sinusoidally oscillated (amplitude 1%) at 15 different frequencies (0.05-30 Hz). The dynamic stiffness of the central segment was calculated from the ratio of force response amplitude to length perturbation amplitude. At low frequencies (below 0.4 Hz), stiffness was approximately constant and reflected the force-length relation. However, in a localized range near 1 Hz, there was a distinct drop in the magnitude of dynamic stiffness to approximately half its low-frequency baseline. This range may reflect the dynamics of attachment and detachment of force generators. The frequency of minimum stiffness was consistent among all muscles (1.3 +/- 0.3 Hz). Moreover, no significant change in this frequency was found over the examined range of lengths (90-100% of the segment length that produced maximal developed force) and activation levels (Ba2+ concentration 0.3-1.0 mM). From 2 to 8 Hz, dynamic stiffness appeared to reflect force-velocity properties, but at higher frequencies, another elastic property emerged. At 30 Hz, stiffness was proportional to force, with an apparent series elasticity less than 1.8%. Even though the muscles had only moderate longitudinal inhomogeneity, quantitatively significant (35%) errors would have been introduced had the study relied on total muscle length instead of central segment length.

Animals↗
PubMed1977

Cineangiographic diagnosis of papillary muscle involvement in rheumatic mitral stenosis.

Left ventricular cineangiography was performed in 25 patients with normal mitral valves and in 49 patients with rheumatic mitral valve disease to estimate the spatial relations between the mitral valve leaflets and papillary muscles. The findings in the pathologic group were compared with observations at operation or with the excised mitral valves. It is concluded that fusion of the papillary muscles with the mitral valve leaflet or severe shortening of the chordae is predicted with a reasonable accuracy preoperatively by means of left ventricular cineangiography. The surgical implications are discussed.

Angiocardiography↗
PubMed1989

Inotropic and chronotropic effects of N6-substituted derivatives of cyclic AMP as assessed in guinea-pig isolated right atria and papillary muscle.

1. The inotropic and chronotropic actions of N6-substituted adenosine 3':5'-cyclic monophosphate (cyclic AMP) derivatives (N6-R cyclic AMPs) were studied in guinea-pig isolated right atrial preparations and in the papillary muscle preparations from guinea-pig right ventricle. 2. All the N6-R cyclic AMPs except N6-C14H29 produced positive inotropic effects in papillary muscle. The C5H11, C6H13, C7H15, C8H17 and C9H19 compounds were the most potent as inotropic agents, the potency being lower with compounds having longer or shorter N6-side chains than these. 3. In right atria N6-C2H5-C7H15 cyclic AMPs produced negative chronotropic effects. However, after treatment of the preparations with 8-phenyltheophylline the negative chronotropic effects were either much attenuated or abolished, indicating the involvement of adenosine receptors. 4. All the N6-R cyclic AMPs except N6-C14H29 were more potent activators of bovine myocardial protein kinase than cyclic AMP. The partition coefficients between octanol and an aqueous phase of N6-R cyclic AMPs became greater as the numbers of carbon atoms increased, and there appeared to be a relationship between partition coefficient and inotropic potency. It was concluded that membrane penetrativeness rather than potency as activators of protein kinase determined the potencies of N6-R cyclic AMPs as positive inotropic agents. 5. Derivatives such as N6-C7H15 cyclic AMP, which have positive inotropic activity without any marked negative chronotropic effect, may be useful as cardiotonic agents in heart failure.

Animals↗
PubMed1981

Multiple effects of putative alpha-adrenoceptor agonists on the electrical and mechanical activity of guinea-pig papillary muscle.

The effects of the putative alpha-adrenoceptor agonists phenylephrine, methoxamine and clonidine on force of contraction and on calcium-dependent action potentials were studied in guinea-pig papillary muscles. Phenylephrine increased the force of contraction by stimulating alpha-adrenoceptors as well as beta-adrenoceptors. It increased the amplitude and duration of slow action potentials, but this effect was exclusively due to stimulation of beta-adrenoceptors. The positive inotropic effect mediated by alpha-adrenoceptors can presumably not be explained by an increase in calcium influx during the action potential via the slow inward current. Methoxamine had no effect on the force of contraction at 10(-5) and 10(-4) mol/l, but at 10(-4) mol/l it slightly decreased amplitude and duration of slow action potentials. Clonidine produced a large increase in force of contraction and in amplitude and duration of slow action potentials. These effects were due to stimulation of H2-histamine receptors. It is concluded that in guinea-pig papillary muscle the tested putative alpha-adrenoceptor agonists do not share a common alpha-adrenoceptor effect, but produce prominent effects which are mediated through either beta-adrenoceptors (phenylephrine), or H2-histamine-receptors (clonidine) or are non-specific (methoxamine) in nature.

Action Potentials↗
PubMed1995

Contractile function of papillary muscles with carbonic anhydrase inhibitors.

Contractile parameters of directly stimulated rabbit papillary muscles were studied during incubation in baths containing the carbonic anhydrase inhibitors chlorzolamide (1*10(-3) M) or ethoxzolamide (1*10(-4) M). Both inhibitors caused an at least partly reversible decrease in isometric force as it has been observed in skeletal muscle, and--in contrast to the results in skeletal muscles--a decrease in time-to-peak and half-relaxation time. It is postulated that inhibition of the membrane-bound carbonic anhydrase of heart muscle might induce an intracellular acidosis and that this acidosis causes the observed effects on contractile parameters.

Animals↗
PubMed2004

Long-term outcome after mitral valve replacement with preservation of continuity between the mitral annulus and the papillary muscle in patients with mitral stenosis.

BACKGROUND AND AIM OF THE STUDY: The effect on left ventricular performance of mitral valve replacement (MVR) with preservation of continuity between the mitral annulus and papillary muscle was studied in patients with mitral stenosis (MS). METHODS: Forty patients with MS who underwent MVR between 1986 and 1995 and had long-term echocardiographic follow up were studied retrospectively. Eighteen patients had conventional MVR (CMVR group), and 22 (PMVR group) had either preservation of autologous chordae tendineae (n = 6) or replacement of the chordae with expanded polytetrafluoroethylene sutures (n = 16). RESULTS: Preoperatively, there were no significant differences between the two groups in age, body surface area, left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), fractional shortening (FS) or ejection fraction (EF). At 3.1-6.5 years after surgery, periodic echocardiography showed significant differences (p <0.05) in LVESD (35.8 versus 31.6 mm, respectively, in the CMVR and PMVR groups) and FS (31.8% versus 38.1%). At 6.6-9.7 years postoperatively, no significant differences were observed between the two groups in FS, but LVESD was significantly greater in the CMVR group than in the PMVR group (37.3 versus 31.5 mm). CONCLUSION: In the long term, MVR with preservation of continuity between the mitral annulus and papillary muscle improves systolic left ventricular performance in patients with MS.

Aged↗
PubMed2002

Effect of class III antiarrhythmic preparation nibentan on extrasystolic and post-extrasystolic contraction of rat papillary muscle.

The effect of nibentan (2.5 and 25 muM) on extrasystolic and post-extrasystolic contraction of isolated and perfused papillary muscle was studied. The muscle contracted in an isometric regimen at a rate of external electrical stimulation of 0.5 Hz in a temperature-stabilized chamber (36.0+0.5 degrees C). The extrasystolic contraction was induced with an extra electrical pulse applied 0.25 sec after the regular stimulus. Nibentan decreased the amplitude of extrasystolic contraction in a dose-dependent manner. At the same time, the effect of nibentan on extrasystolic contraction practically did not depend on its concentration. It is concluded that nibentan produces a dose-dependent effect on excitability of rat ventricular myocardium, and in parallel improves calcium-accumulating capacity of the sarcoplasmic reticulum in cardiomyocytes.

Animals↗
PubMed1991

The effects of halothane, enflurane, and isoflurane on the length-tension relation of the isolated ventricular papillary muscle of the ferret.

The effects of halothane, enflurane, and isoflurane on the length-tension relation were investigated in papillary muscles of the right ventricle of adult male ferrets at 30 degrees C. Isometric twitch contractions were obtained at lengths ranging from the shortest length yielding the greatest active force development under isometric conditions (Lmax) to 86% of Lmax, in two consecutive protocols: first in [Ca2+]o ranging from 0.45 to 2.25 mM, and then in [Ca2+]o 2.25 mM before, during, and after exposure to incremental concentrations of halothane (n = 9 muscles), enflurane (n = 9 muscles), and isoflurane (n = 9 muscles), each in steps of 0.25 MAC to total concentrations up to and including 1.5 MAC. Each of the three anesthetics caused a concentration-dependent decrease in developed force. The relative extent of the negative inotropic effect was not different at various muscle lengths. Because myofibrillar Ca2+ responsiveness (Ca2(+)-affinity of troponin C) decreases at shorter muscle lengths, the results suggest that an alteration in myofibrillar Ca2+ responsiveness by volatile anesthetics is minor relative to the anesthetic-induced decreased intracellular Ca2+ availability in ventricular myocardium.

Animals↗
PubMedDate not supplied

Effects of quinidine on blood flow rate and developed tension in blood-perfused canine papillary muscle.

1. The effects of quinidine on blood flow rate and developed tension were studied in isolated, blood-perfused papillary muscle preparations of the dog. Drugs were injected into the anterior septal artery. 2. Quinidine caused a dose-related increase in blood flow rate; the mean dose producing a 100% increase in blood flow rate was about 0-3 mg. 3. Quinidine in doses of 0-01-0-1 mg produced a positive inotropic response. With 0-3--1 mg of quinidine the positive inotropic response was preceded by a transient negative inotropic response. With 3 mg there was a monophasic negative inotropic response, the developed tension being reduced by about 40% of control. 4. Propranolol had no statistically significant effects on the responses of the blood flow rate and developed tension caused by quinidine. 5. These results indicate that quinidine has an action on coronary vessels in lower doses than on the myocardium, and that in low doses it has a positive inotropic action rather than the well-known negative inotrophic action exerted with higher doses.

Animals↗
PubMed1984

Estimation of cardiodepressant potency of nadolol, alprenolol, propranolol and pindolol, beta-blocking agents, in heart-lung preparation and blood-perfused excised papillary muscle preparation of the dog.

Direct cardiodepressant potency of nadolol was determined by comparing its effect with those of alprenolol, propranolol and pindolol, in both heart-lung preparation and blood-perfused papillary muscle preparation of the dog. In the heart-lung preparation, mean 50% beta-blocking doses of the beta-blockers to inhibit the positive chronotropic action of isoproterenol were 3.75 micrograms for nadolol, 12.5 micrograms for alprenolol, 9.6 micrograms for propranolol and 1.6 micrograms for pindolol. Alprenolol and propranolol in a dose of 10 mg shifted the cardiac function curves rightward and downward, while nadolol and pindolol in the dose of 10 mg did not shift the cardiac function curves. In the blood-perfused papillary muscle preparation, mean 50% beta-blocking doses of the beta-blockers, administered i.v. to the donor dog, to inhibit the positive inotropic action of isoproterenol were 9.1 micrograms/kg for nadolol, 56.6 micrograms/kg for alprenolol, 68.3 micrograms/kg for propranolol and 8.1 micrograms/kg for pindolol. Nadolol did not depress the contractile force in doses up to 1 mg/kg given i.v. or doses up to 10 mg given intra-arterially (i.a.) close to the preparation. Alprenolol and propranolol exerted the dose-related negative inotropic effects, when larger doses (30-300 micrograms) were injected i.a. Thus, it is confirmed that nadolol virtually possesses no direct cardiodepressant activity and also that the depressant activity is exerted only by large doses of the other beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1983

Mitral valve replacement with preservation of papillary muscles and chordae tendineae - revival of a seemingly forgotten concept. I. Preliminary clinical report.

In 45 consecutive patients mitral valve replacement was performed leaving the posterior mitral leaflet and its chordal attachment to both papillary muscles intact (Lillehei's technique). Most patients showed moderate to severe pulmonary hypertension before surgery, 15 of the patients had double valve operations and 4 had a triple valve procedure. All patients survived and were discharged, the postoperative courses being remarkably uneventful with only very limited need of inotropic support in 3 patients and resumption of spontaneous respiration within the first 20 hours after the operation. The clinical courses in these patients seem to indicate that preserving the continuity between papillary muscles and mitral annulus in mitral valve replacement may improve left ventricular function at least early after surgery.

Adult↗
PubMed1988

Electrophysiological effects of amperozide in papillary muscles from ferrets, guinea-pigs and rabbits.

Amperozide, a novel psychotropic agent, in concentrations lower than 10 microM caused a homogenous prolongation only of the action potential in both guinea-pig and rabbit papillary muscle. In concentrations greater than or equal to 10 microM, amperozide caused a flattening of the action potential plateau and the later part of the repolarization phase became slower (longer), probably reflecting an impaired repolarizing Na-Ca exchange current. The overshoot (OS) and the rate of rise of the action potential (dV/dtmax) were depressed. It is concluded that amperozide has a blocking action on the transmembrane calcium current since Isi (second inward current), DIA (depolarization induced automaticity) and the peak force of contraction were depressed. The blocking of the Isi was use-dependent resembling the actions of calcium-antagonists like verapamil, except that it was less potent at equimolar concentrations. Amperozide in concentrations where it acted as an Isi-blocker (above 10 microM), had depressing effects only on ouabain-induced oscillatory events. No major differences in the effects of amperozide were apparent between guinea-pig, ferret or rabbit papillary muscles.

Action Potentials↗
PubMed1987

Effects of bile acids on ventricular muscle contraction and electrophysiological properties: studies in rat papillary muscle and isolated ventricular myocytes.

The effects of sodium salts of various bile acids on the contractile force and the electrophysiological properties of rat ventricular muscle were studied in vitro. Primary, conjugated, and secondary bile acids were studied in a concentration range of 10(-9)-10(-6) mol/l, which corresponds to concentrations found in the plasma of patients with cholestatic jaundice. In general, the bile acid induced a negative inotropic effect which was manifested as a reduction in active tension, maximum rate of tension activation, and maximum rate of tension relaxation. Twitch duration and time to peak tension were unaffected by the bile acids. The negative inotropism was associated with a reduction in ventricular action potential duration. Resting potential, action potential amplitude, and maximum upstroke velocity of phase 0 depolarization were unaffected. Voltage clamp experiments in rat ventricular myocytes demonstrated that sodium taurocholate decreased the slow inward current and slightly increased the outward potassium current. Hence, these effects on the membrane currents are probably responsible for the negative inotropic effect.

Action Potentials↗
PubMed1997

Mitochondrial function is not decreased in stunned papillary muscle at 20 degrees C.

It is unclear to what extent mitochondrial function in vivo is changed after brief anoxia. Heat measurements allow evaluation of mitochondrial function within intact cardiac muscle. Heat production was determined using fast metal-film thermopiles, during contraction and post-contractile recovery in control and stunned superfused rabbit papillary muscles at 20 degrees C. Heat rate was measured for a train of ten twitches (0.2 Hz) before anoxia and after 40 min anoxia followed by 2 h of normoxic recovery. During anoxia muscles were stimulated at 0.2 Hz (group A) or at 1.0 Hz (group B). A normoxic control group C was stimulated at 0.2 Hz. After 2 h recovery, tension was 77 +/- 5% (S.E.M.), 72 +/- 7% and 94 +/- 3% of initial values, for group A, B and C respectively, indicating stunning by anoxia. The economy of contraction or the ratio of recovery heat to initial heat did not change significantly in groups A and B when compared with control, indicating that stunning with this protocol is not associated with mitochondrial uncoupling. Post-contractile recovery heat initially decayed exponentially with time constant 24.9 +/- 2.2 s for all groups and with 22.7 +/- 1.1, 22.0 +/- 0.8 and 41.7 +/- 4.4 s at the end for group A, B and C respectively. The cause of the remarkable slowing of the recovery rate over time in controls is unknown, but is mimicked by blocking fatty acid utilization. No slowing of metabolic recovery is observed in the stunned papillary muscles. We conclude that stunning is not associated with a decrease in mitochondrial function or oxidative capacity in cardiac muscle.

Analysis of Variance↗