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PubMed1987

Performance of papillary muscles from the aging spontaneously hypertensive rat: temporal changes in isometric contraction parameters.

Myocardial mechanics in the male spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) at 18 months of age were studied. Left ventricular hypertrophy was documented in the SHR by an increase in left ventricle/body weight and left ventricle/tibial length ratios when compared to the WKY (P less than 0.001). Isolated left ventricular papillary muscles were studied at 28 degrees C while contracting 12 times/min at the apex of the length-tension curve. Active and passive length-tension relations were measured at relatively early (65 +/- 3 min) and late (200 +/- 5 min) times following sacrifice. No significant differences in passive length-tension relations between strains were observed. Between early and late measurements, a significant decrease in passive tension within the length spectrum 89-100% Lmax occurred in both SHR and WKY, accompanied by a significant increase in passive stiffness (P less than 0.01, SHR; P less than 0.001, WKY). Isometric performance was measured at relatively early (81 +/- 3 min) and later (190 +/- 5 min) times following sacrifice. Strain differences in active muscle performance were of a greater electromechanical delay time (EMD) (P less than 0.05, early: P less than 0.001, late) and time-to-peak tension (TPT) (P less than 0.001, late) in SHR compared to WKY. Between early and late measurements, decreases in EMD (P less than 0.01, SHR; P less than 0.001, WKY), TPT (P less than 0.001; P less than 0.001), the half-time of relaxation (P less than 0.001; P less than 0.001), and the resting tension (P less than 0.01; P less than 0.001) were observed, and the maximum rate of fall of tension increased (P less than 0.01; P less than 0.01). We conclude that studies must be precisely referenced from the time of sacrifice of the animal in order to accurately evaluate the effects of experimental hypertrophy on isolated muscle performance. No evidence for the depression of papillary muscle isometric performance was seen in the 18-month SHR when compared to the WKY, although prolonged EMD and TPT were observed.

Aging↗

PubMed1982

Alterations in mechanical properties of rat papillary muscle during maturation.

Myocardial performance was measured during maturation using isolated left ventricular papillary muscles from female Wistar rats. Muscles were studied isometrically and isotonically, stimulated at 0.1 Hz, perfused with Tyrode solution having an external calcium concentration of 2.4 mM, and maintained at 30 degrees C. Heart and body weight increased rapidly during the first 6 mo and then stabilized. Peak isometric developed tension, time to peak isometric developed tension, and time to half relaxation increased substantially during the 1- to 10-mo period with little change in the peak rate of isometric tension rise and peak rate of isometric tension fall. No difference in resting tension was noted among any groups. Force-velocity curves from muscles from 2-, 6-, and 10-mo-old animals show a significant age-related decrease in the isotonic velocity of shortening by as much as 21% between 2 and 10 mo of age. Thus maturation profoundly affects the contractile state of cardiac muscle, with force of contraction increasing and velocity of shortening decreasing as a function of age in the rat.

Aging↗

PubMed1996

Force-relaxant actions of dimethyl sulfoxide on guinea-pig and rabbit papillary muscles.

Recent voltage-clamp analysis of dimethyl sulfoxide (DMSO: 0.1-10% v/v) action on membrane currents in guinea-pig ventricular myocytes (strong inhibition of delayed-rectifier K+ current, inhibition of Na+ pump current, little effect on L-type Ca2+ current) suggested that the solvent would have a strong positive inotropic effect on guinea-pig papillary muscles. In muscles driven at 1 Hz, the major effects of 30 min superfusion with hyperosmotic 10% DMSO were: (1) a 33% lengthening of the action potential duration; (2) a 23% depression of developed tension; and (3) a pronounced positive inotropy on washout of the solvent. Osmotic change in cell volume was a possible reason for these effects; however, hyperosmotic sucrose solution that shrunk myocyte volume by a DMSO-like 12% failed to elicit the DMSO response. It was postulated that DMSO has both stimulatory and inhibitory actions: during treatment the stimulatory component (Ca2+ accumulation due to action potential lengthening and Na+ pump inhibition) is masked by a concomitant inhibition of Ca(2+)-myofilament interaction; removal of the solvent reveals the Ca2+ overload. In support of this interpretation. (1) DMSO depressed developed tension by up to 85% when the stimulatory influence was attenuated by eliminating action potential lengthening (rabbit papillary muscles), relieving pump inhibition (elevated K+), or preloading Ca2+ (low-K+ or low-Na+ superfusate), and (2) DMSO relaxed Na(+)-free contractures, and nearly abolished caffeine-induced contractures, in quiescent guinea-pig muscles. These data suggest that DMSO has a reversible, powerful inhibitory action on the myofilament force-generating machinery.

Action Potentials↗

PubMed1980

Effect of damaged ends in papillary muscle preparations.

The mechanical characteristics of the central segment of isolated cat papillary muscle were determined with recently developed equipment. Two small sharpened stainless steel pins, inserted transversely through the muscle, were used to mark the ends of a segment not damaged by attachments. Installation of the pins did not affect the performance of the muscle. The distance between the pins was measured and controlled to produce isometric and afterloaded isotonic contractions of the segment of the muscle between the pins. Data from such contractions were compared with traditional whole muscle measurements made on the same preparation. The isometric length-tension curve of the central segment was significantly higher than that of the whole muscle, and there was no plateau of developed force at long lengths in five of six muscles studied. In the resting state, the segment was more compliant than the whole muscle for physiologic lengths and much stiffer for longer lengths. Segment velocity and shortening were significantly higher than whole muscle velocity and shortening at comparable loads.

Animals↗

PubMed1993

Acute myocardial infarction with papillary muscle rupture.

The subject of this report is a 57-year-old obese, hypertensive woman who had been well until the onset of severe chest pain and hypotension. She had to be defibrillated four times on her way to the hospital. The diagnosis of acute inferior-posterior infarction was made by electrocardiogram (ECG) and there was a markedly elevated serum creatine kinase (CK) (including the MB fraction). The patient had a very low cardiac output and ejection fraction. A lung scan revealed possible pulmonary embolism for which she was anticoagulated. She remained hypotensive and hypoxemic and, on Day 17 of her hospital stay, she had a bout of severe dyspnea. A new systolic murmur was heard and the clinical diagnosis of ruptured papillary muscle was made and confirmed by echocardiography, and later at autopsy. All three coronary arteries were severely atherosclerotic and, in addition, the right coronary artery was completely closed by a thrombus. This case clearly illustrates the major pathological changes in the heart that correlate with the clinical findings in patients with a myocardial infarct that is complicated by left ventricular papillary muscle rupture. The pathophysiological effects of this condition, as illustrated in this case report, include the following:1. The posterior papillary muscle wa s almost completely separated from its base, with only a thin strip of muscle intact. The mistral valve thus was insufficient (a "flail valve''); this markedly reduced the ejection fraction of the left ventricle, increased its end-diastolic volume and pressure, produced a damming of blood in the pulmonary circulation, and this resulted in the pulmonary edema seen on the chest x-ray.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗

PubMedDate not supplied

Effects of histamine H1 receptor antagonists on action potentials in guinea-pig isolated papillary muscles.

The effects of histamine H1 receptor antagonists (H1 antagonists) on action potentials in guinea-pig isolated papillary muscles were examined using a microelectrode technique. Terfenadine (0.03 microM) prolonged the action potential duration at 90% repolarization, without affecting the resting membrane potentials, the action potential amplitude or the maximal upstroke velocity, although its metabolite, terfenadine carboxylate, did not affect any action potential parameters. Astemizole, (+)-chlorpheniramine, and clemastine prolonged the action potential duration at 90% repolarization at 0.03, I and 10 microM, respectively. The action potential duration-prolonging effects of terfenadine and astemizole correspond to the reverse use-dependence phenomenon. However, ebastine and its metabolite, carebastine, did not affect the action potential parameters at 3 microM. Mequitazine, diphenhydramine, epinastine, ketotifen and oxatomide were also without effect at 10 microM. These H1 antagonists suppressed the histamine-induced contractions in guinea-pig isolated ileum longitudinal muscles. However, the potency order was inconsistent with that for prolonging the action potential duration. Terfenadine or astemizole prolonged the action potential duration at concentrations lower than each IC50 value for H1 receptor antagonism. Cimetidine, a H2 receptor antagonist, and thioperamide, a H3 receptor antagonist, had little effect on the action potentials. These results suggest that, in guinea-pig isolated papillary muscles, blockade of histamine receptors does not cause prolongation of the action potential duration, leading to prolongation of electrocardiographic QT intervals, and that H1 antagonists may be classified into three groups: (1) drugs causing prolongation of the action potential duration at concentrations producing H1 antagonism and (2) at concentrations higher than those producing H1 antagonism, and.

Action Potentials↗

PubMed2003

Acute and specific collagen type I degradation increases diastolic and developed tension in perfused rat papillary muscle.

Collagen degradation is suggested to be responsible for long-term contractile dysfunction in different cardiomyopathies, but the effects of acute and specific collagen type I removal (main type in the heart muscle) on tension have not been studied. We determined the diastolic and developed tension length relations in isometric contracting perfused rat papillary muscles (perfusion pressure 60 cmH(2)O) before and after acute and specific removal of small collagen struts with the use of purified collagenase type I. At 95% of the maximal length (95%L(max)), diastolic tension increased 20.4 +/- 8.1% (P < 0.05, n = 6) and developed tension increased 15.0 +/- 6.7% after collagenase treatment compared with time controls. Treatment increased the diastolic muscle diameter by 7.1 +/- 3.4% at 95%L(max), whereas the change in diameter due to contraction was not changed. Diastolic coronary flow and normalized coronary arterial flow impediment did not change after collagenase treatment. Electron microscopy revealed that the number of small collagen struts, interconnecting myocytes, and capillaries was reduced to approximately 32% after treatment. We conclude that removal of the small collagen struts by acute and specific collagen type I degradation increases diastolic and developed tension in perfused papillary muscle. We suggest that diastolic tension is increased due to edema, whereas developed tension is increased because the removal of the struts poses a lower lateral load on the cardiac myocytes, allowing more myocyte thickening.

Animals↗

PubMedDate not supplied

Papillary muscle rupture following nonpenetrating chest trauma: report of a case with hemodynamic and serial echocardiographic findings and successful surgical treatment.

The pre- and postoperative echocardiographic features of a patient with severe mitral incompetence due to rupture of a papillary muscle following nonpenetrating chest trauma are presented. The mitral valve echocardiogram showed chaotic diastolic flutter suggestive of a ruptured papillary muscle or ruptured chordae tendineae. The preoperative ultrasound recording of the left ventricle revealed left ventricular enlargement and excessive motion of the interventricular septum. The echocardiogram taken 7 weeks after mitral valve replacement showed considerable regression of the left ventricular enlargement.

Adult↗

PubMed2006

[Case of papillary muscle rupture diagnosed by preoperative transesophageal echocardiography].

A 46-year-old man with severe mitral regurgitation (MR) was scheduled for emergency surgery for chordae tendae repairment. Preoperative transesophageal echocardiography (TEE) revealed massive MR due to a rupture in the antero-lateral papillary muscle. We changed the operation procedure to mitral valve replacement. It is difficult to diagnose papillary muscle rupture. Therefore, we should perform TEE on the patient with acute MR of unknown origin.

Echocardiography, Transesophageal↗

PubMed1974

The actions of a new beta-adrenoceptor blocking drug, ICI 66082, on the rabbit papillary muscle and on the dog heart.

1 The actions of 4-(2-hydroxy-3-isopropylaminopropoxy) phenyl acetamide (ICI 66082), a new beta-adrenoceptor blocking drug, on the twitch response of the isolated papillary muscle of the rabbit and on dP/dt max and free heart rate of a denervated dog heart preparation, are described.2 ICI 66082 (up to 1 mg/ml) did not produce any depression of the twitch response of the rabbit papillary muscle. ICI 66082 antagonized the action of isoprenaline on this preparation at a concentration of 0.01 mug/ml.3 ICI 66082 (0.5-1.0 mg/kg intravenously) reduced the control value of dP/dt max in four dog preparations by a mean value of 529 mmHg/s (s.e. mean +/- 139 mm Hg/s), with no significant change in free heart rate. Antagonism of the effect of isoprenaline on dP/dt max and on free heart rate was demonstrated with ICI 66082 (0.1 mg/kg).4 ICI 66082 (1.0-1.5 mg/kg) produced no significant changes in dP/dt max or in free heart rate in four dogs pretreated with reserpine. A significant reduction (16% of the control value) in dP/dt max was observed with ICI 66082 at a high dose of 40-50 mg/kg.5 It is concluded that ICI 66082 is a competitive antagonist against the actions of isoprenaline on cardiac muscle, has no negative inotropic action (unless the dose exceeds 40 mg/kg) and lacks intrinsic sympathomimetic activity.

Acetamides↗

PubMed1996

[Papillary muscle rupture during subaortic membrane balloon dilatation].

A 37 year-old female patient underwent catheter-balloon dilation for discrete subaortic stenosis. During the procedure severe mitral regurgitation was produced requiring emergency surgery. Transesophageal and intraoperative findings were posteriormedial papillary muscle rupture. Retrospective viewing of the cineangiogram during balloon inflation revealed distal balloon indentation, corresponding to the injured papillary muscle. This severe complication of the left ventricular outflow tract angioplasty should be avoided by careful positioning of the guidewire and balloon before inflation.

Adult↗

PubMedDate not supplied

Stress as an index of metabolic cost in papillary muscle of the cat.

Active stress, stress-time integral (STI) and total heat production of cat right ventricular papillary muscles were recorded during brief trains of isometric twitch contractions at muscle lengths less than or equal to optimal length. Individual muscles were subjected to a 10 degree C change in temperature, a change of stimulus frequency and the addition of isoprenaline sulphate (10(-7) mol. 1(-1). The STI-heat and stress-heat data were subjected respectively to linear and quadratic regression analyses. For both relations, the intercept (stress-independent heat) was unaffected by the frequency change, doubled by the temperature decrease and trebled by the addition of isoprenaline. None of the treatments had a significant effect on the first or second order coefficients of the stress-heat relation. The slope of the STI-heat relation was halved by lowering the temperature, increased 50% by the addition of isoprenaline and unaffected by stimulus frequency. Thus the energetic cost of a given stress increment was constant across conditions while that for a given STI increment was not. Stress is the better mechanical index of myocardial energy cost when the inotropic state is changing.

Animals↗

PubMed2003

Effect of amiodarone on the dynamics of mechanical restitution of rat papillary muscles.

We studied the effect of amiodarone (class III antiarrhythmic drug) on the dynamics of mechanical restitution of rat papillary muscle. Amiodarone produced a weak negative inotropic effect and stimulated potentiation of contractility of the muscle preparation after short-term (4-60 sec) cessation of its electrical stimulation. On the other hand, the time of attaining half-maximum amplitude of contractions after amiodarone treatment did not differ from the control. Analysis of curves presenting the drop of potentiation of muscle preparation contractility after resumption of regular electrical stimulation after 60-sec arrest until attaining a stable level showed that the amplitude returned to the initial level by the 9thcontraction-relaxation cycle both in the control and after amiodarone treatment. Coefficient of the drop of contraction amplitude potentiation was virtually the same in the two groups. Presumably, amiodarone does not modulate calcium-binding capacity of the sarcoplasmic reticulum, but improves Ca retention in the sarcoplasmic reticulum stores.

Amiodarone↗

PubMed1994

Utilization of an isolated, blood-perfused canine papillary muscle preparation as a model to assess efficacy and adversity of class I antiarrhythmic drugs.

To develop a model to predict the efficacy and adversity of class I antiarrhythmic drugs, intraventricular conduction time (IVCT), coronary blood flow (CBF), developed tension of papillary muscle (DT) and idioventricular automaticity rate (VR) were measured following drug administration in an isolated canine papillary muscle preparation cross-circulated with the heparinized blood of a donor dog. Tetrodotoxin, the prototypic fast Na+ channel blocker, and class I drugs increased IVCT and CBF, but decreased DT and VR, in a dose-dependent manner. The profiles of known class I drugs, procainamide, disopyramide, lidocaine, mexiletine and flecainide were similar, but the potencies of each drug were different. Two new class I drugs, ME3202 and AN-132, were also tested and found to have effects that were similar to that of tetrodotoxin. There was a good correlation between the doses of drugs prolonging IVCT by 50% and the canine antiarrhythmic plasma concentrations in our previous study. This model can also be used to estimate the use-dependency and the kinetics of use-dependent sodium channel block; however, it is not suitable for extensive investigation of cellular and molecular mechanisms. Thus, the use of this model facilitates the comparison of multiple cardiac effects of class I drugs and may be an effective way to better assess new antiarrhythmic drugs.

Animals↗

PubMed1990

Changes in the ionic environment may alter the kind of antagonism of some histamine H2-receptor blockers in the guinea pig papillary muscle.

The effect of changes in the composition of the bathing medium on the effect of histamine and histamine H2-receptor antagonists was investigated in the isolated guinea pig papillary muscle. Ringer or Krebs-Henseleit solutions were used as nutrient fluids. They mainly differed with respect to pH and to Mg2+ and H2 PO4- content. Whereas the effect of histamine was not altered by ionic changes, the antagonism by some H2 blockers was different in the two nutrient solutions. The insurmountable antagonism elicited by high concentrations (greater than or equal to 10(-6) M) of famotidine, oxmetidine and mifentidine in Ringer solution was converted to surmountable when these drugs were tested in Krebs-Henseleit solution. Conversely, the antagonism induced by ranitidine was surmountable in both solutions, and that induced by high amounts of Ioxtidine was insurmountable in both nutrient fluids. Results obtained in Ringer solution were not modified by pH adjustments or by the addition of ions present in Krebs-Henseleit medium. These results suggest that the interaction of histamine with H2 receptors in the guinea pig papillary muscle was not influenced by alterations in the ionic composition of the nutrient fluid, whereas the antagonism may be critically dependent on the ionic environment.

Animals↗

PubMedDate not supplied

Manipulation of papillary muscle cyclic nucleotides during anoxia-reoxygenation: effects on contractility.

Endogenous nitric oxide and the accompanying cGMP formation has been postulated to play a role in the pathophysiology of myocardial anoxia-reoxygenation. A direct relationship between cGMP and the alterations observed in contractility under these conditions has never been demonstrated. In this study, cGMP in rat papillary muscles during anoxia and reoxygenation was correlated with mechanical function. Isolated papillary muscles were stimulated continuously and made anoxic for 40 min after a 2-hour stabilisation period. Anoxia caused an abbreviated contraction curve by decreasing the maximum contraction strength, time to peak contraction and relaxation time, accompanied by a significant decrease in tissue cGMP and cAMP levels (controls: 29.09 +/- 1.62 and 568.8 +/- 35.65; anoxia:16.62 +/- 1.51 and 403.3 +/- 30.19 pmoles/gww), which partially returned to pre-anoxic values upon reoxygenation. cGMp levels were significantly elevated by addition of 8-Br-cGMP (a cGMP analogue), but this elevation (154.4 +/- 20.89 pmoles/gww), had no effects on the contractility pattern of muscles during normoxia, anoxia or reoxygenation, suggesting that in isolated ventricular muscle, cGMP levels play a minor role in regulating muscle contractility.

Animals↗

PubMed1993

Implication of ATP released from atrial, but not papillary, muscle segments of guinea pig by isoproterenol and forskolin.

Effects of isoproterenol and forskolin, which increases intracellular cyclic AMP, on contraction and ATP release in atrial and papillary muscles of guinea pig were evaluated. In the electrically driven-left atrial muscle segments, isoproterenol and forskolin at 0.1 microM produced an ATP release coupled with a positive inotropic effect, the values of net ATP release at 5 min after these drugs being 5.20 +/- 0.59 and 5.37 +/- 0.55 nmoles/g wet weight, respectively. The forskolin evoked-ATP release was unaffected by prazosin plus propranolol or by guanethidine, implying that ATP is released from non-neuronal origin. In contrast, in papillary muscle segments, the test cardiotonics did not elicit any ATP release despite producing contractile response similar to that in atrial preparations. However, there is no difference in ectoATPase activities of both tissues. Adenosine added exogenously inhibited electrically evoked-contraction of the atrium, but not that of the papillary, although inhibitions by verapamil of the contractions were approximately equal in these preparations. These findings suggest that cardiotonics such as isoproterenol produce a liberation of ATP from auricle muscles, but not from ventricle muscles, and that the liberated ATP may mainly be catabolized to adenosine by ectoenzymes and the resultant nucleoside may serve as a functional modulator through stimulation of pre or postsynaptic A1-receptors.

Adenosine↗

PubMedDate not supplied

Studies on the mechanism of the positive inotropic effect of piroximone in cat papillary muscle.

The mechanism of the inotropic effect of piroximone HCl [MDL 19205A, 4-ethyl-1,3-dihydro-5-(4-pyridinylcarbonyl)-2H-imidozol-2-on e HCl] was studied in the cat papillary muscle paced electrically in vitro. Piroximone produced a concentration-dependent positive inotropic effect accompanied by an increase in rate of contraction and rate of relaxation, but abbreviated time to peak tension and relaxation time. The positive inotropic effect produced by piroximone was antagonized by carbachol, 3 X 10(-6) M, whereas that produced by increasing calcium concentration was not affected by carbachol. In potassium chloride (22 mM) depolarized muscle, piroximone restored contractility, which was not affected by propranolol (10(-6) M) or by tetrodotoxin (2 X 10(-5) M), but was inhibited by nifedipine (10(-7) M). Piroximine also elevated tissue cyclic AMP (cAMP) content in the papillary muscle. Although nifedipine inhibited the restoration of contractility, it did so without altering the increase of cAMP produced by piroximone. These results suggest that piroximone causes an increase in calcium influx that is mediated by an increase in cAMP, and the results are consistent with the hypothesis that specific inhibition of the high affinity cAMP phosphodiesterase (PDE III) plays a role in the positive inotropic effect of piroximone.

1-Methyl-3-isobutylxanthine↗