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[Replacement of the mitral valve with preservation of the posterior leaflet, papillary muscles and chordae tendineae].

The authors used in 11 patients with chronic mitral regurgitation Lillehei's method of replacement of the mitral valve by a mechanical valve preserving the posterior leaflet of the mitral valve, papillary muscles and chordae tendineae. None of the operated patients died. The authors proved marked functional improvement in the patients, reduction of the size of the left ventricle and left atrium, where by the ejection fraction did not change markedly. These results support the hypothesis that the continuity between the mitral anulus and the left ventricular wall through the valvular leaflet, chordae tendineae and papillary muscles assists the left ventricle on its systolic function.

Adult↗

Length-dependent calcium inotropism in cat papillary muscle.

We studied changes in the relationship of isometric developed force to muscle length when extracellular calcium concentration was altered in isolated cat papillary muscles. In two series of experiments at temperatures of 30 degrees C and 32 degrees C, and rates of 12 and 30 beats/min, 21 muscles were exposed to calcium concentrations of 1.125, 2.25 and 4.5 mM. Muscle lengths were varied between 80% and 100% of the length at which maximum developed force occurred (Lmax). Peak developed force and the time from stimulus to peak were measured. The data indicate that force is not altered proportionately at all lengths when calcium concentration is changed. Rather, we found that a substantially greater modification of force occurs at short lengths than at long lengths. Similarly, the time to peak force increases with length at a rate which is more than 4 times greater at the low calcium concentration than it is at the high concentration. Small but consistent shifts of Lmax also are seen. We observed that Lmax is longer when inotropic changes reduce force and shorter when force is increased. These results indicate that the inotropic effect of extracellular calcium concentration changes is dependent on muscle length.

Animals↗

Internal viscoelastic loading in cat papillary muscle.

The passive mechanical properties of myocardium were defined by measuring force responses to rapid length ramps applied to unstimulated cat papillary muscles. The immediate force changes following these ramps recovered partially to their initial value, suggesting a series combination of viscous element and spring. Because the stretched muscle can bear force at rest, the viscous element must be in parallel with an additional spring. The instantaneous extension-force curves measured at different lengths were nonlinear, and could be made to superimpose by a simple horizontal shift. This finding suggests that the same spring was being measured at each length, and that this spring was in series with both the viscous element and its parallel spring (Voigt configuration), so that the parallel spring is held nearly rigid by the viscous element during rapid steps. The series spring in the passive muscle could account for most of the series elastic recoil in the active muscle, suggesting that the same spring is in series with both the contractile elements and the viscous element. It is postulated that the viscous element might be coupled to the contractile elements by a compliance, so that the load imposed on the contractile elements by the passive structures is viscoelastic rather than purely viscous. Such a viscoelastic load would give the muscle a length-independent, early diastolic restoring force. The possibility is discussed that the length-independent restoring force would allow some of the energy liberated during active shortening to be stored and released during relaxation.

Animals↗

Procaine enhancement of the rapid cooling contracture and inhibition of the decay of potentiated state in rabbit papillary muscle.

We tested the possibility that inhibition of Ca2+ release from the sarcoplasmic reticulum decreases the transsarcolemmal Ca2+ efflux and results in an increased sarcoplasmic reticulum Ca2+ content. We used procaine to inhibit sarcoplasmic reticulum Ca2+ release in rabbit papillary muscles. Rapid cooling-induced contractures were used as an index of sarcoplasmic reticulum Ca2+ content. Decay of potentiated state was measured to study whether the transsarcolemmal Ca2+ efflux is decreased in the presence of procaine. Procaine (0.5, 1.0 mM) inhibited contractions elicited by electrical stimulation and enhanced the rapid cooling-induced contracture. The initial decay of potentiated state that occurs when the muscle was stimulated at a low frequency was slowed in the presence of procaine. These results suggest that procaine inhibition of Ca(2+)-induced release of sarcoplasmic reticulum Ca2+ decreases the transsarcolemmal Ca2+ efflux relative to the influx, resulting in an increased sarcoplasmic reticulum Ca2+ content.

Animals↗

Effects of acetaldehyde on the isolated papillary muscle of diabetic rats.

The effects of acetaldehyde (ACA) were examined in isolated electrically driven papillary muscle preparations from normal and streptozotocin-treated diabetic rats. Muscles from diabetic rats developed greater tension than those from normal rats. In muscles from both groups, ACA caused concentration-dependent negative inotropic effects that were independent of cholinergic or purinergic mechanisms and were not attributable to nitric oxide (NO) release. ACA was three to five times more potent with regard to its negative inotropic effect in diabetic than in normal rat muscles. A propranolol-sensitive, sympathetically mediated positive inotropic effect occurred at certain concentrations. Decreasing [Ca2+]o from 2.7 to 0.5 mM reduced basal developed force to a significantly greater extent in muscles from normal rats than in those from diabetic rats. In low [Ca2+]o, concentration-response curves to CaCl2 in diabetic muscles were displaced to the left of that in normal muscles, suggesting that diabetic muscles are more sensitive to the positive inotropic effect of added CaCl2 at low [Ca2+]o, whereas at higher [Ca2+]o (> 1 mM), normal muscles developed more force in response to added CaCl2. ACA 10 and 30 mM more readily inhibited CaCl2-induced positive inotropic effect in normal than in diabetic muscles. Force-frequency curves, (negative staircase response) were recorded in both normal and diabetic muscles. In diabetic muscles, the curve exhibited a positive component at the lowest frequencies applied and was displaced to the right of that in normal muscle. ACA concentration-dependently inhibited force development, and diabetic muscles were more susceptible to the negative inotropic effect of ACA, when the stimulation frequency was increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗

Effect of hypoxia on myocardial relaxation in isometric cat papillary muscle.

Myocardial relaxation is an important energy-dependent process. Hypoxia, unlike ischemia, has not been shown to impair myocardial relaxation. This difference may be because (a) the traditional index to assess isometric muscle relaxation (half time to relaxation or RT((1/2))) reflects both changes in developed tension as well as relaxation and (b) the relaxation process is highly sensitive to temperature and previous papillary muscle studies have been conducted under hypothermic conditions. The present study examines the effect of hypoxia on the relaxation process of 31 isometrically contracting kitten papillary muscles at hypothermic (29 degrees C) and euthermic (38 degrees C) conditions using RT((1/2)), the peak rate of tension fall (-dT/dt) and -dT/dt normalized for tension ([peak -dT/dt]/T and max [-dT/dt per T]). Hypoxia at 29 degrees C resulted in a fall in RT((1/2)) from 278+/-11 (SEM) to 230+/-17 ms (P < 0.01) and no change in (peak -dT/dt)/T and max (-dT/dt per T). However, at 38 degrees C, hypoxia impaired relaxation as reflected in a prolongation of RT((1/2)) from 101+/-6 to 126+/-8 ms (P < 0.01) in spite of a substantial fall in peak tension. Moreover, (peak -dT/dt)/T decreased from -15.4+/-0.7 to -11.0+/-0.8/s (P < 0.01) and max (-dT/dt per T) decreased from -25.1+/-1.8 to -13.8+/-0.9/s (P < 0.01). In conclusion, the present study demonstrates that hypoxia impairs the relaxation process of cardiac muscle.

Animals↗

Pitfalls in the diagnosis and management of papillary muscle rupture: a study of four cases and review of the literature.

Four cases of papillary muscle rupture occurring in the setting of acute myocardial infarction are presented, which illustrate the following points: the diagnosis may not be apparent at presentation, a mitral regurgitant murmur may be absent, transesophageal echocardiography may establish the diagnosis when transthoracic echocardiography does not, and appropriate surgical correction can lead to excellent functional recovery.

Aged↗

Contractile performance of papillary muscles of renovascular hypertensive and isoproterenol-pretreated rats.

Previous studies suggested that left ventricle papillary muscles from neurogenic hypertensive rats with 15 days of sino-aortic denervation (SAD) develop intense depression of their inotropic state. Considering that these animals have an increased cardiac sympathetic tonus that could produce the observed depression of the contractile response we did the present study simulating a cardiac sympathetic hyperactivity pretreating rats, during 15 days, with isoproterenol (IPA, 0.1 mg/kg, i.p., divided in 3 daily doses). Because SAD rats also develop hypertension, the effect of blood pressure overload was studied in rats with 15 days of renovascular hypertension (RHR), Goldblatt 1K1C, to compare, separated, the effects of sympathetic hyperactivity and hemodynamic overload. Results showed that RHR had muscles that developed larger force than their controls (C: 7.31 +/- 0.34 g/mm2, RHR: 12.8 +/- 0.40 g/mm2), meanwhile IPA pretreated rats had muscles developing less force than their respective controls (C: 13.8 +/- 0.37 g/mm2, IPA: 8.61 +/- 0.24 g/mm2). These results are according to the proposition that the contractile state depression is related to the sympathetic hyperactivity, as suggested by the IPA pre-treated group and because the animals with isolated pressure overload showed a better contractile performance when compared to their uninephrectomized controls.

Animals↗

Effects of non-toxic doses of ouabain on sodium, potassium, calcium distribution in guinea pig papillary muscle. Electronprobe microanalysis.

The mechanisms and the cellular structures which are definitely involved in the accumulation and release of calcium in heart muscle treated with cardiac glycosides are not yet known. The distribution of sodium, potassium and calcium in small papillary muscles of the guinea pig right ventricle was examined with the aid of energy dispersive x-ray microanalysis and cryotechniques. The primary aim of the present study was twofold: firstly, to determine whether an increase in intracellular sodium concentration is detectable in muscles showing positive inotropy resulting from treatment with non-toxic doses of ouabain; and secondly, whether at the end of diastole cellular stores are detectable accumulating Ca which could be responsible for the pronounced contraction which normally would follow. Analyses on interstitium, cell membrane, sarcomeres, Z-lines and mitochondria of 7 muscles strips treated with non-toxic doses of ouabain and frozen at the end of diastole showed the following: sodium concentration in the sarcoplasm was significantly higher than over the mitochondria; it was also higher than over the sarcoplasm of non-treated muscles frozen at the end of diastole. High calcium concentrations were also measured over the cell membrane. These calcium concentrations were higher than that detected in sarcomeres, Z-lines and mitochondria. Over the sarcomeres, the calcium concentration was higher than in experiments on non-treated muscles which were also frozen at the end of diastole. Mitochondria did not accumulate any detectable concentration of calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Rupture of the papillary muscles of the mitrale valve during myocardial infarction].

Between 1967 and 1976, 13 cases of papillary muscle rupture during the acute phase of myocardial infraction were collected. Six patients have been treated surgically during the past three years. Three could undergo surgery by virtue of the use of an intra-aortic counterpulsion balloon. There were no operative deaths. One patient died ten days after surgery as a result of a neurological complication; while a second died 4 months after a successful operation of an undetermined cause. For very satisfactory results were obtained with a follow-up of 7, 16, 18 and 18 months.

Acute Disease↗

[Effects of perindopril on left ventricular hypertrophy, coronary reserve and mechanical properties of the papillary muscle of the rat with renovascular arterial hypertension].

We investigate the effect of a new angiotensin-converting enzyme inhibitor: Perindopril (IRIS) on regression of left ventricular hypertrophy (LVH), coronary blood flow and mechanical performance of isolated papillary muscle in renovascular hypertensive (Goldblatt 2 kidneys-1 clip) Sprague-Dawley male rats. Sham operated rats (G1) and half of hypertensive rats (G2) were studied after 8 weeks. The other half of 8 weeks long hypertensive rats (G3) were treated during 8 weeks with Perindopril in drinking water at a dosage adjusted to maintain blood pressure (BP) measured with tail cuff method under 140 mmHg. The study of each rat included 1) coronary blood flow and resistance measurements under resting conditions and after coronary dilation by carbochrome infusion (9 mg/kg) using left atrial injection of radioactive microspheres (method of Wicker and Tarazi) 2) the study of mechanical performance of the isolated papillary muscle 3) weight of left ventricle after separation of septum and free wall whose subendocardial and subepicardial layers were counted separately. Results (mean +/- SD): (table; see text) MAP: mean pressure. LV/BW: left ventricular mass (mg) per gram of body weight; CR (C): minimal coronary resistance after carbochrome (mmHg/ml/min/100 mg); DL/Dt: peak velocity of shortening at L max preload; Vrelax: peak velocity of relaxation; THR: time of half relaxation; p less than 0.05; p less than 0.01 compared to SHAM. In this model, hypertension induced a 50 p. 100 LVH whose regression was nearly complete after 8 weeks of treatment with Perindopril. Minimal coronary resistance after carbochrome were higher in hypertensive rats compared to sham and return to normal after regression of LVH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of toosendanin on electric and mechanical properties of guinea pig papillary muscles.

Effects of toosendanin (TS) on the action potentials and contractile force in guinea pig papillary muscles were examined using a standard microelectrode technique. TS concentration-dependently increased the action potential duration at 90% repolarization (APD90) of the fast action potentials. In the presence of a Ikl channel blocker BaCl2, the effects of TS on lengthening the APD90 were completely abolished, thereby suggesting that TS inhibited the inward rectifier K+ current Ikl. The APD and contractile force of aminophylline-induced slow action potentials were potentiated by TS in a concentration-dependent manner. In the presence of BaCl2, both effects of TS were completely abolished. The effect of TS on enhancing contractile force was abolished by the addition of CdCl2, with the prolongation of APD preserved. Thus, TS selectively inhibited the inward rectifier K+ current Ikl with a positive inotropic effect, resulting from a delay in Ca channel inactivation which was secondary to delay in ventricular repolarization.

Action Potentials↗

[The curvilinearity of the end systolic tension-length relation of isolated rat papillary muscles].

A series of isotonic tension, shortening and shortening velocity were obtained in isolated rat papillary muscles by varying the ++set point force against which the muscle shortened at optimal length. It was found that (1) end systolic tension-length relation (ESTLR) could be described by an exponential equation. T = ae-bL-k, where a and k represent respectively the total tension and the resting tension and b means curved degree and length-axis intercept (L0) represents maximal shortening. There was a greater correlation index R2 when fitted with the equation compared with linear regression (P less than 0.001). (2) High [Ca2+]0 shifted ESTLR leftward and upward, with increased a, b and maximal shortening L0, so did norepinephrine (NE) but significantly less than high [Ca2+]0, whereas the changes in rates of shortening and tension rise were greater during NE infusion than during high [Ca2+]0 infusion. These results indicated that ESTLR was non-linear in isolated myocardium and exponential parameters a, b and L0 were sensitive to changes in contractile intensity, but less sensitive to changes in contractile velocity when compared with indexes of myocardial mechanics.

Animals↗

[Mitral valve replacement with preservation of papillary muscles and chordae tendineae: a report of 53 cases].

Mitral valve replacement with preservation of papillary muscles and chordae tendineae (MVRP) was carried out in 53 cases in this group, among whom 17 underwent combined mitral and aortic valve replacement (AVR), 36 underwent simple mitral valve replacement (MVR) and tricuspid valve plasty was performed in 28 cases simultaneously. All the patients were given echocardiography one and six months after operation respectively which showed: (1) The left ventrical function of this group was obviously superior to that of the conventional mitral valve replacement (MVRC) group in the same period (SVI, EF, FS, P < 0.05) (2) The open shut velocity of the prosthetic disc was quicker (3) The contradictory movement of the ventrical septum disappeared. The follow-up for 2 to 36 months showed that all the patients were alive and healthy. It is suggested that MVRP can facilitate better recovery of the left ventrical function than MVRC and long-term results are excellent.

Adolescent↗

[Effect of the ionophore A23187 on the contractility and slow action potential of the guinea pig papillary muscle].

Calcium ionophore A23187 (2.10(-6) M) increases contractility of the isolated guinea-pig papillary muscle 3.13 +/- +/- 0.47-fold at 25 degrees C and 1.88 +/- 0.28-fold at 37 degrees C. Prolonged exposure (30 min) to 2 mM of caffeine failed to eliminate positive inotropic effect of ionophore. A23187 (2.10(-6) M) also increased slow response action potential overshoot (18 mM K+ in Tyrode solution, resting potential 46 +/- 1 mV); at 37 degrees C the peak overshoot value was reached by the 2nd min, being equal to 5.2 +/- 0.4 mV; at 25 degrees C the peak value was attained by the 15th min, being equal to 15.5 +/- 0.9 mV with an abrupt increase in the repolarization rate. Overshoot enhancement within the first minutes of A23187 action is concluded to be due to the increased slow inward Ca-current rather than to the decreased outward currents. It is assumed that A23187 facilitates Ca2+ transport to the lipid phase thereby increasing the amount of sarcolemma bound Ca2+ that participates in the development of Ca-current.

Animals↗

Mechanism of the negative inotropic action of cocaine in rat papillary muscle.

We studied the mechanism of the negative inotropic action of cocaine in isolated rat papillary muscles superfused with Tyrode's solution at 31 degrees C while attached to a force transducer to measure peak tension developed (PTD), maximum velocity of development of tension (Vmax T), and time to peak tension (TPT). The results show that in preparations driven at 1 Hz, 5 and 10 mg/liter cocaine had a significant negative effect only on PTD, while 20 mg/liter (58 microM) significantly depressed all three measured parameters. Similar results were obtained in preparations driven at 0.5 Hz, which developed a greater control active tension than those driven at 1 Hz. In preparations driven at 0.5 Hz, propranolol (1 microM) had no significant effect on the active tension developed nor did it modify the negative inotropic action of cocaine. Both nifedipine (1 microM) and caffeine (1.5 mM), on the other hand, significantly reduced PTD, Vmax T, and TPT. The depressant inotropic action of cocaine was accentuated by nifedipine, but was blocked by caffeine. These observations suggest that the primary site of action of cocaine was at the level of the sarcoplasmic reticulum rather than at the sarcolemma.

Animals↗

The murmur of papillary muscle dysfunction in acute myocardial infarction: clinical features and prognostic implications.

The systolic murmur of papillary muscle dysfunction is a well-recognized feature of acute myocardial infarction (AMI), but no large prospective studies have determined its incidence, associated variables, and prognostic implications. Of 1653 patients who entered our data base with MI, 283 (17%) were classified as having a systolic murmur suggesting mitral regurgitation. At hospital discharge, there was a 5% incidence. There was a higher incidence of systolic murmur in non-Q wave AMI than in inferior or anterior Q wave MI (24% vs 13% and 15%, p less than 0.001). Advanced age, previous MI, and heart failure were all associated with systolic murmur (p less than 0.01). Persistent pain in the coronary care unit occurred more often in those with systolic murmur (45% vs 26%, p less than 0.0001). Systolic murmur was associated with an S3 and bibasilar rales (p less than 0.001) in the hospital; however, it was inversely related to peak creatine kinase and unrelated to heart failure or ejection fraction at discharge. Univariate predictors of mortality associated with systolic murmur included complex premature ventricular contractions at discharge and a non-Q wave location. Patients with systolic murmur had higher hospital and 1-year mortalities than those without systolic murmurs (p less than 0.01). When systolic murmur was present during hospitalization, the average time to reinfarction was 2.5 times earlier than when no systolic murmur was present (84 vs 214 days, p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Numerical study of the behavior of an activation parameter in a sliding filament cat papillary muscle model.

A previously existing model of cross-bridge kinetics is modified to make it applicable to cardiac muscle and incorporated into a macroscopic model of isolated heart muscle. Equations are formulated which describe the responses of this model during simulated isometric and isotonic contractions. These equations allow one to calculate the time variation of the activation parameter in the model when given the contraction time history, i.e. the time course of length and tension changes. The activation parameter is defined as the instantaneous rate constant for cross bridge attachment. We calculate the time course of the activation parameter with the model's responses set equal to the measured responses of isolated cat papillary muscle and the model parameters chosen appropriately for cat papillary muscle. It is found that in order for the model and muscle response to match, the degree of activation of the muscle model must first increase and then decrease with shortening. The behavior of the activation parameter in the muscle model is consistent with physiological investigations which suggest that shortening in cardiac muscle is associated with both activation and deactivation.

Animals↗