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Depression of papillary muscle contractility by plasma incubated with pneumococci.

Mechanisms of death in pneumococcal disease are poorly understood. We have previously shown that intravenous pneumococcal products in dogs caused a mean decrease in cardiac output of 58%. The present study used measurements of the force and rate of contraction of isolated rabbit papillary muscle to determine whether pneumococci (PNC) altered myocardial contractility. Nine papillary muscles were superfused with various solutions including Tyrode's, Tyrode's incubated with sonicated type 1 PNC, normal rabbit plasma, and rabbit plasma incubated with PNC. Compared to untreated Tyrode's solution, PNC-treated Tyrode's solution did not alter papillary muscle contractility. However, compared to untreated rabbit plasma, plasma incubated with PNC caused a mean decrease of 18% in the force of contraction and 16.7% in the maximum rate of force development in nine studies. We conclude that PNC do not directly affect papillary muscle contractility. However, the interaction of PNC and plasma does cause a decrease in rabbit papillary muscle contractility.

Animals↗

[A case of emergency surgery for acute mitral regurgitation due to complete papillary muscle rupture as complication of acute inferior myocardial infarction].

We experienced a case with acute mitral regurgitation caused by complete posterior papillary muscle rupture as complication of acute inferior myocardial infarction, who underwent successfully emergency operation of mital valve replacement and coronary revascularization in acute stage. A 64-year-old woman developed sudden cardiogenic shock shortly after the onset of acute inferior myocardial infarction. The diagnosis of acute inferior myocardial infarction was based on the electrocardiographic findings. Under IABP support, preoperative coronary angiography visualized total occlusion of segment 3 of the right coronary artery, and preoperative left ventriculography showed akinesis of inferior wall and severe mitral regurgitation. At 6 hours after onset of papillary muscle rupture, emergency operation was performed. At operation, posterior papillary muscle was found to be totally ruptured. Coronary artery revascularization and mitral valve replacement were performed. Postoperative course was uneventful, with 4 days of IABP and 5 days of ventilatory support. She was discharged on the twentieth postoperative day in NYHA class I. Reports of successful emergency operation for total papillary muscle rupture following acute myocardial infarction are rare. Early diagnosis and surgical treatment are mandatory to save this group of patients.

Emergencies↗

Mitral regurgitation in ventricular premature contractions. The role of the papillary muscle.

In view of the possibility that the mechanism of mitral regurgitation following premature ventricular contractions may contribute to the understanding of mitral regurgitation in clinically important causes of nonrheumatic mitral insufficiency, we studied 320 premature ventricular contractions in eight dogs. Since the papillary muscle is an important component of the mitral valvular complex, the extent and course of lengthening and shortening of the papillary muscle was investigated with ultrasonic crystals implanted within the anterolateral papillary muscle. Lengthening and shortening of a segment of the free wall of the left ventricle was measured simultaneously with identical crystals in three dogs. During sinus rhythm, lengthening of the papillary muscle always began well before the onset of isovolumic contraction of the left ventricle and continued throughout isovolumic contraction, indicating that lengthening occurred during closure of the mitral valve. When lengthening was prevented by premature ventricular contractions, left atrial v waves occurred. These observations indicate that lengthening of the papillary muscle during the latter part of diastole is required for proper closure of the mitral valve and that inadequate lengthening can result in mitral regurgitation.

Animals↗

Intracellular chloride activity in rabbit papillary muscle: effect of serum.

The intracellular chloride activity (aiCl), measured with Cl-selective microelectrodes on stimulated rabbit papillary muscles (1 Hz) incubated in serum, was 7.2 +/- 2.2 mM (48 measurements). Under the same condition, on the quiescent muscle, aiCl was 7.5 +/- 2.8 mM (45 measurements). The membrane potential of quiescent papillary muscles and diastolic potential of stimulated papillary muscles were -79.0 +/- 0.7 (50 measurements) and -83.5 +/- 0.5 mV (50 measurements), respectively. The experimental conditions were chosen to reproduce the in vivo conditions where the Cl equilibrium potential is close to the membrane potential or to the diastolic potential. After correcting for cytoplasmic interference (4 mM) on the aiCl measurements, the Cl equilibrium potential (ECl) was -84 mV. In conclusion, the Cl distribution in cardiac cells bathed in serum is passive as for in vivo cardiac cells.

Animals↗

Effects of sodium substitutes on transient inward current and tension in guinea-pig and ferret papillary muscle.

We used ouabain-treated guinea-pig and ferret papillary muscles to study transient inward current (Iti), after-contractions, and tonic tension development during voltage-clamp pulses. Li, sucrose and choline were used isosmotically as Na substitutes to evaluate the effect of altering the Na equilibrium potential. We were unable to detect outward Iti at any potential up to +30 mV in normal or Na-depleted solutions. However, reduction of Na had a biphasic effect on Iti, initially increasing it and then reducing it at all clamp potentials from -50 to +20 mV. After-contractions were also initially increased and, in sufficiently Na-depleted solutions, decreased by reduction of extracellular Na. However, the peak in the after-contraction always occurred later than the increase in Iti and frequently coincided with the maximum suppression of the current. Complete suppression of after-contractions was not often achieved and always required more complete Na replacement than Iti suppression. Tonic tension responses were reduced by Na replacement, usually in synchrony with the reduction of Iti. The responses of Iti to Na replacement are consistent with a model of electrogenic Na-Ca exchange over the potential range positive to -50 mV. The responses deviate from the predictions of the model at more negative potentials. The results are consistent with the previous proposal that oscillatory changes in internal free Ca concentration underlie both Iti and after-contractions.

Action Potentials↗

Ultrasound intensity and contractile characteristics of rat isolated papillary muscle.

The effect of graded intensities of continuous wave ultrasound on the contractile performance of isolated papillary muscle of rat was tested. Under isometric conditions rat left ventricular papillary muscles (n = 48) were electrically stimulated to contract at rates of 30, 60, 120 and 240 beats per minute. Muscles were perfused with a Tyrode solution at 30 degrees C under normoxic conditions. Ultrasound at intensities of 0.25, 0.50, 1.0 and 2.0 W/cm2 spatial average temporal average (SATA) at 963 kHz was applied to the muscles while recording muscle contractile characteristics. The analog data were digitized and stored on disk for analysis by computer. This revealed a significant (p less than 0.001) increase in peak developed force (F), peak rate of force development (+dF/dt) and peak rate of myocardial relaxation (-dF/dt) that was linearly related to ultrasound intensity. The muscles were more sensitive to ultrasound at 240 contractions per minute. Resting force was significantly decreased by ultrasound. Although bath temperature increased according to the ultrasound intensity, control studies in papillary muscles (n = 24) on the correlation between contractile parameters and temperature revealed that bulk heating could not account for the positive inotropic action with ultrasound. These data confirm the inotropic effect of continuous wave ultrasound on myocardial tissue and point to the possibility of applying this phenomenon therapeutically.

Animals↗

[Effects of nizofenone on the action potential of guinea-pig papillary muscle and S-A node and dog Purkinje fibers].

Effects of nizofenone, an agent which has been known to have a protective effect against experimental cerebral ischemia or anoxia, on the action potential of guinea-pig papillary muscle and S-A node and dog Purkinje fibers were studied. Nizofenone (10(-6) and 10(-5) M) significantly prolonged the action potential duration of guinea-pig papillary muscle and dog Purkinje fibers accompanying prolongation of the effective refractory period in dog Purkinje fibers. Nizofenone decreased Vmax at the concentrations of 10(-5) and 10(-4) M in guinea-pig papillary muscle and at 10(-4) M in dog Purkinje fibers. Nizofenone suppressed the spontaneous activity of dog Purkinje fibers and guinea-pigs S-A node at the concentrations of 3 X 10(-5) to 10(-4) M and 10(-5) M, respectively. Nizofenone (10(-4) M) decreased the contractile force of guinea-pig papillary muscle. In the guinea-pig papillary muscle, the effect of nizofenone on action potential duration was almost the same as that of quinidine, but the inhibitory effect on Vmax was slightly weaker than quinidine. These results suggest that nizofenone has a so-called "quinidine-like action" on cardiac membrane.

Action Potentials↗

Reoxygenated effluent of Tyrode-perfused heart affects papillary muscle contraction independent of cardiac perfusion.

OBJECTIVE: We determined, via a bioassay, if inotropic factors are released in the coronary circulation of the rat heart and if changes in cardiac perfusion change papillary muscle inotropy. METHODS: An isolated isometrically contracting rat papillary muscle (n = 5, acceptor) was superfused with Tyrode or with reoxygenated coronary venous effluent from an isolated isovolumically beating rat heart (donor) at 27 degrees C, which was perfused with Tyrode according to Langendorff. The superfusion solution in the muscle bath was exchanged completely in 90 s. During coronary venous effluent superfusion, the flow of the heart (donor) was changed in steps. RESULTS: The peak force of the papillary muscle (acceptor) was unaffected by a change from Tyrode to coronary venous effluent superfusion, but time to half relaxation (RT 1/2) significantly increased by 23.0 +/- 9.0% (mean +/- s.d.) and positive dF/dtmax significantly decreased by 14.6 +/- 4.7%. These twitch characteristics were unaffected by changes in coronary perfusion while in the heart isovolumic developed left ventricular pressure did increase with perfusion (the Gregg phenomenon). CONCLUSIONS: Factors that affected papillary muscle contractility are released into the coronary circulation, but their effect is independent of the magnitude of coronary perfusion.

Animals↗

Frequency-dependence of the positive inotropic effect of methoxamine and naphazoline mediated by alpha-Adrenoceptors in the isolated rabbit papillary muscle.

Under the conditions of different stimulation frequencies the inotropic effects of the alpha-adrenoceptor stimulationg agents, methoxamine, naphazoling and oxymetazoline were studied on the isolated rabbit papillary muscle. 1. On the papillary muscle stimulated at 0.5 Hz methoxamine in concentrations from 10(-5)M caused a significant and dose-dependent positive inotropic effect. At 10(-3)M methoxamine decreased the developed tension. With increasing frequency of stimulation (0.5--1--1.5Hz), the positive inotropic effect became smaller, while the negative inotropic one was more pronounced. The time course of the disappearance of the negative inotropic effect of methoxamine by washout differed from that of the positive inotropic effect: the negative component disappeared within 30 min, whereas the positive one lasted for about 100 min. The positive inotropic effect of noradrenaline (10(-6)M), in contrast ot that of methoxamine, was not influenced by the frequency under the same conditions of stimulation. Also naphazoline (10(-5)M) caused a significant positive inotropic effect on the papillary muscle stimulated at 0.5 Hz, while oxymetazoline induced exclusively a negative inotropic effect. 2. The positive inotropic effect of metoxamine (10(-4)M) as well as of naphazoline (10(-5)M) evoked at a frequency of 0.5 Hz was abolished by phentolamine (10(-6)M). Methoxamine (10(-4)M) induced a significant negative inotropic effect in the presence of phentolamine. Phentolamine antagonized the positive inotropic effect of methoxamine in a non-competitive manner: the pD2-value was 7.76. 3. In the presence of methoxamine (10(-4)M) the developed tension in the lower range (0.05--1 Hz) of the frequency-force relationship was enhanced, while that in the higher range (greater that 1.5 Hz) was decreased. The enhancement was abolished by phentolamine (10(-6)M). 4. Papaverine (2x10(-5)M) did not affect the positive inotropic effect of methoxamine. 5. The present results show that methoxamine and naphazoline induced a positive inotropic effect via alpha-adrenoceptor in the ventricular myocardium of the rabbit. These effects were caused only at low, but not at high frequencies of stimulation.

Animals↗

Electrophysiological effects of CI-980, a tubulin binding agent, on guinea-pig papillary muscles.

1. The electrophysiological effects of CI-980, a new tubulin-binding agent that inhibits assembly of cytoplasmic microtubules, on transmembrane action potential characteristics were studied in right ventricular papillary muscles from guinea-pig hearts. 2. In papillary muscles driven at 1 Hz, CI-980 at concentrations > or = 10(-5) M produced a concentration-dependent increase in the maximum upstroke velocity (Vmax) and a lengthening of the action potential duration at 50% (APD50) and 90% (APD90) of repolarization without affecting the resting membrane potential. Prolongation of the APD90 was accompanied by a parallel lengthening of the effective refractory period (ERP) so that the ERP/APD90 ratio remained unaltered at all drug concentrations tested. 3. CI-980 exhibits a reverse use-dependent effect on APD90 values, that is, drug-induced APD90 prolongation become exagerated at slow rates and attenuated at fast rates. 4. CI-980 at concentrations > or = 10(-6) M lengthened the APD of the slow action potentials elicited by isoprenaline in papillary muscles depolarized by high K+ (27 mM) solution. 5. At 10(-5) M, CI-980 produced a small tonic Vmax block. However, in muscles driven at rates between 0.5 and 3 Hz it produced an exponential decline in Vmax (use-dependent Vmax block) which was augmented at higher rates of stimulation. At 3 Hz the onset kinetics of the use-dependent Vmax block was fitted by a monoexponential function with a K value 0.07 +/- 0.01 per AP. The recovery time constant (tau re) from the use-dependent Vmax block was prolonged from 21.6 +/- 2.6 ms to 3.5 +/- 0.2 s. 6. The curve relating membrane potential and Vmax was shifted by CI-980 (10(-5) M) in the hyperpolarizing direction by 2.3 +/- 1.1 mV. 7. It is concluded that in guinea-pig papillary muscles, CI-980 produces a use-dependent inhibition of Vmax and a reverse use-dependent prolongation of the ventricular action potential, thus exhibiting class I and class III antiarrhythmic actions, respectively. From the onset and offset kinetics of use-dependent Vmax block, CI-980 can be considered to be an intermediate kinetics (IA) Na+ channel blocker.

Action Potentials↗

[A case of mitral regurgitation caused by total rupture of the posterior papillary muscle after acute myocardial infarction].

We observed a case of severe mitral regurgitation caused by total rupture of the posterior papillary muscle 13 days after acute myocardial infarction. The patient was a 76-year-old man who suddenly felt anterior chest pain. He was admitted to another hospital with the diagnosis of acute myocardial infarction. Electrocardiogram suggested a posterior infarction. He did well during the first 12 days of hospitalization, but at noon on the 13th day he developed anterior chest pain and dyspnea. Echocardiography demonstrated rupture of the posterior papillary muscle. He was subsequently transferred to our hospital with acute heart failure. He was initially treated with an intra-aortic balloon pump. Cardiac catheterization demonstrated 99% stenosis of segment 2 of the right coronary artery and mitral regurgitation, Sellers' stage IV. Intraoperative findings included total rupture of the posterior papillary muscle. Mitral valve replacement was performed using a Carbomedics prosthetic valve. The patient was discharged 53 days after surgery without heart failure or angina pectoris. This case represents the 6th successful operation of total papillary muscle rupture in Japan.

Aged↗

Evolution of echocardiographic modalities in detection of postmyocardial infarction ventricular septal defect and papillary muscle rupture: study of 62 patients.

Diagnostic sensitivity of various echocardiographic modalities was assessed for postinfarct ventricular septal defect (40 patients) and papillary muscle rupture (22 patients). Two-dimensional transthoracic echocardiography enabled direct visualization of ventricular septal defect in 68% and combined two-dimensional Doppler echocardiography was diagnostic in 95%. Papillary muscle rupture was directly visualized in 45%, and severe mitral regurgitation was present on Doppler color flow images in 100%. Transesophageal echocardiography was diagnostic in all nine patients (five with ventricular septal defect and four with papillary muscle rupture) in whom this modality was applied. Thus two-dimensional Doppler echocardiography (transthoracic and transesophageal if necessary) is highly sensitive in detecting postinfarct ventricular septal defect and papillary muscle rupture.

Aged↗

[Diagnosis of papillary muscle rupture in acute myocardial infarction by transesophageal Doppler echocardiography].

Three patients, two females, ages ranging from 62 to 78 years were studied, evolving with hypotension, acute pulmonary edema and cardiogenic shock. One had anterior myocardial infarction, and in two, infero-posterior. Due to severe hemodynamic instability and necessity of vasoactive drug therapy to maintain adequate arterial pressure, coronary angiography was performed in two, showing total occlusion of the circumflex artery and severe mitral regurgitation. In one case, angioplasty on the circumflex artery was successfully achieved. No hemodynamic improvement was observed, however. Doppler echocardiography depicted mild to moderate mitral regurgitation in the three cases. Transesophageal echo confirmed the clinical suspicion of papillary muscle rupture: total rupture of antero-lateral papillary muscle in one patient, as well as total and partial rupture of the postero-medial papillary muscle in the other two patients. Two patients were submitted to mitral valve replacement, and the surgical findings confirmed the transesophageal echo conclusions. One of them died in the immediate pos-operative period, whereas the other was discharged from the hospital and is doing well. The third patient died before operation. Differential diagnosis of acute mitral regurgitation due to papillary muscle dysfunction or rupture was not possible by left ventriculography or by transthoracic echo. Transesophageal echo was the only exam to clearly confirm papillary muscle rupture, as should be done promptly after clinical suspicion of this severe condition arises.

Aged↗

An effective morphometric method for electron microscopic studies on papillary muscles.

Morphometry was performed on the left ventricular posterior papillary muscles of seven Wistar rats. The volume densities of myocardial cells, interstitial space, myocardial nuclei, sarcoplasm, mitochondria, myofibrils, ground substance and T tubules, and the surface densities of myocardial cells, mitochondrial membranes and T tubules, were calculated. Though only 1 ultrathin section per animal was evaluated the low standard errors of the means indicate that the method described here will be adequate in most experimental studies. Due to the anisotropy of the surfaces within myocardial cells, the papillary muscles were cut at an angle of 32.4 degrees to their longitudinal axis. This angle is derived from an equation published by Whitehouse (1974). The procedure to correct the loss of cristal membrane images from oblique sectioning is discussed.

Animals↗

Chronic diabetes decreases the ouabain inotropic response in rat left atria and papillary muscles.

The inotropic response to ouabain in rat left atria were markedly depressed in animals made diabetic for 6 months. Similarly, ouabain inotropy was also decreased in papillary muscles obtained from 70-day diabetic rats. The effect of isoproterenol was not reduced in the above papillary muscle experiments and was not tested in the atria experiments. Ouabain produced a monophasic dose-response curve in atria but a biphasic curve in papillary muscles. Timolol had no effect on the ouabain response. Left atria and papillary muscles from animals made diabetic for 7 days responded in a normal fashion to both ouabain and isoproterenol.

Animals↗

Peculiar mitral valve and papillary muscle lesions induced by vagus manipulations in rabbits. An experimental model for nonrheumatic mitral regurgitation.

Peculiar lesions of mitral valves and papillary muscles developed in 50 to 80% of rabbits after clipping (N = 38), crushing (N = 15) or electrical stimulation (N = 44) of their cervical vagi. Both right and left vagus manipulations induced similar cardiac lesions. The earliest manifestation was bleeding of the mitral leaflets, which was followed by swelling and fibrosis of the papillary muscles. Ventricular arrhythmias and systolic murmurs were frequently associated with the vagus manipulations. During or just after electrical stimulation of the vagus, ventricular premature contractions (VPCs) were observed in 30 of 44 animals. Twenty-nine of these 30 animals with VPCs (96.7%) were found to have mitral valve and/or papillary muscle lesions at autopsy, whereas only 5 of 14 animals without VPCs (35.7%) had the cardiac lesions. These results indicate that the occurrence of these ventricular arrhythmias during vagus manipulations was closely related with the mitral valve and papillary muscle lesions.

Animals↗

Application of papillary muscle sling concept in an infant as a biological bridge to transplantation.

We successfully applied the papillary muscle sling concept in mitral valve reconstruction of an infant with dilated cardiomyopathy. This new method of banding the two papillary muscles together can shorten the distance of the base between the two papillary muscles, reduce the severity of mitral regurgitation, and remodel the dilated left ventricle without any mitral stenosis. The infant survived after this bridge-to-transplantation procedure and was successfully transplanted.

Cardiomyopathy, Dilated↗

No evidence for involvement of dopaminergic receptors in the positive inotropic action of dopamine on the isolated rabbit papillary muscle.

Experiments were carried out on the isolated rabbit papillary muscle driven at 0.5 Hz in order to further elucidate the mechanism of the positive inotropic effect evoked by dopamine. The dose-response curve for dopamine was not affected by the antagonists pimozide (10(-6) M), yohimbine (10(-5) M) pindolol (3 x 10(-8) M) and phentolamine (10(-6) M) when these agents were given separately. Only the simultaneous administration of yohimbine plus pindolol and phentolamine plus pindolol, respectively, shifted the entire curve to the right. This shift was not further influenced by pimozide. Dopamine (10(-4) M) increased the cyclic AMP content of the papillary muscle by about 50%; this increase was not affected by pimozide, but was markedly elevated by yohimbine and completely depressed by pindolol. From the present results it is concluded, that dopamine produces its positive inotropic effect through stimulation of myocardial alpha-as well as beta-adrenoceptors to about the same degree; stimulation of specific dopaminergic receptors, however, is not involved. The stimulation of beta-adrenoceptors is accompanied by an increase of the cyclic AMP level, while that of alpha-adrenoceptors is not.

Animals↗