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Postnatal developmental changes in the electrophysiological properties of cat right ventricular papillary muscles.

Cellular electrophysiological properties of cat right ventricular papillary muscles were studied during postnatal development using intracellular microelectrodes. Animals were studied in the neonatal period (less than 75 h of age), in infancy (16 to 18 days old) and in adult life (1.8 to 2.3 kg body weight). Resting membrane potential, action potential amplitude, Vmax and action potential duration increased significantly with age. The age related changes in action potential duration were independent of stimulation frequency. Conduction velocity was measured using two simultaneous impalements and increased significantly with age. Exposure to low [Ca]o (0.2 mmol X litre-1) caused a prolongation in action potential duration which was greater in infant and adult than neonatal myocardium, and was greatest at low stimulation frequencies. High [Ca]o shortened action potential duration and this was also greater in infant and adult tissue. Action potential duration was prolonged by low [K]o (0.5 mmol X litre-1) and shortened by high [K]o. Both of these effects appeared to be independent of age. Exposure to ouabain, 10(-8) and 10(-7) mol X litre-1 caused a dose related shortening of action potential duration. This effect was significantly greater in adult and infant than neonatal myocardium. The results indicate that the electrophysiological properties of the cat myocardium continue to develop during early postnatal life. These findings are discussed in relation to changes in morphology and transmembrane ionic gradients occurring at this time.

Action Potentials↗

Mechanical restitution at different temperatures in papillary muscles from rabbit, rat, and hedgehog.

Mechanical restitution curves, i.e., peak isometric force as a function of the duration of the preceding test interval, were investigated in papillary muscles from rabbit, rat, and hedgehog. Peak force of rabbit papillary muscle increased with prolongation of the test interval from about 0.3 s to about 1.0 s and for longer intervals peak force declined (called type I mechanical restitution). On the other hand, in rat and hedgehog, papillary muscles' force reached a maximum value at intervals of 30-120 s (called type II mechanical restitution). When temperature was decreased from 35 to 15 degrees C, maximum force of type I mechanical restitution shifted from 1.0 to 10 s, whereas maximum force of type II restitution did not change significantly. Type II mechanical restitution consisted of two different phases, designated phase A and phase B, respectively. As temperature was decreased from 35 to 0 degree C in the hedgehog preparation, the two phases became even more separated. At 35 degrees C, the rising part of mechanical restitution in the rabbit muscle could not be distinguished from phase A of the hedgehog preparation and was also very similar to phase A of the rat muscle. Phase A is thus present in both type I and type II mechanical restitution, but phase B is a special feature of type II mechanical restitution. Phase A and phase B might be a manifestation of activator calcium originating from two different sources, e.g., the sarcoplasmic reticulum and the sarcolemma.

Animals↗

[Successful surgical treatment in a case of complete rupture of the posterior papillary muscle of the mitral valve caused by infective endocarditis].

Forty three year-old male who had cough and easy fatigability since three weeks prior to admission was diagnosed to have acute pulmonary edema with severe mitral regurgitation caused by active infective endocarditis. Transesophageal echocardiograms under the endotracheal intubation for controlled respiration suggested rupture of the posterior papillary muscle of the mitral valve and the emergency surgical treatment was performed. Intraoperatively the total rupture of the posterior papillary muscle was confirmed and mitral valve replacement was carried out with a SJM prosthetic valve. Histological examination of the ruptured papillary muscle revealed hemorrhage, muscle necrosis and small cell infiltration suggesting the presence of active inflammation with bacteria on it. Staphylococcus epidermidis was demonstrated by the bacteriological studies of the ruptured papillary muscle.

Adult↗

A multitissue organ bath evaluated using new rabbit papillary muscle isolation methods.

A multitissue organ bath was developed to study four isolated muscle preparations simultaneously under identical conditions. The multitissue bath was evaluated by determining the dose-response curves to dobutamine in isolated rabbit right ventricular papillary muscles. Several new procedures were developed to diminish the contracture shortening that often accompanies papillary muscle excision in this species. The excised heart was dissected in a hypothermic (22 degrees C) 'relaxing solution' containing 180 mM NaCl and 5.6 mM glucose, and a 'transfer clip' maintained constant, reproducible resting tension on the isolated muscle after its excision. Rabbit papillary muscles (n = 13) isolated with these procedures and studied in the multitissue bath were stimulated at a frequency of 20/min at 30 degrees C in a modified Krebs solution containing 2.5 mM Ca2+. Mean developed tension was 3.3 +/- 0.5 g/mm2. The dose-response curve for dobutamine demonstrated a maximal increase of dT/dt, an index of contractility, at 10(-4) M (173.6 +/- 35%, p less than 0.01). The multitissue bath may be useful for simultaneous comparison of chronotropic and inotropic effects of interventions on right atrial and ventricular preparations, respectively, or for comparison of intervention effects on selected vascular strips.

Animals↗

Oxidative and glycolytic ATP formation of rabbit papillary muscle in oxygen and nitrogen.

Contraction-related O2 consumption of rabbit papillary muscles was determined at 20 degrees C by measuring change in saline PO2 during and after trains of 120 twitches at 0.125-1 Hz in a microrespirometer. Although anoxic cores occurred at twitch frequencies greater than 0.2 Hz, no lactate was found in saline after twitch train. To measure lactate accumulation in muscle, fully oxygenated muscles were frozen at rest and during steady-state twitches at 0.2 Hz. We also measured nucleotides and creatine (Cr) compounds. There were no differences in lactate, ATP, and phosphocreatine (PCr) content between the resting and active muscles. When a P-to-O2 ratio of 6.3 is assumed, aerobic ATP formation was compared with glycolytic ATP formation during anoxia at a stimulus frequency of 0.2 Hz. The latter value was obtained by freezing muscles between 6 and 25 min after changing from O2- to N2-saturated saline. Withdrawal of O2 caused the ratio of PCr to total Cr to fall in less than 6 min from 0.77 to 0.23, while ATP remained at approximately 15 mumol/g dry wt. Force fell initially within 4 min to approximately 70% of control value, decreasing thereafter more slowly to approximately 40% at 20 min. From the relationship between amount of lactate formed and duration of anoxia, rate of anaerobic ATP formation was calculated assuming a P-to-lactate ratio of 1. We found that despite continuing contractile activity, anaerobic ATP formation was less than that required by a fully oxygenated resting muscle and was about the same magnitude as the estimated ATP hydrolysis for the contractions in N2. We conclude that in fully oxygenated rabbit papillary muscles no net lactate is produced during stimulation and that in anoxia anaerobic glycolytic capacity may not provide sufficient ATP for processes other than the uptake of Ca by the sarcoplasmic reticulum and cross-bridge cycling.

Adenosine Triphosphate↗

Effects of dipfluzine on delayed afterdepolarizations and triggered activity induced by ouabain in guinea pig papillary muscles.

AIM: To investigate the effects of dipfluzine (Dip) on delayed afterdepolarizations (DADs) and triggered activity (TA) induced by ouabain and high Ca2+ in guinea pig papillary muscles. METHODS: Stable and reproducible DADs and TA in guinea pig papillary muscles were induced by ouabain (1 micromol/L) and high Ca2+ (5.4 mmol/L). DADs and TA were recorded using intracellular glass microelectrode technique. RESULTS: (1) DADs and TA were markedly inhibited by pretreatment with Dip (10, 30 micromol/L). The amplitude and duration of DADs were reduced by Dip (30 micromol/L) from 10.5 mV +/- 2.2 mV and 230 ms +/- 19 ms to 3.6 mV +/- 0.3 mV and 152 ms +/- 14 ms, respectively, and the induced time of DADs was prolonged from (21+/-5) to (66+/-11) min. TA was not observed. (2) Dip (10, 30 micromol/L) had significant therapeutic effects on DADs and TA. The amplitude and duration of DADs were reduced by Dip (30 micromol/L) from 10.4 mV +/- 1.2 mV and 218 ms +/- 22 ms to 3.3 mV +/- 0.6 mV and 159 ms+/-26 ms. The occurrence of TA was also abolished. CONCLUSION: Dip has inhibitory effects on DADs and TA induced by ouabain and high Ca2+ in guinea pig papillary muscles, which might be related to alleviation of intracellular calcium overload through inhibiting calcium channel and/or calcium release from sarcoplasmic reticulum. The effects of Dip on DADs and TA might produce anti-arrhythmic effects.

Animals↗

Toxic concentrations of selenite shortens repolarization phase of action potential in rat papillary muscle.

Selenium (Se) has long been recognized as both an essential mammalian nutrient and a hazardous element. Sodium selenite is commonly used as a dietary supplement for the treatment of Se deficiency. On the other hand, chronic Se toxicity has been demonstrated to affect the major organs, including the heart, in experimental animals. This study examines the effects of high concentrations of extracellular selenite (in the range of 0.001-1 mM) application into the recording bathon the electrical properties of rat papillary muscles. Conventional glass semifloating microelectrodes were used to record intracellular action potentials (APs) in isolated rat papillary muscles. The amplitude of APs and the resting membrane potential of papillary muscles were not changed following a 20-min selenite (1 mM) application compared to the first minute of its application. Freshly isolated ventricular myocytes by an enzymatic method were used to determine the selenite-induced alterations in Na+ currents. Na+ currents, measured at 22 degrees C, by the whole-cell patch-clamp technique, decreased by 38 +/- 8% in the presence of 1 mM selenite for 5 min. These selenite-induced effects were not reversed, but are restored by dithiothreitol (1 mM). These results demonstrated that toxic concentrations of selenite induced a significant shortening in AP duration as a result of an increase in the rate of repolarization. Our findings also suggest that a decrease in Na+ currents, in addition to Ca2+ currents, may play a role in the shortening of AP duration in rat papillary muscles.

Action Potentials↗

Two-dimensional echocardiographic recognition of papillary muscle fibrosis in pediatric patients.

Two-dimensional echocardiographic examinations were performed in seven infants with anomalous origin of the left coronary artery from the pulmonary artery (ALCA), in one infant with myocardial infarction and left main coronary obstruction, and in eight with critical valvar aortic stenosis (AS). Comparative qualitative echo density assessment demonstrated that each infant had a marked increase in the echo density of one or both left ventricular papillary muscles. The increased echo density was considered to represent fibrosis and scar formation as a result of ischemia and infarction. Pathologic proof of excessive fibrosis of the papillary muscles was obtained in three cases. In an additional case, calcification of the papillary muscle was noted on fluoroscopic examination. The echocardiographic appearance of papillary muscle fibrosis provides a useful indicator of severe subendocardial ischemia in patients with either critical AS or ALCA.

Aortic Valve Stenosis↗

The effects of potassium channel modulators on the simulated ischaemia-induced changes in contractility and responsiveness to phenylephrine of rat-isolated papillary muscle.

The aim of the present study was to compare the influence of terikalant, a blocker of inwardly rectifying K+ channels, galanin, a neuropeptide of 29 aminoacids with a complex mechanism of action including an activation of inwardly rectifying K+ channels and glibenclamide, a blocker of ATP-sensitive K+ channels, on simulated ischaemia-induced changes in contractility and response to phenylephrine of rat-isolated heart muscle. Experiments were performed on isolated rat heart papillary muscles. The following parameters were measured: force of contraction (Fc), velocity of contraction (+dF/dt) and velocity of relaxation (-dF/dt), time to peak contraction (ttp) and relaxation time at 10% of total amplitude of contraction (tt10). In the presence of 1 microM of galanin, as well as terikalant, simulated ischaemia caused a decrease in Fc, +dF/dt and -dF/dt, however, it significantly increased a drop in Fc and -dF/dt. After 60 min of reperfusion, all the measured parameters recovered completely except Fc in the galanin group. Terikalant, but not galanin, prevents the negative inotropic action of phenylephrine observed in the control group. On the other hand, addition of 1 microm of glibenclamide to the no-substrate solution prevented the simulated ischaemia-induced decrease in Fc, +dF/dt and -dF/dt. In this group phenylephrine did not cause the negative inotropic action. The above mentioned data reveal that pretreatment with the inhibitors of ATP-sensitive and inwardly rectifying K+ channels protect rat-isolated papillary muscle against ischaemia-induced disturbances in contractility.

Animals↗

Acute infarction of the left ventricular papillary muscle: electrocardiographic pattern and recognition of its location.

BACKGROUND AND HYPOTHESIS: ST-segment depression during acute myocardial infarction (AMI) is known to herald serious hemodynamic complications. Since the mechanism of this dependence is not clear, we reinvestigated the old concept of papillary muscle infarction (PMI) as a cause of marked ST depression. METHODS: Autopsies and morpho-electrocardiographic cor-relations were performed in 53 patients with AMI involving one or both left ventricular papillary muscles, and in 10 patients with AMI, but without acute PMI. RESULTS: ST-segment depression > or = 1 mm in at least two leads (mean 3.6 +/- 2.2 mm) was found in 46 (86.8%) patients with, and in one without acute PMI. Thus, the sensitivity and specificity in selecting patients with acute PMI from among those with AMI were 86.8 and 90%, respectively, with an overall accuracy of diagnosis of acute PMI in the course of AMI of 87.3%. Among 26 patients with ST elevation consistent with diagnosis of AMI, ST depression, recorded in 22 patients, was insignificantly greater than in 24 of 27 patients without ST elevation: 4.1 +/- 2.9 versus 3.1 +/- 1.2 mm. Localization of ST depression in the limb leads allowed recognition of which papillary muscle suffered from acute infarction: ST depression in the inferior leads was seen only in patients with anterolateral PMI, whereas in leads I and/or a VL it was seen only in cases with posteromedial PMI. This rule was also valid in patients without concomitant ST elevation. CONCLUSION: Patients with acute PMI show marked ST-segment depression. Its location in the limb leads allows recognition of which papillary muscle has undergone necrosis. This cause of marked ST depression in patients with AMI may explain the high mortality in this particular group.

Aged↗

[Emergency operation for complete papillary muscle rupture after myocardial infarction--a case report of 81-year-old patient].

Mitral regurgitation due to complete rupture of the papillary muscles after myocardial infarction has a very poor prognosis, even if diagnosed and operated on at an early phase. Recently, we performed an emergency operation for mitral regurgitation due to complete papillary muscle rupture after myocardial infarction in an 81-year-old patient. This is probably the oldest case in Japan. Operation revealed complete rupture of the posterior papillary muscle, and valve replacement with a Carpentier-Edwards bioprosthesis was performed.

Aged↗

[Rupture of the papillary muscle after percutaneous transvenous mitral commissurotomy (PTMC)--a case report].

We experienced a rare case of the mitral regurgitation due to papillary muscle rupture after percutaneous transvenous mitral commissurotomy (PTMC). This case was a seventy years old female who underwent PTMC. The cardiac tamponade and mitral regurgitation occurred after PTMC. Pericardial drainage was done immediately, and the next day the emergency operation was required. Rupture of the posterior papillary muscle was found at the operation, and mitral valve replacement was performed. Her postoperative course was uneventful and she discharged on the 26th day after the operation. We should take the papillary muscle rupture into consideration if there are severe sub-valvular lesion and shorting of the chorda.

Aged↗

Influence of glucose on the transmembrane action potential of papillary muscle. Effects of concentration, phlorizin and insulin, nonmetabolizable sugars, and stimulators of glycolysis.

The action potential duration (APD) of isolated guinea pig papillary muscle is directly related to the medium glucose concentration regardless of the gas mixture with which it is in equilibrium. The APD can be maintained at control value for many hours by a glucose concentration of 50 mM in the complete absence of oxygen. Following reduction of the APD by incubation of the muscle in medium containing 5 mM glucose, adjustment of the glucose concentration to 50 mM will cause restoration of normal APD. Phlorizin has been shown to competitively interfere with the effect of glucose on the APD and insulin to prevent or reverse the effect of phlorizin. Nonmetabolizable sugars cannot produce glucose-like effects on the APD. Adrenaline, noradrenaline, and isopropylnoradrenaline increased the reduced APD of papillary muscles incubated in the absence of oxygen in a medium containing 5 mM glucose coincident with an increase in contractile force. The effect of isopropylnoradrenaline was blocked by acetylcholine and propranolol. In the presence of iodoacetate and 2-deoxyglucose, isopropylnoradrenaline increased contractile force but not the reduced APD. Aminophylline was found to produce changes in the reduced APD similar to those caused by the sympathomimetic amines. The findings clearly support the hypothesis that anaerobic metabolism utilizing either glycogen or exogenous glucose is capable of maintaining normal transmembrane electrical activity in guinea pig papillary muscle.

Action Potentials↗

Effect of length and contraction on coronary perfusion in isolated perfused papillary muscle of rat heart.

We studied the impeding effect of cardiac muscle contraction on coronary arterial inflow in six isolated, perfused papillary muscles of the rat. Special attention was given to the effect of changes in muscle length and contractility on flow impediment in systole. Contractility was changed by resumption of pacing after a quiescent period of 60-100 s or by doubling the calcium concentration in the perfusate and the superfusion fluid from 1 to 2 mM. The vascular bed was maximally dilated with adenosine, and perfusion pressure was kept constant at 69 +/- 3 cmH2O. We found that contractions impede arterial inflow by 29% [from 17.3 +/- 2.2 ml.min-1.g-1 during diastole to 12.4 +/- 1.8 (SE) ml.min-1.g-1 at peak systole, P < 0.001] while the muscle was kept at 90% of maximum muscle length (MLmax). When the muscle was stretched from 80 to 97% of MLmax, diastolic force increased from 0.5 +/- 0.3 to 11.1 +/- 1.2 mN/mm2, systolic force increased from 11.1 +/- 1.5 to 44.6 +/- 4.0 mN/mm2, diastolic flow decreased by 12% (from 18.2 +/- 2.3 to 15.9 +/- 1.9 ml.min-1.g-1, P < 0.05), and systolic flow decreased by 3% (12.4 +/- 2.3 to 12.0 +/- 1.6 ml.min-1.g-1, P = NS). Increased contractility by elevated [Ca2+] did not affect diastolic flow but increased systolic flow impediment from 29 to 39% (systolic flow decreased from 12.4 +/- 1.8 to 10.3 +/- 1.4 ml.min-1.g-1, P < 0.01). The results are qualitatively similar to findings in the intact heart. Limitations on quantitative comparison due to differences in muscle architecture and differences in force vectors in the papillary muscle and the left ventricle are discussed. The results show that ventricular pressure is not essential in systolic coronary arterial flow impediment. The findings are in agreement with the varying elastance concept where the flow impediment is predicted to depend on myocardial elastic properties.

Animals↗

Single papillary muscle of the left ventricle associated with persistent common atrioventricular canal: variant of parachute mitral valve.

Six cases of single papillary muscle of the left ventricle in persistent common atrioventricular canal (AVC) are described. Except for one case with double outlet right ventricle and AVC, in the other five cases AVC occurred with normally related great vessels. Down's syndrome was present in two cases. The mitral valvular condition in AVC is not the classic parachute mitral valve since the separation between the common anterior and the common posterior leaflet leaves a space (cleft) oriented toward the ventricular septum. This mitral valve in AVC may or may not be obstructive. The common anterior leaflet fixed to the ventricular septum may result in obstruction. Clinically, single left ventricular papillary muscle should be suspected if the AVC is associated with coarctation of the aorta or tubular hypoplasia of the aortic arch. This type of mitral valve in AVC may also be associated with double outlet right ventricle. Preoperative recognition of the single papillary muscle by echocardiogram or left ventriculogram will prevent postoperative mitral obstruction following closure of the mitral cleft.

Aortic Coarctation↗

On the relationship between action potential duration and tension in cat papillary muscle.

Tension and action potentials have been measured simultaneously from isolated cat papillary muscles. Two groups of experiments are described. In the first group, the external conditions under which the muscle contracted were changed. Specifically, stimulation rate, extra-cellular [Ca++], extracellular [Na++] were altered, and adrenaline was added to the bathing fluid. A tendency for given levels of tension to be accompanied by action potentials of constant duration is demonstrated under some of these conditions. In the second group of experiments, tension and action potentials were recorded following some change in external conditions; specifically, after a long rest, after a change in muscle length, and after the muscle had been set up in the experimental apparatus (the 'running-in' period). In the period that followed each of these interventions, peak tension increased substantially over at least several minutes but all external conditions (for example, temperature, muscle length, stimulation rate, and composition of the bathing fluid) remained constant. In each of these three situations tension increased but in one case the action potential duration increased, in another it decreased, and in the third it was unchanged. It is concluded that change in action potential durations do not necessarily make an important contribution to the changes in tension of papillary muscles.

Action Potentials↗

Contribution of angiotensin II, endothelin 1 and the endothelium to the slow inotropic response to stretch in ferret papillary muscle.

We investigated the contribution of angiotensin II and endothelin I to the slow positive inotropic response observed following stretch of isolated ferret papillary muscle from 88% to 98% of the length at which maximum force is generated. Angiotensin antagonists losartan and saralasin did not affect the magnitude of the slow response in ferret papillary muscle. The ETA-selective antagonist BQ123 slightly reduced the magnitude of the slow response (P > 0.05). In the presence of PD145065 (an ETA and ETB antagonist), the magnitude of the slow response was reduced significantly by 50%. Removal of the endothelium with 1% Triton X-100 reversed the slow response to stretch. We conclude that, in the ferret, endothelin I acting through ETA and ETB receptors, contributes to the slow response although it is not the sole mediator. Angiotensin II is not a prerequisite for the slow response to stretch. We have shown for the first time that the endocardial endothelium plays a pivotal role in this phenomenon in cardiac papillary muscle.

Angiotensin II↗

Acute papillary muscle rupture in a patient with clostridial sepsis.

We describe the clinical course of a 58-year-old man who died from acute papillary muscle rupture as a complication of clostridial sepsis. There was no evidence for myocardial infarction, infective endocarditis, prior chest trauma or other known causes of papillary muscle rupture. Histological specimens taken at autopsy demonstrated clostridial infection of the heart. To our knowledge the occurrence of papillary muscle rupture in the setting of clostridial sepsis has not yet been reported in the literature.

Acute Disease↗