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PubMed1991

The effect of acidosis on the interval-force relation and mechanical restitution in ferret papillary muscle.

1. The effect of a respiratory acidosis on the interval-force relation and on mechanical restitution was investigated in ferret papillary muscles. 2. Acidosis (pH 6.85) decreased developed force over a range of stimulation frequencies (1.0.06 Hz); the percentage decrease was greatest at the lowest stimulation frequencies. Qualitatively similar effects of acidosis on developed force were observed in the presence of the sarcoplasmic reticulum (SR) inhibitor ryanodine. 3. Mechanical restitution curves were constructed by interpolating extra-systoles at different test intervals following a train of steady-state beats. Mechanical restitution in ferret papillary muscle was triphasic: an initial, rapid, exponential increase in force with test intervals to 2 s, a further increase with test intervals between 60 and 90 s and then a slow decline, with a plateau at about 30 min (0.33 Hz, 30 degrees C). 4. Acidosis slowed the initial phase of mechanical restitution. The degree of slowing depended on the steady-state stimulation frequency, being greatest at low frequencies. 5. Inhibition of the SR abolished the initial phase of mechanical restitution, suggesting that this phase depends on Ca2+ release from the SR. 6. The strength of the first contraction after the extra-systole varied inversely with the size of the extra-systole under all conditions studied. 7. It is concluded that acidosis may inhibit the SR by altering the time required for Ca2+ recycling between contractions. This effect may alter Ca2+ release from the SR during acidosis, and may underlie the mechanical alternans (the alternation of small and large contractions) that can occur during acidosis.

Acidosis, Respiratory↗

PubMed1976

Age-changes of the force-frequency-relationship and the duration of action potential of isolated papillary muscles of guinea pig.

The force-frequency-relationship and the duration of the action potential recorded intracellularly were compared on isolated isometrically arranged papillary muscles of young (3--4 months old) and senile (36--40 months old) guinea pigs. The muscles were in Krebs-Henseleit-solution at 37 degrees C electrically stimulated with frequencies between 30 and 420 imp./min. The following results were obtained: 1. The isolated papillary muscles of the two groups are almost similar with respect to length, weight and cross-sectional are. 2. In the range of stimulation rate from 30--420 imp./min the duration of action potential in the senile group was 120--135% of that in the young group. 3. The shape of slow repolarization of action potential was steeper in the senile group. 4. The time to peak tension and the relaxation time were longer in the senile group. 5. The maximally developed tension was the same in both groups, but in the senile group it was reached at a stimulation rate of 120 imp./min whereas in the young group, the optimal frequency was 290 imp./min. 6. The greatest value for the maximal rate of tension rise was 2.4 times smaller in the senile group. The results are discussed in relation to the age dependent intensity of membrane currents and to a possible altered activity of sarcoplasmic reticulum.

Action Potentials↗

PubMed1978

[Surgical treatment by valve replacement and aorto-coronary bypass in mitral valve insufficiency caused by chronic dysfunction of the posterior papillary muscle].

Nine patients with cardiac failure which was refractory to medical treatment, and which was caused by chronic malfunction of the posterior papillary muscle, as a result of a myocardial infarction, were studied by cardiac catheterisation and coronary arteriography. The mean pulmonary capillary pressure was 31+/-16 mm of mercury with a nu wave at 51+/-27 mm of mercury. The end diastolic volume was increased (141+/-68 ml/m2) and the ejection fraction lowered (0.40+/-0.13). The left ventricle had overall hypokinesia in 5 patients and akinesia of the inferior wall, representing 21+/-24% of the end diastolic perimeter, in 3 others. All these patients had significant lesions of two or three of the main coronary trunks. At operation lengthening of the posterior papillary muscle and/or the cordae was found. All patients had a replacement mitral valve of the Starr-Edwards type, associated with an aorto-coronary bypass of the anterior descending artery. The operative mortality was zero. At a mean follow-up period of 21 months, there had been no late death, and all the patients were improved.

Aged↗

PubMed1987

Changes in intra- and extracellular potassium and intracellular sodium activities induced by repetitive stimulation and their relation to membrane potential in guinea-pig papillary muscle.

We measured changes in membrane potential (MP), extra- and intracellular potassium and intracellular sodium ion activities (aKo, aKi, and aNai) in papillary muscle of the guinea-pig heart induced by repetitive stimulation at various frequencies and periods in vitro, using double-barrelled ion-selective microelectrodes. Stimulation (2-4 Hz) depolarized the cells, and termination of stimulation induced hyperpolarization. The aKi and aNai (stimulated at 0.2 Hz) were 92.3 +/- 4.6 and 7.8 +/- 2.0 mM (mean +/- S.D.), respectively. Prolongation of the stimulation period (0.5-2 min) increased aNai time-dependently, but there was no further increase by stimulation for longer than 3 min. The increase in aNai was dependent on stimulus frequency. After termination of the stimulation aiNa declined exponentially. aKi slightly decreased by the stimulation (3-4 Hz). aKo increased during the stimulation period, and decreased below the initial level after termination of the stimulation. Results suggest that in guinea-pig papillary muscle, the contribution of an electrogenic component of Na-K pump to the hyperpolarization after stimulation would be small, since the hyperpolarization could be explained mostly by depletion of aKo induced by Na-K pump activity.

Animals↗

PubMed1991

Adenosine receptors mediate a pertussis toxin-insensitive prejunctional inhibition of noradrenaline release on a papillary muscle model.

The effects of adenosine receptor agonists and antagonists on field-stimulated release of radioactivity from superfused guinea-pig papillary muscles preincubated with [3H] noradrenaline were studied. N6-cyclopentyladenosine (CPA), N6-(R-phenylisopropyl)-adenosine, and 5'-N-ethylcarboxamidoadenosine caused concentration-dependent inhibition of evoked overflow with a rank order of potency typical for interaction of the compounds with the A1-subtype of adenosine receptors. Maximum inhibition was 80%. The A1-selective antagonist 8-cyclopentyl-1,3-dipropyl-xanthine (DPCPX) induced a rightward shift of the concentration-response curve for CPA with a pA2 of 8.35. However, DPCPX per se had no effect on stimulation-evoked tritium overflow. On the other hand, in the presence of 4-nitrobenzylthioinosine (2 mumol/l) and deoxycoformycin (1 mumol/l), inhibitors of adenosine uptake and deamination, respectively, DPCPX produced a concentration-dependent increase in overflow with a pD2 of 8.1. Pretreatment of the animals with pertussis toxin caused a substantial reduction in the activity of toxin-sensitive G proteins, as indicated by a lack of [32P]ADP ribosylation in a ventricular membrane preparation. Nevertheless, the inhibitory effect of the adenosine receptor agonists on stimulus-evoked overflow remained unaffected. These results are compatible with the existence of inhibitory prejunctional adenosine receptors in guinea-pig papillary muscle, which appear to be coupled to a pertussis toxin-insensitive G protein. The role of endogenous adenosine in occupying these receptors seems minimal under basal conditions.

Animals↗

PubMed1989

Diazepam does not improve the mechanical performance of rat cardiac papillary muscle exposed to chloroquine in vitro.

Diazepam has been reported to decrease the cardiac toxicity of chloroquine but the precise mechanism involved remains unknown. Left ventricular papillary muscles from adult Wistar rats were exposed to 10(-4) M chloroquine and assigned to three groups: group I (n = 10) exposed to chloroquine alone; group II (n = 8) exposed to chloroquine and 10(-5) M diazepam; group III (n = 8) exposed to chloroquine and 10(-4) M diazepam. The main mechanical parameters measured were: maximum unloaded shortening velocity (Vmax), maximum lengthening velocity (maxVr), active force normalized per cross-sectional area (AF/s), contraction-relaxation coupling under low load (R1), load sensitivity of relaxation (Isot.A/Isom.A), and peak power output (Emax) determined from Hill's equation of the force-velocity curve. Data are expressed as mean percent of control values +/- SD, for groups I, II, III respectively. No differences between groups I, II, and III were noted for Vmax (87 +/- 13, 82 +/- 9, 86 +/- 7), maxVr (47 +/- 6, 48 +/- 11, 52 +/- 11), AF/s (87 +/- 16, 91 +/- 10, 83 +/- 11), Isot. A/Isom. A (113 +/- 9, 108 +/- 3, 109 +/- 7), or Emax (75 +/- 10, 81 +/- 12, 72 +/- 16). Chloroquine was shown to be a negative inotropic agent since it decreased Vmax, AF/s and Emax, but diazepam did not restore the intrinsic mechanical performance of rat cardiac papillary muscle exposed to chloroquine, therefore 1) the protective cardiovascular effects of diazepam in chloroquine poisoning are not related to an improvement in intrinsic cardiac mechanical properties; 2) inotropic agents are therefore necessary in combination with diazepam for the treatment of severe chloroquine poisoning.

Animals↗

PubMed1990

Electrophysiological effects of AN-132, a new antiarrhythmic compound, in guinea pig papillary muscles.

We used electrophysiological techniques to examine the effects of AN-132, a new antiarrhythmic agent, on transmembrane action potentials of isolated papillary muscles of guinea pigs. AN-132 (1-90 microM) produced a dose-dependent decrease in the maximum upstroke velocity of the action potential (Vmax). The resting potential and the amplitude, overshoot, and the duration of the action potential were not affected, even at the highest concentration of the drug used (90 microM). In the presence of AN-132, trains of stimuli at a rate of 0.5, 1, 2, and 4 Hz led to an exponential decline in the Vmax, reaching a new steady state (use-dependent block, UDB). The UDB was augmented by higher stimulation frequencies or lower membrane potentials. In the presence of the drug (60 microM), the time constant and the rate of onset of UDB of Vmax were 13.4-4.5 s and 0.141-0.053 AP-1 at stimulation frequencies of 0.5-4.0 Hz, respectively. The time constant for the recovery of Vmax from the UDB was 81.2 +/- 17.2 s. AN-132 (60 microM) only slightly depressed the Vmax of the first action potential elicited after an 8-min quiescent period (tonic block, TB). In papillary muscles depolarized with 8.4 and 10.4 mM [K+]0, both UDB and TB were augmented, but the augmentation was greater with the former. None of the parameters of the slow response elicited in the presence of 27 mM [K+]0 and 0.2 mM Ba2+ were affected by the drug (30-90 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1989

Electrophysiological effects of lidocaine on isolated guinea pig Purkinje fibers: comparison with its effects on papillary muscle.

1. The effects of lidocaine on action potentials of isolated guinea pig Purkinje fibers were examined and compared with those on the papillary muscle, by use of conventional microelectrode techniques. 2. Lidocaine 2.1 x 10(-4) M significantly depressed the resting membrane potential, amplitude, overshoot, maximum upstroke velocity, and duration of action potential of the Purkinje fibers stimulated at cycle length (CL) 1 sec, while the lower concentration (2.1 x 10(-5) M) produced no significant effect. 3. Various parameters of action potentials from the papillary muscle at CL = 1 sec were also depressed by lidocaine 2.1 x 10(-4) M, but the extent of the depression was less marked than in Purkinje fibers. 4. When the Purkinje fibers were stimulated at various CLs (0.3-10 sec), the shortening of action potential duration induced by lidocaine was more evident at slower stimulus rate.

Action Potentials↗

PubMed1989

Electrophysiological effects of OPC-88117, a new antiarrhythmic agent on papillary muscles and single ventricular myocytes isolated from guinea-pig hearts.

1. The effects of OPC-88117, a new antiarrhythmic agent, on transmembrane action potentials were examined in right ventricular papillary muscles and in single ventricular myocytes isolated from guinea-pig hearts. 2. In papillary muscles, OPC-88117 above 3 x 10(-6) M caused a dose-dependent prolongation of action potential duration (APD). 3. OPC-88117 above 3 x 10(-5) M caused a significant decrease in the maximum upstroke velocity (Vmax) of the action potential without affecting the resting membrane potential. The inhibition of Vmax was enhanced at higher stimulation frequencies. 4. In the presence of OPC-88117, trains of stimuli at rates greater than or equal to 1.0 Hz led to a use-dependent inhibition of Vmax with rapid onset. The time constant for the recovery of Vmax from the use-dependent block was 456 ms. 5. The curves relating membrane potential and Vmax were shifted by OPC-88117 to the direction of more negative potentials (9 mV at 10(-4) M). 6. In single ventricular myocytes treated with OPC-88117 (1-3 x 10(-4) M), the Vmax of test action potentials preceded by conditioning clamp pulses to 0 mV was decreased progressively as the clamp pulse duration was prolonged. 7. These findings suggest that the primary electrophysiological effect of OPC-88117 on the cardiac muscle cell is prolongation of APD (Class III action) and that at high concentrations, it may also possess a lignocaine-like sodium channel inhibitory effect (Class I action).

Action Potentials↗

PubMed2006

Complete rupture of the posterior papillary muscle caused by late reperfusion for acute myocardial infarction.

We describe a patient with acute mitral regurgitation due to complete rupture of the papillary muscle immediately after successful late reperfusion for inferior myocardial infarction. An 81-year-old woman was admitted complaining of mild chest discomfort. Although the electrocardiograms, biochemical test results, and her clinical history showed that several days had passed since the onset of acute myocardial infarction, a late coronary stenting was performed. Immediately after successful stenting, she suddenly developed acute pulmonary edema, leading to cardiogenic shock. In addition to high pulmonary capillary wedge pressure (mean 35 mmHg), color Doppler imaging revealed massive mitral regurgitation caused by complete rupture of the posterior papillary muscle. Emergent mitral valve replacement with a prosthetic valve was performed, saving the patient. Hence, late reperfusion should be considered carefully when treating a patient with a high risk, such as an elderly patient or a patient with single-vessel disease or initial transmural myocardial infarction.

Aged, 80 and over↗

PubMed1987

Changes in LV papillary muscle performance and myosin composition with aortic insufficiency in rats.

Aortic insufficiency was induced in rats. Left ventricular papillary muscle function was studied after 5, 12, and 40 wk and compared with the papillary muscles from sham-operated animals. The maximum unloaded velocity of shortening, Vmax, was decreased in the rats with aortic insufficiency relative to controls by 15, 20, and 34% at 5, 12, and 40 wk, respectively. The decrease in Vmax occurred concomitantly with a change in the myosin isoenzyme composition such that the V1 isoform content decreased and the V3 isoform increased. Relative to age-matched controls, the V3 content in the hearts with aortic insufficiency had increased by 80, 180, and 125% at 5, 12, and 40 wk, respectively. The decrease in Vmax in the aortic insufficiency group muscles correlated with the change in myosin isozyme composition and could not be explained by changes in collagen content. Thus aortic insufficiency induced changes in myosin isozyme content and Vmax similar to those previously observed with aortic stenosis, thus suggesting a common mechanism of myocardial adaptation to different types of mechanical overload.

Animals↗

PubMed1993

Cocaine enhances postrest and paired-stimulation potentiation in rat papillary muscle.

We studied the effects of cocaine (20 mg/l; 58 microM) on paired-stimulation potentiation and rest-potentiation in isolated rat papillary muscles superfused with Tyrode's solution at 31 degrees C. A force transducer was used to measure peak tension developed, maximum velocity of development of tension and time to peak tension. The results show that, in preparations driven at a basic constant rate (0.5 Hz), cocaine had a depressant effect on peak tension developed and maximum velocity of development of tension and shortened time to peak tension. Propranolol or nifedipine did not modify the negative inotropic action of cocaine, whereas this action was blocked by caffeine. The results also show that cocaine enhanced rest-potentiation and paired-stimulation potentiation. In the presence of propranolol, the enhancement of paired-stimulation potentiation caused by cocaine remained intact, whereas it failed to do so under the influence of nifedipine. On the other hand, nifedipine did not affect the enhancing action of cocaine on rest-potentiation. Caffeine reversed both rest-potentiation and paired-stimulation potentiation; this action was not modified by cocaine. Thus, even though cocaine exerted a negative inotropic action on rat papillary muscles driven at a constant rate, it enhanced the potentiating action of maneuvers which modify the force-interval relation. Cocaine appears to cause these effects by acting at various levels of electro-mechanical coupling, such as the sarcolemma, the sarcoplasmic reticulum and the myofilaments sensitivity to calcium.

Animals↗

PubMed1985

Influence of thyroid hormone levels on the electrical and mechanical properties of rabbit papillary muscle.

We have examined the influence of chronic in vivo alterations of thyroxine levels on the electrophysiological and mechanical properties of rabbit ventricular papillary muscles measured in vitro. Marked changes in the repolarization phase of the action potential and the time to peak tension of isometric twitches were observed when thyroid hormone levels were increased above or decreased below normal. The time to peak tension was consistently shorter than normal in hyperthyroid and longer than normal in hypothyroid preparations. In hypothyroid preparations the action potential duration was greater than that of controls at all stimulation frequencies tested (0.1 to 1.0 Hz). In hyperthyroid preparations, the repolarization phase consisted of an initial phase of fast repolarization to membrane potential values between -20 and -40 mV followed by a plateau. The early phase of repolarization persisted at all stimulation frequencies tested (0.1 to 1.0 Hz) but the plateau component increased markedly as the stimulation frequency was decreased. The early phase of repolarization was markedly reduced in the presence of 4-aminopyridine. These results suggest that thyroxine levels may modulate the kinetics of a transient outward current which in rabbit papillary muscle normally is responsible for the frequency dependence of action potential duration. Action potential amplitude, maximum rate of rise, resting membrane potential, and peak isometric twitch tension were not markedly different between the three classes of preparations. A second depolarizing response occurred in all hyperthyroid preparations at low stimulation frequencies (0.1 to 0.4 Hz) but not in control or hypothyroid preparations. This second depolarizing response, which was eliminated by D-600 treatment, was similar to the calcium-dependent slow action potentials recorded in other cardiac preparations. These two component action potentials could represent either intrinsic single cell activity, or a re-entry wave of depolarization which results from nonhomogeneous excitation.

4-Aminopyridine↗

PubMed2001

A case of papillary muscle rupture caused by acute myocardial infarction.

A 63-year-old female was admitted because of cardiogenic shock due to complete rupture of the posterior papillary muscle. The diagnosis was made by echocardiography. She was treated successfully by an emergency replacement of the mitral valve. Early diagnosis and surgical treatment are mandatory and life-saving in the case of complete papillary muscle rupture.

Coronary Angiography↗

PubMed1997

Action potential configuration in heart papillary muscles from female rats in different thyroid states.

We have studied the effects of thyroidectomy and the in vivo administration of different triiodothyronine (T3) doses in thyroidectomized female rats on electrophysiological properties, measured in vitro, of the anterior and posterior papillary muscle fibers from the right ventricle. In each thyroid state, the action potential duration (APD) measured by stimulating at 1 Hz was shorter for the posterior papillary muscle. APD from both preparations was found significantly lengthened in thyroidectomized animals in comparison to euthyroid controls. APD was shortened owing to treatment of thyroidectomized rats with T3 doses up to 10 micrograms/100 g body weight every second day. Treatment with larger doses of T3 tended to restore the values of APD found for ventricular fibres from both controls and thyroidectomized animals treated with substitutive T3 doses (5 micrograms/100 g body weight every second day). As the stimulation rate was increased from 1 to 5 Hz, APD increased in both preparations of all groups. The changes were of different amounts but the APD difference between the rat groups, which were significant at 1 Hz, remained significant at 5 Hz, while the differences between anterior and posterior preparations were cancelled in animals treated with 50 micrograms of T3 and reversed in those treated with 100 micrograms.

Action Potentials↗

PubMed1980

Effects of acetaldehyde upon mechanical properties of isolated rat papillary muscle.

The acute effects of acetaldehyde upon the performance of isolated rat papillary muscle were studied. At high concentrations (50 and 100 mg/100 ml), acetaldehyde demonstrated a negative inotropic effect and abbreviated relaxation time. Pretreatment with either propranolol or reserpine unmasked a direct negative inotropic effect of acetaldehyde at concentrations as low as 5 mg/100 ml. The shortening of relaxation was also blocked by propranolol and reserpine. These findings are compatible with both a direct myocardial depressant effect and an indirect beta-stimulatory effect of acetaldehyde. In the range of concentrations encountered clinically, however, acetaldehyde is not likely to have a significant acute effect upon cardiac muscle performance.

Acetaldehyde↗

PubMed1985

Intracellular pH and contraction of isolated rabbit and cat papillary muscle: effect of superfusate buffering.

The influence of external buffering on surface pH (pHs), intracellular pH (pHi) and developed twitch tension was investigated in rabbit and cat papillary muscle. pHs and pHi were measured using single and double-barreled microelectrodes respectively. In 20 mM HEPES buffered solution, steady state pHi is close to that in control CO2/HCO-3 (25 mM HCO-3, 5% CO2) solution. pHs and developed tension also do not differ greatly from their control values. Decreasing the HEPES concentration to 5 mM, at constant external pH, lowers pHs considerably. The surface acidosis is associated with a small intracellular acidification; steady state pHi in 5 mM HEPES is always more acid than that in control CO2/HCO-3. A significant decrease in developed tension is also seen in 5 mM HEPES. Alteration of the superfusion velocity influences pHs only slightly. Stimulation of the muscle at high frequency is shown to increase surface acidification, the extent of which is dependent on the buffer concentration. The conclusion from the present experiments is that in papillary muscle external buffering influences intracellular pH and contraction via its effect on pHs.

Acid-Base Equilibrium↗

PubMed1999

Effects of agmatine on afterdepolarizations induced by isoproterenol in guinea pig papillary muscles.

AIM: To study the effects of agmatine (Agm) on early afterdepolarizations (EAD) and delayed afterdepolarizations (DAD) induced by isoproterenol (Iso) in guinea pig papillary muscles. METHODS: EAD and DAD were recorded using intracellular glass microelectrode technique. RESULTS: (1) EAD and DAD induced by Iso 20 nmol.L-1 were markedly inhibited by pretreatment with Agm 1.0-2.0 mmol.L-1 in a concentration-dependent manner. (2) NG-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol.L-1), a NOS inhibitor, did not affect the inhibitory effects of Agm (1.0 mmol.L-1) on EAD and DAD induced by Iso. (3) The inhibitory effects of Agm (1.0 mmol.L-1) on EAD and DAD induced by Iso (20 nmol.L-1) were eliminated by pretreatment with idazoxan (Ida, 0.1 mmol.L-1), an alpha-2 adrenergic receptor (alpha 2-AR) and imidazoline receptor (IR) antagonist. CONCLUSION: The inhibitory effects of Agm on EAD and DAD induced by Iso in papillary muscles is related to the reduction in calcium influx and mediated by alpha 2-AR and/or IR.

Adrenergic alpha-2 Receptor Agonists↗