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PubMed1993

Effect of dysfunctional vascular endothelium on myocardial performance in isolated papillary muscles.

Vascular endothelium has been shown to modify the contractile characteristics of vascular smooth muscle, and endocardial endothelium has been shown to modify the contractile characteristics of adjacent myocardium. In this study, whether vascular endothelium also modifies the contractile characteristics of adjacent myocardium and whether these effects are additive to those of endocardial endothelium were investigated. Rabbit hearts (n = 54) were excised and mounted in a Langendorff preparation. Vascular reactivity was verified by acetylcholine infusion. One group of these hearts had Triton X-100 injected as a bolus into the coronaries to render the vascular endothelium dysfunctional. The other portion served as control hearts. Triton X-100 bolus injection resulted in little or no pathological changes on morphological examination; however, the vasodilatory response to acetylcholine in these hearts was abolished, suggesting vascular endothelial dysfunction. Vascular smooth muscle reactivity was verified in Triton X-100-injected hearts by nitroprusside infusion. In the control Langendorff-perfused hearts, there was little evidence of vascular endothelial dysfunction, with the coronary perfusion rate increasing from 8.9 +/- 0.4 to 11.0 +/- 0.3 ml/g per minute (p < 0.01) in response to acetylcholine. All hearts were then removed, and right ventricular papillary muscles were excised for myocardial mechanical studies. Control Langendorff-perfused hearts had myocardial mechanical characteristics similar to those of muscles from 18 other control hearts without Langendorff perfusion, indicating that the Langendorff perfusion itself had little effect on myocardial mechanics. The muscles from the Triton X-100-injected Langendorff hearts had marked changes: a shortening of twitch duration (363 +/- 16 versus 449 +/- 9 msec, p < 0.01) and decreases in total tension (2.2 +/- 0.2 versus 2.9 +/- 0.2 g/mm2, p < 0.01), dT/dt (9 +/- 1 versus 12 +/- 1 g/mm2 per second, p < 0.05), and maximum velocity of unloaded muscle shortening (Vmax) (0.89 +/- 0.06 versus 1.14 +/- 0.07 length at which maximum developed tension occurred [Lmax]/sec, p < 0.05). Endocardial endothelial removal of the papillary muscles in the two control groups (with and without Langendorff perfusion) by Triton X-100 caused the same changes in twitch characteristics as occurred in muscles from the Langendorff-perfused hearts injected with Triton X-100 but with intact endocardial endothelium, suggesting that vascular endothelial dysfunction had similar effects on contractile characteristics as endocardial endothelial removal.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

The electrophysiologic effects of bupivacaine on adult, neonatal, and fetal guinea pig papillary muscles.

The authors used standard microelectrode techniques to study developmental changes in the effects of bupivacaine on the transmembrane potentials of adult, neonatal, and fetal guinea pig papillary muscles. Bupivacaine hyperpolarized membrane potential in the adult and neonatal muscles but not the fetal muscles. In all three age groups, action potential overshoot and the maximum rate of increase of phase 0 (Vmax) were significantly reduced by bupivacaine greater than or equal to 1.0 microgram/ml. Bupivacaine 1.5 micrograms/ml reduced action potential duration at both 50% and 100% repolarization in the fetal tissues, but not in adult or neonatal tissues. Tonic block was not induced by bupivacaine in any of the three groups. Use-dependent block was variable at bupivacaine 0.2 micrograms/ml in all three groups and was consistent and equivalent at higher concentrations. The onset and offset of use-dependent block were the same in all three groups, with onset occurring between 6.0 and 6.7 beats and the time constant for recovery being 1.9-2.3 s. The authors conclude there is an age-related bupivacaine effect on action potential duration but no age-related change in bupivacaine-induced use-dependent block.

Action Potentials↗

PubMed1994

Effects of gadolinium on length-dependent force in guinea-pig papillary muscle.

The degree to which stretch-activated channels operate during physiological length changes in multicellular heart preparations, or how much the channels could contribute to length-dependent activation, is not known. We studied the relationship between muscle length and contractile force in guinea-pig papillary muscles superfused with gadolinium chloride (10 microM), a stretch-activated channel blocker, and compared the effects to those with nifedipine (0.25 microM), a calcium channel blocker. Gadolinium reduced contractile force statistically significantly more at the longer muscle lengths than at the short muscle lengths. This did not apply with nifedipine, although a marginally greater effect at longer lengths was perceptible. The results can only partly be explained by gadolinium having a non-specific action via the calcium channel, or Na(+)-Ca2+ exchange, and are consistent with the possibility that stretch-activated channels contribute to length-dependent activation in cardiac muscle, and thus to 'Starling's Law of the Heart'.

Animals↗

PubMed1995

Positive action of propionyl-L-carnitine on mechanical performance of papillary muscle from Syrian hamsters with hereditary dilated cardiomyopathy.

Propionyl-L-carnitine has been shown to exert a beneficial effect on cardiac function in different experimental models of cardiomyopathy in the rat, most likely by improving cardiac metabolism and energy production. We have previously shown that, in a strain of hamsters with hereditary dilated cardiomyopathy (BIO TO.2), the mechanical activity of papillary muscle (length-tension, velocity of shortening, shortening, work and power relationship) is significantly depressed when compared to the same parameter in normal hamsters (BIO F1.B). The repeated oral treatment with propionyl-L-carnitine (60 mg/kg per os for 7 weeks) to BIO TO.2 hamsters had a significant positive inotropic effect, as indicated by an increase in developed tension up to the levels observed in papillary muscles from normal hamsters. This action is most likely associated with metabolic effects similar to those observed in rats.

Administration, Oral↗

PubMed1985

Contractile performance of papillary muscles of sinoaortic denervated rats.

The effects of sinoaortic baroreceptor denervation (SAD) was studied in left ventricle papillary muscles from rats with 15 days of hypertension, compared to sham operated normotensive controls (SO). SAD muscles develop less force (F) with slower force development (dF/dt) than SO ones, characterizing a depressed contractile performance. To verify if the mechanical response produced by cardiac beta-adrenoceptors stimulation displays a desensitization similar to what is observed for rate changes, percentual changes of F and dF/dt resulting from isoproterenol (IPA) actions were compared in SO and SAD muscles, being similar in both groups. Rest potentiation was analyzed to test if this behavior only occurs during beta-adrenoceptors stimulation or if it is an interference with the contractile machinery. Absolute and percentual changes of F and dF/dt, in SO and SAD rats were again similar, as observed before. The results suggest that in this model of experimental hypertension it is not possible to demonstrate beta-adrenoceptors desensitization in ventricular myocardium. The behavior of SAD muscles must result from changes occurring in a common place for both inotropic interventions probably at the contractile machinery level.

Animals↗

PubMed2002

Cardiac tamponade masking clinical presentation and hemodynamic effects of papillary muscle rupture after acute myocardial infarction.

A 67-year-old woman sustained an acute lateral-wall myocardial infarction and was treated with thrombolytic therapy. Postinfarction hypotension developed 3 days later. Clinical findings at that time were consistent with cardiac tamponade, and an echocardiographic study revealed a moderate-sized pericardial effusion. She underwent urgent pericardiocentesis with transient improvement in hemodynamics, followed by deterioration associated with the development of acute pulmonary edema. Follow-up transesophageal echocardiographic imaging revealed papillary muscle rupture with severe mitral regurgitation. The patient underwent urgent surgical intervention consisting of coronary artery bypass grafting and mitral valve replacement. The presence of cardiac tamponade in this patient masked the clinical manifestations of papillary muscle rupture through the hemodynamic effect of tamponade physiology on mitral regurgitation.

Aged↗

PubMed1979

[Increase of force of concentration under hypoxic conditions by glucose-insulin. Experiments in isolated papillary muscles of the guinea pig (author's transl)].

The minimally remaining force of contraction under the influence of hypoxia was measured in isolated right-ventricular papillary muscles of the guinea-pig, incubated in hypoxic (pO2 90 mm Hg) and oxygenated (pO2 630 mm Hg) buffer solution. With insulin (0.05 IE/ml) and elevated glucose (300 mg% compared to 100 mg%) the force of contraction fell to only 70 +/- 9% minimally instead of 38 +/- 11% (control, p less than 0,001). Elevated glucose or insulin alone had less pronounced effects which were not statistically significant for insulin. The results show an increase of tolerance against hypoxia of isolated papillary muscles under the influence of glucose and insulin.

Animals↗

PubMed1987

Arrhythmic activity in reoxygenated guinea pig papillary muscles and ventricular cells.

Aftercontractions, delayed afterdepolarizations, and automaticity occurred in guinea pig papillary muscles that were reoxygenated after hypoxic conditioning. The emergence of dysfunction was dependent on the severity of hypoxic conditioning and on stimulation during reoxygenation. After 60 minutes of substrate-free hypoxia, reoxygenation induced automaticity in a high proportion of stimulated muscles; the automaticity appeared within 1 minute and lasted for 10-20 minutes. After similar conditioning, muscles reoxygenated for 7-15 minutes were stimulated at various cycle lengths. The incidence of automaticity and the amplitudes of delayed events had W-shaped dependencies on cycle length (200-1,000 msec), whereas coupling intervals had M-shaped dependencies. In ventricular myocytes that displayed automaticity after reoxygenation, extrasystolic upstrokes arose smoothly from delayed afterdepolarizations that reached threshold. In tissue, extrasystolic upstrokes usually rose sharply from delayed afterdepolarizations that were distinctly subthreshold. Thus, threshold was reached elsewhere in the tissue. Further evidence of electrical heterogeneity was obtained from surface mapping of delayed-afterdepolarization amplitude in reoxygenated muscle. There were no detectable aftercontractions, delayed afterdepolarizations, or signs of automaticity in quiescent reoxygenated muscles or in stimulated reoxygenated muscles that were treated with 1 microM ryanodine. We conclude that the dysfunction precipitated by reoxygenation is due to synchronized spontaneous releases of calcium from overloaded sarcoplasmic reticulum.

Animals↗

PubMed1977

Relationship between sarcomere length and active force in rabbit papillary muscle.

Isometric peak twitch force (stimulation frequency 0.5/s; 29.5-30.5 degrees C) was correlated with sarcomere length in isolated papillary muscles of the rabbit. Sarcomere length was measured from photographic recordings (1.5 ms exposure time) performed at rest between contractions and at the time of isometric peak twitch force. The sarcomere length at rest was found to be relatively uniform throughout the preparation and to be linearly related to the overall muscle length within the range Lmax-0.85Lmax. The distribution of sarcomere lengths increased considerably as the muscle went from rest to activity. Studies of surface markers showed different degrees of shortening (or elongation) of individual segments along the length of the preparation. The mean resting sarcomere length at Lmax (the optimum muscle length for force production) was 2.44 +/- 0.01 micron (grand mean +/- S.E., 7 muscles). The means active sarcomere length at Lmax was 2.29 +/- 0.04 micron. Active force declined steeply as the muscle length was reduced below Lmax. At a resting sarcomere length of 2.0 micron, active force was approximately 1/3 of the maximum. The observed differences between the length-tension relat-onships in myocardium (twitch responses) and skeletal muscle (tetanic contractions) are discussed on the basis of a length dependency of the activation process in cardiac muscle.

Animals↗

PubMed1992

Differential effects of halothane, enflurane, and isoflurane on Ca2+ transients and papillary muscle tension in guinea pigs.

These studies were designed to examine the effects of inhalational anesthetics on rapid changes in myocardial intracellular Ca2+ and Ca2+ sensitivity of the contractile apparatus. The effects of halothane, enflurane, and isoflurane on rapid changes in intracellular Ca2+ (Ca2+ transients as measured with bioluminescent protein aequorin) and contractile characteristics were compared in guinea pig right ventricular papillary muscles. In addition to examination of their potencies at equianesthetic concentrations, the effects of these agents on alterations in Ca2+ sensitivity at myofilaments were also investigated. The negative inotropic effects of halothane (0.65 and 1.15%) and enflurane (1.0 and 2.2%) were dose-dependent and closely related to a decrease in Ca2+ transients. In the presence of isoflurane (0.77 and 1.6%), the contractile force decreased in a dose-dependent manner, but the decrease was significantly less as compared to that with equianesthetic concentrations of halothane and enflurane. An additional feature observed in the presence of isoflurane was a dissociation between intracellular Ca2+ availability and contractile force. Although the magnitude of the Ca2+ transients did not change when the percentage of isoflurane was increased from 0.77 to 1.6, the contractile force decreased. Because of these findings, the effects of halothane (1.2%), enflurane (2.2%), and isoflurane (1.6%) on the relationship between intracellular Ca2+ and tension developed in the papillary muscle were examined in order to assess myofibrillar responsiveness to Ca2+. The results indicate that only isoflurane slightly but significantly shifted the Ca2+/isometric tension curve toward higher intracellular Ca2+ concentrations; no differences were observed in the absence and presence of equianesthetic concentrations of halothane and enflurane.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Electrophysiological effects of homocysteine in isolated rat right ventricular papillary muscles and left atria.

There is clinical and epidemiological evidence that elevated plasma homocysteine (Hcy) levels are associated with increased myocardial infarction mortality; however, very little is known about Hcy's direct cardiac effects. Thus, we aimed to characterize the cellular electrophysiologic effects of Hcy, a sulfur-containing amino acid in isolated rat hearts. A conventional microelectrode technique was used in left atria and right ventricular papillary muscles. At concentrations higher than 10(6) M, Hcy significantly decreased the maximum rate of rise of the depolarization phase (Vmax) in both cardiac preparations in a dose-dependent manner. Hcy at 10(-4)-5 x 10(-4) M concentrations increased the action potential duration (APD) at late stages of repolarization (at 75% and 90% of APD) both in atria and in ventricles. There was a slight decrease in action potential amplitude in ventricular papillary muscles and atria at concentrations higher that 10(-5) M. The resting membrane potential and the early repolarization phase (APD25 and APD50) remained unchanged in every preparation studied at all concentrations of Hcy administered. The present data suggest that homocysteine may decrease the Na+ channel activity in in vitro cardiac preparations. reserved.

Action Potentials↗

PubMed1995

A xanthine derivative denbufylline inhibits negative inotropic response to verapamil in guinea pig ventricular papillary muscles, independent of its phosphodiesterase inhibitory activity.

A phosphodiesterase (PDE) III inhibitor, amrinone, inhibited both the negative inotropic actions of verapamil and nicardipine in guinea pig ventricular papillary muscle; this effect was canceled by the protein kinase A inhibitor H-89. The PDE IV inhibitor 1,3-di-n-butyl-7-(2'-oxopropyl)xanthine (denbufylline), which elicited a negative inotropic action by itself, attenuated the action of verapamil up to 10 microM, without any interaction with nicardipine. The attenuation by denbufylline was not influenced by H-89. This suggests that in the ventricular papillary muscle, denbufylline acts on some verapamil-sensitive site(s) in the membrane and interferes with the calcium channel function without involvement of its PDE inhibitory activity.

Animals↗

PubMed1984

Effect of platelet activating factor on guinea-pig papillary muscle.

Platelet activating factor (PAF) induces a biphasic effect on guinea-pig papillary muscle: 1. a transient positive inotropic effect preceded by an increase in action potential duration (APD); 2. a marked negative effect on inotropism and on APD. Since Ca++ slow action potentials were initially enhanced by PAF and then markedly depressed, it is suggested that PAF specifically interferes with the Ca++ slow channel.

Action Potentials↗

PubMed1984

Mechanisms of hypoxia-induced decrease of load dependence of relaxation in cat papillary muscle.

Relaxation of mammalian cardiac muscle is very sensitive to the prevailing load, but becomes largely load-independent during hypoxia. This effect was previously ascribed to a delayed removal of activating myoplasmic calcium. To further elucidate the underlying mechanisms of this effect of hypoxia, relaxation was now studied in 26 cat papillary muscles, in which hypoxia-induced decrease of load dependence of relaxation was compared with the effects of low [Ca2+]o (1.0, 0.5, 0.375 mM), verapamil (1 microM) and nifedipine (0.1 microM). Load dependence of relaxation was quantified by comparing force and time coordinates at the onset of the isometric relaxation phase in several after-loaded isotonic twitch contractions with the relaxation of the isometric control contraction. Hypoxia, low [Ca2+]o, verapamil and nifedipine decreased load dependence of relaxation. Although low [Ca2+]o, verapamil and nifedipine had a more marked negative inotropic effect on the contraction phase than hypoxia, the decrease of load dependence with hypoxia was significantly more pronounced and it included two phases: an early and fast drop, followed by a slower and longer-lasting decrease. The early fast phase was neutralized in low [Ca2+]o and also diminished after administration of verapamil or nifedipine. An impaired calcium reuptake by the sarcoplasmic reticulum would underly only the second phase of decreased load dependence. The first phase on the other hand originated mainly from changes in the isometric relaxation of the papillary muscles.

Animals↗

PubMed1988

Critical tricuspid insufficiency due to papillary muscle rupture. A result of prenatal hypoxic insult.

Fatal tricuspid insufficiency secondary to papillary muscle rupture due to prenatal hypoxic insult occurred in a full-term newborn. The diagnosis of flail tricuspid valve should be considered when fetal distress is encountered in a newborn with persistent hypoxemia. Prenatal diagnosis of this condition combined with prompt delivery, prostaglandin E1 therapy, and possible surgical repair of the tricuspid valve may improve chances of survival.

Female↗

PubMed1973

The time courses of the changes in contractile force and in transmembfane potentials induced by cardiac glycosides in guinea-pig papillary muscle.

1. The effects of ouabain, digoxin, digoxigenin monodigitoxoside, digoxigenin bisdigitoxoside and digitoxigenin bisdigitoxoside on the force of contraction and on the transmembrane action potential were compared in isolated papillary muscles of guinea-pigs.2. All cardiac glycosides studied had a dose-dependent positive inotropic effect and simultaneously shortened the duration of the action potential at all levels of repolarization from the start of drug action.3. In every instance, the reduction of the action potential duration developed more slowly than the increment in contractile force. However, the ratios between the two rates were independent of the concentrations used and seemed to be characteristic for the individual cardiac glycosides.4. All cardiac glycosides had a biphasic effect on the time-to-peak tension. An initial increase was followed by a dose-dependent decrease.5. The results are discussed with respect to the possible sites of action. Taking into account the different rates as well as the different ratios, it is proposed that more than one site of action is involved in producing the different effects of cardiac glycosides on heart muscle.

Action Potentials↗

PubMed1987

Qualitative characteristics of the mechanical response in rat papillary muscles to increase in extracellular calcium concentration.

The qualitative characteristics of the inotropic response to increase in extracellular calcium (Cao) were studied in isolated, electrically driven, isometrically contracting rat papillary muscles. All experiments were done in the presence of adrenergic receptor blockers. Cao was increased in a cumulative way by exchanging a small fraction of the incubation solution with a corresponding solution with higher calcium concentration (8 mmol l-1). At any Cao level there was an almost proportional increase in parameters describing different parts of the contraction-relaxation cycle as compared with results at the preceding lower Cao level. Time to peak tension was prolonged at high compared with low Cao levels. The response to increased Cao was very similar to the cyclic AMP (cAMP)-independent inotropic response elicited through activation of alpha-adrenergic receptors (alpha-type response, Skomedal et al. 1982) and strikingly different from the cAMP-dependent inotropic response elicited, for example, through activation of beta-adrenergic receptors (beta-type response, Skomedal et al. 1982). As the inotropic response to increased Cao is known to be cAMP-independent (Dönges et al. 1977), the present results demonstrate the interrelationship between the regulatory function(s) and the direct effector function(s) of calcium in the myocardium.

Adrenergic alpha-Agonists↗

PubMed1993

Differential effects of propofol and enflurane on contractions dependent on calcium derived from the sarcoplasmic reticulum of guinea pig isolated papillary muscles.

We investigated the possibility that the effects of propofol on sarcoplasmic reticulum (SR) function may contribute to the myocardial depression induced by this anesthetic. With guinea pig isolated papillary muscles, the effects of propofol on transient alterations in contractility (termed "potentiated-state" contractions), after abrupt changes in stimulation frequency and brief periods of rest, were compared with those of enflurane and the inhibitor of SR function, ryanodine. These potentiated-state contractions are mediated by calcium derived largely from the SR. Propofol, enflurane, and ryanodine were applied at concentrations that produced approximately 50%-60% inhibition of "steady-state" contraction. Ryanodine abolished and enflurane attenuated the potentiated-state contractions, whereas propofol had no apparent effect. Although impairment of SR function may contribute to the depression of contractility induced by enflurane, propofol has no major effect on SR function.

Animals↗