[Characteristics of myocardial contraction in myocardial infarct].
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Acute Disease↗
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Studies on myocardial contraction. Right ventricular contraction and local myocardial contraction measured by the transcatheter method.
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Animals↗
Effects of platelet-activating factor on myocardial contraction and myocardial relaxation of isolated perfused guinea pig hearts.
Platelet-activating factor (PAF) is an important mediator of cardiovascular shock owing to immunologic reactions, including anaphylaxis and endotoxaemia. Previous studies have shown that PAF is a potent cardio-depressive agent causing a marked coronary constriction and a sustained impairment of myocardial contractility. In this study, we attempted to characterize further the prolonged PAF effects on coronary circulation and myocardial contractile force in isolated guinea pig hearts perfused at constant pressure (60 cm H2O) or constant flow which was adjusted to a level of 100% above basal flow. In addition, the PAF-induced changes of ventricular systolic and diastolic function were distinguished. In the hearts perfused at constant pressure, PAF induced a dose-dependent (0.57, 5.7, and 57 pmol/min) decrease of coronary flow rates, left ventricular pressure (LVP), LV contraction (peak positive dP/dt) and LV relaxation (peak negative dP/dt). The decrement of peak negative dP/dt was more pronounced than that of peak positive dP/dt. Maintenance of coronary flow rates only attenuated, but did not suppress, the PAF-induced ventricular malfunction, and it improved ventricular relaxation less than it did ventricular contraction. Pretreatment with the PAF antagonist WEB 2086 (19.7 nmol/min) almost completely abolished the effects of the highest PAF dose on coronary circulation and ventricular contractile parameters. We conclude that the cardiodepressive effects of PAF are due to coronary constriction and direct contractile events. Furthermore, PAF impairs ventricular diastolic function more than ventricular systolic function.
Animals↗
Increased uncoupling of beta-, beta 1- and beta 2-adrenoceptor to myocardial contraction in failing human myocardium.
Coupling of myocardial beta-, beta 1-, beta 2- and alpha-adrenoceptors (AR) to myocardial contraction was investigated in patients with various degrees of heart failure. With the use of delta Vcfc, a load independent parameter of myocardial contraction, AR mediated contraction was evaluated. beta-AR mediated contraction, delta Vcfc by infusion of a beta-AR agonist, isoproterenol, declined with the advancement of heart failure from 0.41 Circ/sec (NYHA I) to 0.31 (NYHA II), 0.22 (NYHA III) and 0.12 (NYHA IV). Dobutamine, a beta 1-AR full agonist, mediated delta Vcfc was 92-97% of that of isoproterenol. On the other hand, terbutaline sulfate, a full agonist to beta 2-AR, increased delta Vcfc partially in comparison with isoproterenol; 51% in NYHA I, 52% in NYHA II, 36% in NYHA III and 17% in NYHA IV. An alpha 1-AR agonist, methoxamine had little effect on myocardial contractility beta-AR and alpha-AR densities were analyzed by saturation binding isotherms of myocardial membrane fraction with 125I-Iodocyanopindolol (ICYP) and 3H-Bunazosin, respectively. beta-1 and beta 2-ARs were separated by competition binding of 125ICYP with a highly selective beta 1 AR antagonist, CGP20712A. There was a progressive down regulation of beta, beta 1- and beta 2-ARs with the advancement of heart failure. A new index was used to examine coupling of ARs to myocardial contraction; Coupling Index. The index was slightly decreased in NYHA II in beta- and beta 1-ARs. In beta 2-AR, the coupling index declined as heart failure advanced from NYHA I to NYHA IV.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Cardiac output and regional myocardial contraction in anorexia nervosa.
The study measured cardiac output and assessed regional myocardial contraction in 14 patients with anorexia nervosa, some of whom also had bulimia, and in 15 controls. The experimental and control groups were not significantly different in age or body surface area (p = greater than 0.05). To evaluate regional myocardial contraction, 12 of 14 anorexia nervosa-bulimia (ANB) patients were studied in the acute phase and once serially at a mean interval of 1.5 years by assessing the movement of each left ventricular wall segment toward the center of the ventricle as imaged in the precordial short axis. Cardiac output was measured in the ascending aorta by pulsed Doppler for control subjects and for 13 ANB patients. Regional myocardial contraction was normal for all controls, but eight of 14 ANB patients showed regional myocardial contraction abnormalities. Between studies, four of these eight demonstrated improved regional myocardial contraction, three remained unchanged, and one was worse. Mean cardiac output was markedly reduced in ANB patients (2.6 L/min) compared to controls (4.5 L/min) (p = less than 0.001). The low cardiac output in ANB patients was reflected as reduced mean ascending aortic velocity/second (18.5 cm/s) compared to a mean of 22.8 cm/s for controls (p = less than 0.02). Mean ascending aortic area was slightly smaller for ANP patients. Mean peak ascending aortic velocity was significantly lower in ANB patients than in controls (p = less than 0.02). Mitral valve prolapse was seen during at least one examination in seven of 14 ANB patients (0/15 controls) and disappeared in two of three patients following hydration.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Characteristics of myocardial contractions activated under depolarizing conditions.
Guinea pig papillary muscles were used to study the activation of myocardial contractions under depolarizing conditions. Depolarization promoted by TKBa (normal Tyrode solution containing KCl and BaCl2) and TKAdr (normal Tyrode solution containing KCl and adrenaline) inactivates the fast Na current and under these conditions only slow responses are available to activate contractions. Since the slow response is sensitive to changes in rate and rhythm, we searched for mechanical correlates using isometrically contracting preparations to study the force-frequency relationship as well as rest potentiation. We also investigated if contractions are dependent only on the slow response or if the complete action potential plays a special role in the activation of contractions. We conclude that the slow response is the main mechanism for the activation of myocardial contraction, because complete mechanical activation was observed under depolarizing conditions. However, the electrical behavior of the slow response is reflected in the mechanical behavior of the depolarized preparations. At high rates, disturbances of excitation occur in depolarized cells and contractions appear to be bigeminal or with 2:1 block. Furthermore, after long pauses, post-rest contractions are depressed and increase progressively with repetitive stimulation, probably due to changes in the latency and threshold of the slow response. The complete action potential also plays a role in the activation of myocardial contractions which is necessary for the resting potentiation phenomena and also to avoid the larger depression of the rest contractions that can be seen in depolarized muscles when the pause is prolonged. This behavior seems to be related to the decrease of intracellular Na concentration produced by the inhibition of the fast inward Na-current.
Action Potentials↗
[Myocardial contraction and coronary circulation in experimental myocardial hypertrophy].
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Animals↗
[Effect of strophanthin and cytochrome C on myocardial contraction and the incidence of shock and ventricular fibrillation in experimental myocardial infarct].
High ligation of the interventricular artery caused ventricular fibrillation in the first 2--4 minutes in 20% of cats. In the remaining animals myocardial contractility diminished to half its initial value. After that, contractility increased gradually. In cardiosclerosis myocardial contractility reduced by 20--30%. Ligation of the interventricular artery on the background of cardiosclerosis induced cardiogenic shock in half of the animals. Cytochrome C does not reduce the diminution of myocardial contractility after ligation and has a marked antifibrillatory effect. Strophantin does not affect the diminution of contractility of a healthy myocardium but reduces the decrease in contractility of a sclerosed myocardium and also promotes the development of ventricular fibrillation following ligation of the interventricular artery.
Animals↗
Myocardial contraction band lesions in patients with fatal asthma: possible neurocardiologic mechanisms.
Myocardial contraction band necrosis (MCBN) occurs in catecholamine infusion, central nervous system stimulation, stress, and transient myocardial ischemia with reperfusion. In 4 of 13 children who died with asthma, MCBN was present, suggesting that this cardiac lesion may contribute to the deaths of some asthmatic patients. Two of the 4 patients who had MCBN had not received sympathomimetics intravenously or by an intracardiac route. Therefore, mechanisms other than infusions of large doses of catecholamines are probably involved in production of this cardiac lesion in asthmatics.
Adolescent↗
[Correlation of the parameters of myocardial contraction and relaxation in compensatory cardiac hypertrophy].
The parameters of myocardial contraction and relaxation were determined from the left ventricular pressure curves obtained in closed chest rabbits. One month after the creation of ascending aorta stenosis when the relative weight of the left ventricle increased by 54% as compared to the control, systolic pressure was higher by 42% and maximum rate of pressure development by 47%. This increase corresponded to the degree of left ventricular hypertrophy so that the load on the unit of myocardial mass did not change. No changes were found in the contractility index. The index of relaxation, however, determined by the relation between the maximum rate of relaxation and the developed pressure and characterizing the function of the myocardial relaxation system was 20% lower than that of the control. This was associated with the decrease of the diastolic pause by 27%. The slowing down of relaxation is one of the first and must' signs of compensatory function of the heart.
Animals↗
Action potential duration and endocardial modulation of myocardial contraction in the ferret.
OBJECTIVE: Endocardial endothelium releases substances which modulate myocardial contraction. Selective endocardial removal abbreviates contraction by removing a contraction prolonging substance "endocardin". The aim of the study was to investigate whether changes in action potential duration underlie these contractile effects. METHODS: The contractile effects of shortening the action potential were first characterised, using a potassium channel "opener" cromakalim (3 microM). Transmembrane action potentials were then recorded in isolated ferret papillary muscles before and after endocardial removal. RESULTS: Cromakalim-induced action potential abbreviation reduced contractile twitch duration. Endocardial removal itself however did not alter action potential duration. CONCLUSIONS: Endocardial modulation of cardiac contraction does not involve changes in action potential duration.
Action Potentials↗
Effect of myocardial contraction on systolic coronary resistance in conscious dogs.
We studied the effect of cardiac contraction on systolic coronary resistance under the conditions of maximally dilated coronary resistance vessels in six conscious dogs. Subendocardial segment length in areas supplied by the left circumflex coronary artery, left ventricular pressure and left circumflex coronary artery flow were simultaneously measured. At 5 sec after release of the first 2 min of left circumflex coronary artery occlusion, diastolic coronary blood flow revealed its peak value in association with markedly depressed regional contractile function. With collateral development induced by repeated 2 min left circumflex coronary artery occlusions, segmental dysfunction during occlusion and early reperfusion was progressively attenuated. Before and after collateral development, diastolic coronary resistance at 5 sec of reperfusion remained unchanged, but systolic coronary resistance increased by 41% secondary to restoration of regional myocardial shortening. In each animal, normalized regional shortening correlated well with changes in systolic coronary resistance. The fraction of systolic coronary resistance due to active regional myocardial contraction was 52%. These studies demonstrate that when coronary vasomotor tone is abolished, regional myocardial contraction impedes the coronary systolic flow in proportion to the extent of shortening.
Animals↗
Mechanisms of transient augmentation of myocardial contraction after a brief coronary occlusion.
The purpose of this study was 1) to clarify whether augmented myocardial contraction after a brief coronary occlusion, i.e. post-ischemic hypercontraction, depends on a transient increase in coronary blood flow or preceding myocardial ischemia, and 2) to identify the role of catecholamines or calcium flux in this phenomenon. Sixteen mongrel dogs were examined in open-chest anesthetized condition. One-minute reperfusion after two-minute total coronary occlusion of the left anterior descending artery resulted in a transient increase in segment shortening. Intracoronary administration of adenosine caused hyperemia without any changes in segment shortening. Two minutes of total coronary occlusion with adenosine caused post-ischemic hypercontraction to the same degree, but without any additional hyperemia. Two minutes of partial occlusion with 75% flow reduction caused less post-ischemic hypercontraction. Post-ischemic hypercontraction did not occur after partial occlusion with 50% flow reduction, irrespective of hyperemia with adenosine during reperfusion. Propranolol or verapamil did not prevent this phenomenon. Thus, post-ischemic hypercontraction is not dependent on the transient increase in coronary blood flow, but is related to the preceding myocardial ischemia. Local release of catecholamines is not likely to be the cause. A calcium antagonist, verapamil, did not modify this phenomenon. The precise mechanism of this phenomenon is still uncertain, although some alterations in cellular hemostasis, such as ionic changes, are likely to be the cause.
Animals↗
Correlation of myocardial contraction band necrosis and vascular patency. A study of coronary artery bypass graft anastomoses at branch points.
Eleven patients who died within 1 week of operation and in whom saphenous vein bypass graft anastomoses were located at or extended across coronary artery branch points were studied at autopsy. New surgically introduced narrowings of greater than 75% in one branch of the 13 anastomoses studied were more frequent (six of eight) when the arteriotomy extended into a branch artery than when the arteriotomy ended proximal to the flow divider of the branch point (zero to five). Obstruction was most frequently caused by suture compression of the arterial lumen. In five of the six anastomoses, where one branch contained a significant new narrowing and the other did not, a striking difference in the severity of myocardial contraction band necrosis in the distribution of the two arteries was found. In each such case the severe necrosis was in the distribution of the patent branch artery and the obstructed branch had slight or trivial injury. The results are interpreted as showing that myocardium that has the potential for developing contraction band necrosis may not develop it if the reflow phase is suppressed.
Adult↗
The influence of endocardial endothelium on myocardial contraction.
A novel unidentified agent, provisionally named 'endocardin', has been shown to be released from endocardial endothelium. Endocardin has a unique prolonging effect on myocardial contraction. In contrast, endothelium-derived relaxing factor released from endocardial endothelium has the opposite effect of abbreviating contraction. Jerry Smith and colleagues discuss the mechanisms of action of these agents and their possible physiology and pathophysiology.
Animals↗
Effects of ischemia, bypass surgery and past infarction on myocardial contraction, relaxation and compliance during exercise.
Abnormalities of left ventricular function during ischemia have been described in animal models and in humans. Exercise, while a physiologic means of inducing ischemia, has a complex effect on left ventricular function by itself. In addition, patients with coronary artery disease have a diversity of chronic changes in myocardial structure and function. Therefore, with use of micromanometer left ventricular pressure measurements and ventricular volumes, calculated from biplane cineangiograms, left ventricular function at rest and during exercise was studied in 57 patients. Exercise-induced ischemia produced a decrease in ejection fraction, an increase in end-systolic volume, dramatic increases in diastolic pressures and an upward shift in the diastolic pressure-volume relation. Central to these changes was abnormal myocardial contraction and relaxation, with reduced regional shortening and impaired left ventricular pressure decay. However, nonischemic areas were capable of augmented shortening, and global pressure decay did accelerate slightly. These findings demonstrate that exercise-induced adjustments in contraction and relaxation are intertwined with ischemia-related abnormalities. Exercise studies in patients after bypass surgery and in patients with scars from distant myocardial infarction were useful in clarifying confounding factors. For example, asynchrony of contraction and relaxation, and chronic changes in passive chamber properties, also compromise systolic and diastolic function during exercise. In patients with coronary artery disease without ischemia during exercise, left ventricular end-diastolic pressure, but not early diastolic pressure, increased during exercise. The increase in pressure was appropriate for a slight increase in end-diastolic volume in a ventricle with a steep pressure-volume relation. Furthermore, end-systolic volume, while maintained during exercise, was not reduced, as occurs normally.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Catheterization↗
Oscillation of cyclic adenosine monophosphate concentration during the myocardial contraction cycle.
The concentration of adenosine 3',5'-monophosphate (cyclic AMP) rises and falls during each myocardial contraction cycle. Peak concentrations of cyclic AMP precede peak development of systolic tension. Epinephrine alters the normal oscillation in myocardial cyclic AMP and increases both diastolic and systolic concentrations of the cyclic nucleotide. These transient changes in myocardial cyclic AMP indicate a potential role for cyclic AMP as a beat-to-beat regulator of myocardial contractility.
Animals↗
[Relationship between the amplitude of myocardial contractions in frogs and the frequency of electrical stimulation. Role of external and intracellular calcium in the coupling of excitation and contraction].
Ionic currents were studied on the frog atrial trabeculae (Rana ridibunda) at 20 degrees C using a double sucrose gap voltage clamp arrangement. The net inward current peaks did not change in the course of repetitive stimulation (0,5/s) in contrast to the increase of the contraction amplitude (isometric tension) in the similar conditions (Bowdich staircase). The slow component of the net inward current revealed under the action of TTX (2-10(-8) g/ml) was increased upon the increase of external Ca concentration but was blocked when D-600 was introduced into the solution. The inhibitory action of D-600 on the contraction amplitude was frequency independent (in the ranges: 0,1--0,7/s). The decrease of external Na+ (isoosmotic replacement of 70% NaCl by sucrose) or the increase (5-fold) of the external Ca2+ significantly enhanced the myocardial contraction depressed with D-600. However these contractions fall in the course of rhythmical stimulation, and the effect being strongly dependent on the rate of stimulation. The results confirm the assumption (see: Biophysics, 6, 1024, 1976), that intracellular Ca stores (sarcoplasmic reticulum, internal surface of the cellular membrane) are involved in the control of the contractility in the amphibian myocardial cells. Many peculiarities of the excitation-contraction coupling in the frog myocardial cells can be explaned if one assumes that: 1) there is no space separation of primary uptake and release of Ca ion sites in the frog myocardium; 2) the system of "resting Ca chanels" in the frog myocardial cells is not so well developed as in the mammalian myocardial cells.
Animals↗