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The tricuspid valve and the right ventricle are hemodynamically closely related. Pathological changes of the valve or of the ventricle itself and also various diseases beyond that can result in a downward spiral of mutual interference, which is of prognostic importance for the patient. The development of a functional tricuspid regurgitation is of great importance. Especially with the help of 3D-echocardiography, more and more changes and mechanisms have been identified that are crucial in this process. This article provides a review of the relationship between the tricuspid valve and the right ventricle emphasizing the current knowledge of the causes, the pathophysiological concepts, the underlying structural changes and the therapeutic approaches based on this.

Pathologies of the right heart and the tricuspid valve were not recognized to be of prognostic relevance for many years. Available evidence showing the progressive nature of right heart diseases with direct impact on patient survival have changed current understanding of its clinical importance. Visualization and a profound understanding of the right heart anatomy are prerequisites for the development of modern and still experimental treatment strategies. Transthoracic and transesophageal echocardiography enable a standardized and clear visualization and assessment of the right heart anatomy and its pathological changes.

Intoxications in children still account for a large part of the cases reported to poison control centres. Among drug intoxications, substitution drugs have gained in importance lately. Careless storage of take-home medications puts children living in the same household at risk. The authors report on a fatal case of a 10-year-old girl who died from intoxication with methadone belonging to a carer. The accidental intoxication had not been diagnosed at the hospital where the girl was treated for suspected meningitis. The question of medical malpractice is discussed.

The aim of the study was to compare the diagnostic accuracy in imaging viability of the myocardium with a multislice inversions recovery 2D single shot TrueFISP sequence and an established inversion recovery TurboFlash sequence.Twelve patients with myocardial infarction were examined at a 1.5 tesla MR system (Sonata, Siemens, Medical Systems) 10 min after application of a single dose multihance (0,1 mmol/kg body weight) with a 2D multislice technique (inversion recovery single shot TrueFISP), that allows to image the entire short axis during one breathhold and a 2D single slice technique (inversion recovery TurboFlash), that requires one breathhold per slice. Signal intensity was determined in normal myocardium, in the infarcted myocardium and in the left ventricle. The contrast/noise ratio of normal and infarcted myocardium was determined. The areas of hyperintense infarction were compared for both sequence techniques.The multislice single shot 2D IR-TrueFisp sequence has a lower contrast/noise ratio than the IR-TurboFlash sequence (mean values 6.9 vs. 12.5) for viable and non viable myocardium. The assessment of the volume of the infarction is possible with excellent correlation of both techniques (r=0.97, p0.036). In addition, an assessment of the transmural extent of the infarction is possible with identical spatial resolution.The inversions recovery 2D single shot TrueFisp technique allows for accurate detection of the infarction, for accurate determination of the area of the infarction and for assessment of the transmural extent of the infarction with high spatial resolution.

The case of a primary cardiac epithelioid hemangioendothelioma (EHE) arising multifocally in the papillary muscle of the tricuspid valve and the deeper trabecular muscle in a 68-year-old male with myelodysplastic syndrome is presented. The tumor was an incidental autopsy finding. Histologically the tumor is characterized by proliferation of plump epithelial-like endothelial cells with the vascular differentiation being mostly expressed at a cellular level in the form of cytoplasmic vacuoles. In the differential diagnosis, metastatic carcinoma, cardiac myxoma as well as other epithelioid vascular neoplasms should be considered. EHEs are indolent tumors of intermediate malignancy with the potential to metastasize, even after a long time. Primary cardiac EHE is extremely rare. To our knowledge, only four EHEs of the heart have been reported in the literature. We believe, this is the first report of a cardiac EHE in this localization and the first one in association with myelodysplastic syndrome.

Heutzutage stellt der Erhalt des posterioren Halteapparates beim Mitralklappenersatz (MKE) ein Routineverfahren dar. Das Ziel dieser Studie war es festzustellen, ob der komplette Erhalt der subvalvulären Strukturen beim Mitralklappenersatz Vor- oder Nachteile hat. Es wird über die Erfahrungen mit 48 Patienten berichtet. Die Gruppe MKEh bestand aus 15 Patienten, bei denen beim MKE der komplette subvalvuläre Halteapparat erhalten wurde. Die Gruppe MKEo, bei denen beim MKE nur der posteriore Halteapparat erhalten wurde, bestand aus 9 Patienten. Die dritte Gruppe (MKR) enthielt 12 Patienten, bei denen die Mitralklappe rekonstruiert worden war und die vierte Gruppe (KG) bestand aus 12 Herzgesunden ohne Klappendefekt, die die Kontrollgruppe darstellte. Die Patienten wurden einer ausführlichen Befragung unterzogen sowie prä- und postoperativ echokardiographisch untersucht und die Ergebnisse verglichen. Bezüglich der Ergebnisse der Befragungen und der präoperativen echokardiographischen Ergebnisse fanden sich bei den drei operierten Gruppen (MKEh, MKEo, MKR) keine signifikanten Unterschiede. Demgegenüber wurden postoperative Unterschiede festgestellt: Bei den Patienten mit MKE, bei denen aber der vordere Halteapparat nicht konserviert wurde (MKEo), fand sich eine signifikant geringere systolische Verkürzung zwischen dem Apex und der Mitralklappenbasis (6,5 mm - 15 mm), die systolische Kontraktion begann bei diesen Patienten außerdem nicht im Bereich des Apex und der posteriore Papillarmuskel führte in diesen Fällen keine aktive Kontraktion aus. Es konnte somit die Schlußfolgerung gezogen werden, daß der komplette subvalvuläre Apparat notwendig ist, damit der linke Ventrikel eine physiologische Kontraktion durchführen kann. Er sollte somit immer beim Mitralklappenersatz komplett erhalten werden, sofern die Papillarmuskeln und die Chorden intakt sind und keine Mitralklappenrekonstruktion durchgeführt werden kann. Today preservation of the chordal attachment to the posterior leaflet in mitral valve replacement (MVR) is a routine, universally accepted procedure. The aim of this study was to show the advantages and disadvantages of the preservation of the entire subvalvular structures. Our institution's experience with 48 patients in four groups is reported. The MKEh group consists of 15 patients who underwent MVR with preservation of the entire subvalvular structures. The MKEo group, treated with MVR and preservation of the posterior subvalvular structures only, consists of 9 patients. The third group (MVR) consists of 12 patients with mitral valve reconstruction and group 4 (CG) of 12 healthy individuals without heart valve dysfunction, as a control group. The patients were assessed by questioning and echocardiography pre- and postoperatively and the results compared. In questioning and in the preoperative echocardiography results no differences were seen between the three surgical groups (MKEh, MKEo, MKR). However, considerable differences were present in the postoperative echocardiography results: in patients without preservation of the anterior subvalvular structures (MKEo group) the shortening between the apex and the mitral valve basis is significantly less (6.5 mm - 15 mm), the systolic contraction does not begin at the apex and the posterior papillary muscle does not actively contract. It is concluded that preservation of the entire subvalvular structures is important to ensure physiological contraction of the left ventricle. They should be preserved in all mitral valve replacement operations when the papillary muscles und chordae are intact and mitral valve reconstruction cannot be performed.

We report a female patient with mitral valve replacement and preservation of subvalvular apparatus in which parts of the papillary muscle ruptured postoperatively. During systole the ruptured papillary muscle prolapsed through the native aortic valve. Echocardiographic documentation and operative procedure were demonstrated.

The case of a 57 year old patient is reported, who suffered from an acute myocardial infarction with maximum CK and CKMB values of 821 and 84 U/l, respectively. The patient underwent bicycle exercise testing 9 days after a myocardial infarction in 25 W steps every 2 min starting with 50 W. The ergometry was interrupted at 125 W because of ST segment depression of 0.28 mV in V6. Systolic blood pressure dropped to 55 mm Hg, combined with severe angina and shock. Volume substitution and catecholamines did not elevate blood pressure. Immediate M-mode and Doppler echo revealed a "stiletto"-shaped mitral regurgitation profile typical of acute mitral valve insufficiency. The transesophageal echocardiogram showed a distinct mass moving between the left ventricle and left atrium, diagnostic of papillary muscle rupture. Despite of shock, mitral valve replacement was performed successfully. To our knowledge, this is the first report of a papillary muscle rupture during exercise testing after myocardial infarction. Papillary muscle rupture can be induced by exercise. This fateful event may not be predicted by the course of the ergometry. In case of hypotension during exercise, papillary muscle rupture should be considered. The diagnosis is to be established by transesophageal echocardiography.

It has been shown that dihydropyridines exert a cardioprotective effect during experimental ischemia. This effect is reflected in a reduced K-efflux from the ischemic tissue. Recently we have shown that ischemic K-efflux is largely mediated by ATP-dependent K-channels. Using K-selective microelectrodes we studied the effect of nisoldipine on K-efflux during simulated ischemia (guinea pig papillary muscle immersed in paraffin oil; normal Tyrode solution, HEPES buffered, 100% O2-equilibrated, 37 degrees C). While ischemic K-efflux was Ca-dependent in stimulated preparations, it was independent of extracellular Ca in resting preparations. Our results show that nisoldipine leads to an inhibition of ischemic K-efflux during simulated ischemia. In resting preparations this inhibition is not a direct Ca-antagonistic effect, since withdrawal of extracellular Ca does not inhibit ischemic K-efflux but nisoldipine does. We suggest a direct effect of nisoldipine on the KATP channel which is mainly responsible for ischemic K-loss.

Myocardial rupture is the second most common reason for in-hospital mortality in patients with acute myocardial infarction, accounting for 8-17% of deaths. The clinical presentation varies due to the possibility of rupture in three main locations: free left ventricular wall (85%), interventricular septum (10%), and papillary muscle (5%). Hypotension, long persisting or repeated chest pain, syncopes, new heart murmurs or weak action should draw attention to the possibility of myocardial rupture, apart from the classical sign of upper inflow congestion. In about 48% of cases immediate surgical intervention can save life. We present two unusual cases of myocardial rupture. Case 1 shows left ventricular free wall rupture with additional rupture of an accessory posterior papillary muscle but without changes in hemodynamic parameters; case 2 involves a rupture of the free left ventricular wall which the patient survived without surgical intervention.

Despite numerous improvement in cardiac surgery the results in mitral valve replacement are still not satisfactory, since impaired left ventricular function continues to be a problem during the postoperative course. In order to investigate the effect of mitral valve replacement on left ventricular function canine experiments were performed: During extracorporeal circulation bileaflet mitral valve prostheses were implanted preserving the ventriculo-annular continuity. Flexible wires were slung around the chordae of the subvalvular mitral apparatus and brought to the outside through the left ventricular wall. Left ventricular diameters were measured by sonomicrometry, left ventricular stroke volume, left ventricular enddiastolic volume and ejection fraction by dye dilution technique as well as left ventricular and aortic pressure by catheter tip manometers. After finishing cardiopulmonary bypass control values were registered and different preload values achieved by volume loading with blood transfusions to left ventricular enddiastolic pressures of 12 mm Hg. Subsequently under normovolumic conditions the chordae tendineae of the anterior and posterior papillary muscles of the mitral valve were cut from the outside, while the heart was beating, by application of electrocautery on the steel wires. Following severance of the ventriculo-annular continuity of the mitral valve again function curves of left ventricular hemodynamics were made during volume transfusions. When the chordae had been divided the left ventricular enddiastolic diameter increased by 10% in the major axis, while in the minor axis no significant changes occurred. The systolic shortening was impaired substantially by reduction of 43% during the ejection phase when the subvalvular mitral apparatus had been severed. Left ventricular enddiastolic volume was increased by 18% at any preload level, while left ventricular ejection fraction was reduced by 16%. Consequently left ventricular stroke volume was decreased by 24% at any left ventricular enddiastolic volume, when the chordae had been divided. It can be concluded that left ventricular geometry is changed when the annulo-ventricular continuity has been interrupted at mitral valve replacement: The major axis of the left ventricle is increased and the enddiastolic volume is augmented. The left ventricle is only able to eject the same stroke volume at higher preload levels when the chordae tendineae have been divided. The same cardiac performance can only be achieved by volume loading and at the expense of higher wall tension, which leads to unfavorable conditions in terms of cardiac muscle mechanics with reduced exercise tolerance. These data speak for preservation of the annulo-ventricular continuity in mitral valve replacement. Provided that these results from acute canine experiments can be transferred to humans, one would suggest that preservation of the mitral subvalvular apparatus is of importance in patients with dilated hearts and with impaired left ventricular function.

Intracellular calcium homoeostasis is greatly altered in heart failure. This does not seem to be due to altered calcium influx through L-type calcium channels but rather due to altered calcium uptake mechanisms of the sarcoplasmic reticulum. Recently, a negative force-frequency behaviour of the human myocardium has been detected in hearts from patients with severe heart failure. In the myocardium from these patients, SR-Ca(2+)-ATPase activity was decreased. The same defect has been reported in human isolated cardiac myocytes. A disturbed calcium release from the SR may also contribute to this finding of the inverse force-frequency-relationship in the failing myocardium. The altered intracellular calcium handling is connected with the diastolic and systolic failure of the myocardium. Mg++ and Na(+)-channel modulators are able to restore the positive force-frequency-relationship even in severely failing myocardium.

Es werden Dialkylaminoalkyl-isothiochroman-S,S-dioxide und Dialkylaminoalkyl-ethylsulfonyl-isothiochroman-S,S-dioxide synthetisiert. An zwei Verbindungen wird ein allgemeines Screening durchgefuhrt. Dialkylaminoalkyl-isothiochroman S,S-dioxide Dialkylaminoalkyl-isothiochroman S,S-dioxides and Dialkylaminoalkyl-ethylsulfonyl-isothiochroman S,S-dioxides are synthesized, and two of these compounds are generally screened.

A 63-year-old male patient suffered an acute myocardial infarction entirely confined to the posterior wall. As symptoms persisted and cardiogenic shock developed immediate heart catheterization was performed, which demonstrated an occlusion of the left circumflex branch. Right-heart catheterization demonstrated an enlarged v-wave. Thus, acute infarct associated mitral regurgitation was suspected. In the catheterization laboratory transesophageal echocardiography including Doppler- and contrast echocardiography was then performed, which revealed the diagnosis of posterior papillary muscle rupture. The patient proceeded immediately to emergency surgery during which mitral valve replacement with a St. Jude prothesis was performed in addition to venous bypass revascularization of the occluded and a further stenosed coronary artery. The postoperative follow-up was without any complications and the patient recovered satisfactorily from the acute event. This case demonstrates the excellent diagnostic utility of emergency transesophageal echocardiography in the situation of infarct related myocardial rupture, which has to precede the life-saving operation.

Connatal heterotopies are rare accidental findings fore-most without clinical symptoms. The present case report describes an asymptomatic multilocular bronchial cyst of a 72 years old woman which occurred in the left ventricular endocard of the anterior papillary muscle and which was covered with ciliated and occasionally multilayered epithelium. Today the knowledge about these rare cardial heterotopies is important, because they are not only accidental postmortal findings but also the clinical importance is rising as consequence of the improved diagnostic imaging procedures with a high resolution. The histogenesis and the classification of cardial heterotopies is discussed.

The in vitro and in vivo effects of endocardial laser ablation were assessed. Energy was supplied by a Nd-YAG laser (wavelength approximately 1064 nm) and transmitted via a quartz core fiber (phi: 0.4 mm) housed within a specially designed 7 F catheter. In vitro, the effects of increasing output power (5, 10, 20, 40 watt) and impulse duration (1, 2, 4, 8 s) on lesion size were assessed in myocardial preparations of canine hearts. Preparations were superfused with saline or blood, respectively; the distance of the optical fiber to the endocardium was 5 mm. Lesion size increased in diameter (range: 0-4.0 mm) and depth (range: 0-5.2 mm) in a power- and time-dependent manner. Superfusion with blood significantly enhanced the diameter of the lesions, whereas depth of the lesions significantly decreased. In 16 anesthetized mongrel dogs, a total of 52 laser impulses (output power: 10, 20, 40 w; impulse duration: 1, 2, 4 s; energy: 10-160 J) were delivered to apical and apico-inferior sites of the left ventricle. Postmortem, 40 lesions with a diameter of 2.6-19.4 mm and a depth of 3.7-16.2 mm were found. 19 lesions revealed central vaporized craters with a depth up to 11.2 mm. Perforation of the left ventricle occurred in two cases following 80 and 160 J, respectively. In vitro and in the intact animal (in apical and apico-inferior sites of the left ventricle) endocardial laser ablation is feasible to induce distinct myocardial lesions in a power- and time-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Anatomical variations of the peripheral conduction system are a very common finding. One of these variations are the so-called aberrant tendons, which are found in about 67% of the hearts. In this paper the possible correlation between these anatomical variations and disturbances of conduction in the electrocardiogram is discussed.

Forty one cardiac rupture complicating acute myocardial infarction (AMI) were studied in a ten-year period. The anterior AMIs are most likely to be observed with ruptures. The interval from the onset of AMI to the clinical detection of rupture was short (acute period). Some factors such as physical work in the acute period and transmural infarctions strongly infiltrated with leukocytes cause a higher frequency of rupture. Diabetes and hypertension might be predisposing factors.

The direct effects of midazolam on isometric force of contraction (Fc) and on transmembrane action potential (AP) in electrically driven right ventricular papillary muscles were investigated. The results were compared with the effects of thiopental. Midazolam (0.01-200 mumol/l) had a concentration-dependent maximal negative inotropic effect of 94 +/- 4% compared with the pre-drug value on the papillary muscles of animals pretreated with reserpine (RES) [7.5 mg/kg b.wt. i.p., 16-18 h prior to the study]. The IC25 and IC50 values were 2.9 mumol/l (2.0-4.5; n = 9) and 12.4 mumol/l (6.5-30; n = 9) respectively. However, on the papillary muscles of untreated animals (nRES) midazolam developed a concentration-dependent positive inotropic effect (maximal 20 +/- 7%). Midazolam at a clinically relevant concentration of 2.8 mumol/l (= 1 microgram/ml; equivalent with the maximum plasma level following a midazolam i.v. bolus injection of 0.15 mg/kg b. wt.) reduced Fc by 15 +/- 3% (p less than 0.05) compared with the pre-drug value on the RES papillary muscles (n = 6) and increased Fc by 3 +/- 0.3% (p less than 0.05) on nRES animals. The resting membrane potential (RMP), the AP amplitude (APA) and the AP duration at 20% (APD20) and 90% (APD90) repolarisation showed no significant differences with midazolam (2.8 mumol/l; n = 5). Thiopental (0.01-200 mumol/l) produced a concentration-dependent maximal negative inotropic effect of 86 +/- 2% compared with the pre-drug value on the papillary muscles of nRES animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Up to six arteries traverse from the interventricular septum to the M. papillaris magnus in the trabecula septomarginalis (moderator band) of swine and pygmy goat. Musculo-elastic intimal thickenings, many of them quite extensive, are recordable from along the entire length of all these intramural coronary arteries which are between 50 microns and 300 microns in diameter. The conclusion may be drawn from the results of morphometric analysis that coronary arteries undergo enlargement in response to increased intimal thickening and that such enlargement does not lead to narrowing of the lumen. Peculiarities in wall structure of the arteries in the trabecula septomarginalis are interpreted as adaptive processes of the vascular wall to the extraordinary stress on those vessels.

Myocardial lesions occuring in diseases with acute increase of intracranial pressure were investigated. Morphologic alterations in heart muscle in spite of different lengh of surviving and various causes of the death were of similar type. In every case subendocardial haemorrhage could be observed on the septal surface and on the papillary muscle of the left ventricle. Focal intracellular edema, myocytolysis were revealed in 76%, focal necrosis of hypercontractic type developed in 52% of the cases. Cellular infiltration occurred around the alternations observed in 3 cases. It is concluded, that damage to the heart muscle is not caused directly by the increased intracranial pressure or catecholamine mobilisation, but seems to be the consequence of the acute myocardial hypoxia.

1. Nonanoic acid causes a depression in the contractile force of rat papillary muscles working isometrically. The effect depends on both the concentration of the fatty acid (0.1-1 mM) and the time of exposure (2-12 min), and shows a nearly complete reversibility. 2. Vmax-values derived from the force-velocity relation as well as the index of relation suggested by Meerson do not change in muscles exposed to nonanoic acid. During paired pulse stimulation with a 400 ms-delay of the second impulse, both the postextrasystolic potentiation and the time to reach a new steady level in the contraction amplitude are significantly increased. The speed of restituting the contraction after a twitch (resitution) is descreased. 4. The results suggest that the action site of nonanoic acid may be the excitation-contraction coupling system (including the action potential) rather than the contractile element or the relaxation of the muscle.

Physiological hypertrophy is present when the increase in myocardial mass resulting from chronic mechanical loading is associated with normal or enhanced myocardial function and myosin ATPase activity. Morphological alterations occurring during the formation of hypertrophy are fully reversible in physiological hypertrophy. In pathological hypertrophy myocardial function and myosin ATPase activity are depressed and morphological changes do not or only incompletely regress following the elimination of the stimulus of hypertrophy. In the experimental animal myocardial hypertrophy resulting from exercise conditioning or slight to moderate ventricular pressure overload fulfills the criteria of physiological hypertrophy. More severe sudden pressure overload is accompanied by depression of contractile function. These pressure overload models have however, little analogy to the more progressive development of pressure loading in humans. In young dogs and in cats with a gradually increasing pressure load, in vivo ventricular ejection fraction remained within normal limits 37 to 60 weeks after banding of the ventricular outflow vessel. In vitro myocardial function evaluated in the hypertrophied papillary muscle was, however, at least in part depressed, notably when hydroxyproline concentration was augmented. Following debanding in rats with aortic constriction hydroxyproline content did not regress suggesting that fibrosis once established is not reversible. In man myocardial hypertrophy from exercise conditioning is associated with normal ventricular function except in older athletes, who may show a subtle reduction in ventricular shortening. Patients with chronic pressure overload from aortic stenosis or volume overload from aortic insufficiency in whom the angiographic muscle mass is severely increased (greater than or equal to 180 g/m2) elicit a depressed left ventricular contractile function. Preserved left ventricular ejection performance in aortic valve disease is however not associated with normal myocardial structure because interstitial fibrosis evaluated from endomyocardial biopsies or biopsies obtained at surgery was found to be increased. Patients with depressed left ventricular contractility were characterized by having an abnormally high muscle fibre diameter. Normal function after surgery was not accompanied by normalization of myocardial structure: Interstitial fibrosis increased, fibrous content remained the same and cellular hypertrophy regressed incompletely regardless whether angiographic muscle mass had regressed to normal or remained still increased after surgery. In summary, the bulk of available functional and morphological data suggests that the occurrence of true physiological hypertrophy is probably limited to exercise conditioning and eventually to mild chronic mechanical overload. The more severe secondary hypertrophy such as in patients with aortic valve disease who undergo valve replacement, is not a physiological adaptation, but must be considered as a pathological process.

In guinea pigs the toxic effect of beta-acetyldigoxin was not increased by simultaneously administered 3-(beta-hydroxy-alpha-methyl-phenethyl-amino)-3'-methoxy-propiophenone (oxy-fedrine). There was no evidence of a potentiation of the glycoside effect by the combination with oxyfedrine (ildamen-Novodigal). The threshold dose for arrhythmia was increased: typical glycoside tachyarrhythmias only occurred after higher infused doses. In anesthetized dogs with heart failure by overdosed pentobarbital, the therapeutic effects of beta-acetyldigoxin were sustained and enhanced by oxyfedrine.

Two-dimensional echocardiographic (2D-Echo) studies were performed in 51 healthy subjects to set up normal ranges of regional left ventricular (LV) wall motion for three different standard planes: the short axis (SA), recorded at a level between the mitral valve and the papillary muscles, the apical two-chamber view (2 CV) and the apical four-chamber view (4 CV). Wall motion analysis was performed using a fixed (Fix) as well as a floating reference system (Float). For regional wall motion, calculated by segmental area shortening, tolerance limits were estimated by using two well established statistical methods. The lowest coefficient of variation (V) was found for the SA (VFix = 0.18; VFloat = 0.11). The apical planes showed higher variations (2 CV: VFix = 0.20, VFloat = 0.20; 4 CV: VFix = 0.26, VFloat = 0.19). Defining the normal LV contraction ranges, a comparison of the reference systems showed advantages of the floating procedures, mainly in the SA and in the 4 CV. The obtained normal contraction ranges can be used for the evaluation of regional LV contraction abnormalities after acute myocardial infarction (AMI) if the 2D-Echo images are of excellent quality. We suggest an "index of dyssynergy" as a measure of wall motion abnormality.

Mechanical Parameters of the whole, Langendorff-perfused cat heart and of isolated right ventricular papillary muscles are depressed in chronic potassium deficiency. 45Ca binding of sarcoplasmic reticulum (SR) was found to be diminished and correlated with a reduced contractility of the perfused hearts. 45Ca uptake of sarcoplasmic reticulum isolated from potassium deficient hearts was also reduced. The mitrochondrial 45Ca binding and endogenous Ca concentration were increased and there was a positive correlation between these two parameters. The data suggest that a reduced SR Ca binding plays a role in the depression of myocardial contractility in chronic potassium deficiency. Increased mitochondrial 45Ca binding in the presence of reduced 45Ca binding and uptake of sarcoplasmic reticulum suggests the possibility that mitochondria are an additional myocardial calcium pool in chronic potassium deficiency.

Histamine-H1-receptors are only present in the left atrium of guinea-pig hearts, whereas the ventricular myocardium contains histamine-H2-receptors exclusively. Although the stimulation of both receptor types causes positive intropic effects, only the H2-receptor response is closely associated with increases of cyclic AMP. H1- as well as H2-receptors are present in the rabbit mesenteric artery. Cyclic AMP serves as a messenger for H2-receptor mediated relaxation only and not for H1-receptor mediated contraction. Thus, the different effects on the cyclic AMP-system must also be considered in H1- and H2-receptor differentiation.

A rapid change in length of cat papillary muscle induces two reciprocal diastolic and systolic processes: stretching causes a viscoelastic relaxation of the muscle. The opposite behavior is observed after abrupt releases when - subsequent to an increase in resting tension - diastolic force attains its new equilibrium. The stretch-induced process of relaxation is accompanied by a transient decrease in mechanogram amplitudes; a release is accordingly followed by a temporary increase in isometric muscle performance. The mechanograms of the steady state prove to be the function of the degree of stretch or release, whereas muscle contractions in the early phase of stress relaxation depend on the contractile state before the change in length. All interventions which augment developed tension (increased calcium, decreased potassium, increased or decreased sodium concentrations, strontium, postextrasystolic potentiation, sympathicomimetic agents, frequency potentiation) diminish the transient phenomena due to stretch, whereas low frequency or a lesser intensity of electromechanical coupling (Hexobarbital, Iproveratril, Desoxycorticosteron, Ryanodine) increases them. A decrease of bath temperature enhances the transient increase in force due to a release or an initial reduction of isometric tension after a sudden stretch, although the absolute forces increase. No substantial changes could be observed in reserpinized cats with beta-blocking agents or under hypoxia. It is supposed that alterations in the time course of the action potential could be related to post-stretch and post-release systolic phenomena. A final interpretation of mechanical and electrical events after stretch and release is not possible with the methods used in these experiments.

The contractile function of the non-infarcted myocardium was examined in adult cats following myocardial infarction produced by ligation of several branches of the LAD and circumflex coronary artery. Two and seven days following infarction, after determination of intracardiac pressures, papillary muscles were excised from the non-infarcted portion of the right ventricle and transferred into a myograph for analysis of contractile function. One week following infarction, force-velocity relations of the surviving myocardium showed a shift downward and to the left in comparison to sham-operated controls. At the same time, there was a decline in actively developed force at Lmax to be deserved, which appeared to be caused by a decrease in the rate of force development. Two days following infarction, similar changes were to be observed, although to a lesser extent. There appears to be a distinct loss of contractility in the remaining viable myocardium following experimental infarction.

Specific binding of cardiac glycosides to their receptors precedes their actions on the myocardium. Thus changes in the number and affinity of these membrane bound receptors will vary the response to cardiac glycoside therapy and the incidence of side-effects. Several studies have reported an age-dependent decrease in the number of cardiac glycoside receptors in animals as well as in human erythrocytes. These results may explain the increase in cardiac glycoside sensitivity with age which is not accounted for by the reduction in kidney function. Furthermore, changes in both binding affinity and capacity are known to occur in several diseases which are more common in older patients. Therefore, we have measured the number and affinity of cardiac glycoside receptors in atrial samples from 209 patients and in papillary muscle samples from 59 patients taken during coronary bypass graft surgery or mitral valve replacement. Further, the maximal increase in force of contraction was measured using papillary muscle strips from some of these patients. Our results show no significant age-dependent alteration in the characteristics of the cardiac glycoside receptors but a reduced myocardial receptor density in males (3.47 +/- 0.14 X 10(14)/g protein) compared with females (4.44 +/- 0.21 X 10(14)/g protein) (p less than 0.001) which is more pronounced in older patients. About 30% fewer cardiac receptors either per g protein or per g wet weight are present in patients with coronary heart disease or dilative cardiomyopathy. The maximal inotropic effect of ouabain in human papillary muscle strips is correlated with the number of cardiac glycoside receptors present.(ABSTRACT TRUNCATED AT 250 WORDS)

To characterize consequences of cholesterol induced increases of the Na content on the Ca regulation in rabbit myocardium the influence of increasing extracellular Ca (Cae) on isometric contraction and relaxation of papillary muscles has been investigated after a 12 weeks lasting cholesterol-rich diet. After cholesterol-rich diet increasing Cae caused a higher augmentation in peak tension T, accompanied by a decreased index in contractility [Formula: see text], an insignificantly prolonged time to peak tension TPT, and a decrease in the refractory period, which was extended compared with the control group. A delay in relaxation is demonstrated by the maximum relaxation rate [Formula: see text], the half time of relaxation RT 1/2 and more pronounced by a prolonged relaxation time RT. The results correspond with changes in the Na content published earlier and are in agreement with the assumption that a Na-Ca exchange is involved in beat-to-beat regulation in rabbit myocardium; thereby the cholesterol component of atherogenic diet promotes Ca enhancement in rabbit cardiac cells.