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At least 109 records · Page 6Linked to original sources
PubMed2000

Impaired sarcoplasmic calcium release inhibits myocardial contraction in experimental sepsis.

PURPOSE: In septic shock, myocardial dysfunction develops over the course of illness, but the mechanism of this depression is not clear. In this study, mechanisms of myocardial dysfunction were examined in a porcine model of Escherichia coli sepsis. MATERIALS AND METHODS: Animals were subjected to 4 hours of bacteria infusion (n = 5) (septic group) or saline infusion (n = 5) (nonseptic group), after which trabeculae were removed from the right ventricle and placed into a recirculating water bath. Measurements of steady-state contraction (SSC) were obtained at 0.5, 1, and 2 Hz. Indirect indices were used to assess abnormalities in myocardial calcium metabolism in sepsis. Extrasystoles (ES) were used to assess transsarcolemmal (TSL) calcium flux and were measured at 300 milliseconds, 400 milliseconds, and 500 milliseconds after the preceding stimulus. Postrest contraction (PRC) is an indicator of SR recirculation from the uptake to the release site and was obtained after interposing intervals of rest between steady-state beats at 0.5 Hz. Rapid-cooling contracture (RCC) is an indicator of sarcoplasmic reticulum (SR) content and was obtained at 0.5, 1, and 2 Hz and after interposing intervals of rest at 0.5 Hz. RESULTS: SSC was not different between groups at 0.5 Hz, but compared with the nonseptic group, SSC decreased at 1 and 2 Hz in the septic group (P < .05). PRC and TSL were not different between groups. During rest intervals, calcium leaks out of SR through the ryanodine channel (ie, SR calcium release channel). In the septic group, as assessed by RCC, SR calcium leak was less than that found in the nonseptic group. CONCLUSION: These results indicate that myocardial dysfunction in sepsis is frequency dependent, and that the mechanism is most likely caused by inhibition of SR calcium release owing to blockade of the ryanodine channel.

Analysis of Variance↗
PubMed1995

[Effect of diazepam on myocardial contraction and on the response to dopamine. Study in isolated rat hearts].

PURPOSE: The myocardial contractility variations and the cardiac rate were studied in isolated hearts of rats with injection of diazepam, dopamine and the association of both. METHODS: In all animals, after anesthesia, the hearts were removed and perfused with Krebs-Henseleit solution enriched by 95% O2 under a constant pressure of 90 cm H2O, until complete stabilization, for control value recordings. The following groups were studied: I) ten hearts: after stabilization the control values were recorded and dopamine (3 micrograms/ml) injected; IIA and IIB): also ten hearts were used and submitted to 50 micrograms and 100 micrograms of diazepam injections respectively. III) ten hearts studied with 50 micrograms of diazepam and 3 micrograms/ml of dopamine injection in a sequential form. RESULTS: Myocardial contractility arose in group I, from 37 g.seg-1 (control mean-value) to 70 and 53 g.seg-1 (1st and 3rd min); p < 0.001. In the groups IIA and IIB the dT/dt fell considerably in relation to the control: 35 g.seg-1 to 24 and 30 g.seg-1 (1st and 3rd min)--group IIA; p < 0.001 -32 g.seg-1 to 22 and 25 g.seg-1 (1st and 3rd min)--group IIB; p < 0.001. In the group III, a partial inhibition of the inotropic effects of dopamine by the injection of diazepam was observed. Heart rate follows fully the dT/dt variations in the groups IIA, IIB and III. CONCLUSION: Diazepam presents inotropic and chronotropic negative effects with the 50 micrograms as well as with 100 micrograms injection and the chronotropic and inotropic effect of dopamine (3 micrograms) injection was partially inhibited by the previous injection (50 micrograms) of diazepam.

Animals↗
PubMed1999

Early changes in the time course of myocardial contraction after correcting aortic regurgitation.

BACKGROUND: Correcting aortic regurgitation causes significant changes in left ventricular loading conditions, but few observations have been made intraoperatively of early effects on myocardial function. METHODS: We studied 18 patients (mean age, 59+/-12 years; 14 men) in whom aortic regurgitation was corrected with a stentless biologic valve. Overall left ventricular function was studied by thermodilution cardiac output, ventricular filling pressure, and systemic arterial pressure. Regional myocardial function was assessed from intraoperative transesophageal M-mode echocardiography and high fidelity ventricular pressure recordings before cardiopulmonary bypass, and 0.5, 1, 3, 6, 12, and 20 hours after operation. Time course of contraction, and magnitude of left ventricular systolic wall stress, dimensional shortening, myocardial power, and stroke work were measured. RESULTS: Global hemodynamics: there was an immediate decrease in left ventricular stroke volume (58+/-31 mL versus 80+/-30 mL, p = 0.004) and stroke work index (250+/-86 mJ/m versus 401+/-198 mJ/m, p = 0.005), but systemic arterial pressure (79+/-11 mm Hg versus 65+/-10 mm Hg, p = 0.002), increased at constant heart rate and end-diastolic pressure. Regional myocardial function and timing: peak systolic wall stress, dimensional shortening rate, and myocardial power production were all unchanged with operation. However, myocardial stroke work decreased (3.0+/-1.3 mJ/cm versus 4.8+/-2.4 mJ/cm, p = 0.009), attributable to shortening of the duration of systole (475+/-91 ms versus 543+/-67 ms, p<0.001). Diastolic time increased from 34%+/-18% to 71%+/-33% of systolic pulse duration (p<0.001). CONCLUSIONS: Correcting aortic regurgitation causes an early decrease in regional and global stroke work and increases diastolic time, although systolic wall stress does not decrease immediately. These beneficial effects are achieved by reducing the duration rather than altering the peak intensity (power) of myocardial contraction.

Adult↗
PubMed1995

L-methionine augments mammalian myocardial contraction by sensitizing the myofilament to Ca2+.

L-Methionine is an essential amino acid that has been reported to have a potent positive inotropic effect on the mammalian myocardium. We studied the mechanisms of the inotropic effect in ventricular myocardium from the rabbit. In the isolated coronary-perfused whole heart, L-methionine in a millimolar range exerted concentration-dependent positive inotropic effects on the isovolumic left ventricle, which were associated with negative lusitropic effects (prolonged time course of relaxation). The chronotropic state and the coronary perfusion pressure were not affected. These complex effects on the isolated whole heart were not blocked by pretreatment with (mumol/L) propranolol 1, prazosin 1, carbachol 3, staurosporine 1, or [Ser1,Ile8]angiotensin II 0.1. To further study the subcellular mechanisms, isolated ventricular papillary muscles from the same species were loaded with a bioluminescent indicator, aequorin, to monitor [Ca2+]i. In the presence of 3 mmol/L L-methionine, the isometric tension showed a similar combination of the positive inotropic and negative lusitropic effects as observed in the whole heart. In contrast, the simultaneously recorded intracellular Ca2+ signals did not increase in amplitude but instead decreased. The [Ca2+]i-tension relation shifted to the left compared with that obtained in response to [Ca2+]o. In saponin (250 micrograms/mL)-treated skinned preparations, 3 mmol/L L-methionine also shifted the force-pCa curve to the left by 0.16 pCa units. This is the first demonstration that an essential amino acid directly acts on the myofilaments and modulates their responsiveness to Ca2+, thereby producing a positive inotropic effect.

Actin Cytoskeleton↗
PubMed1987

The control of myocardial contraction with skeletal fast muscle troponin C.

The present study describes experiments on the myocardial trabeculae from the right ventricle of Syrian hamsters whose troponin C (TnC) moiety was exchanged with heterologous TnC from fast skeletal muscle of the rabbit. These experiments were designed to help define the role of the various classes of Ca2+-binding sites on TnC in setting the characteristic sensitivities for activations of cardiac and skeletal muscles. Thin trabeculae were skinned and about 75% of their troponin C extracted by chemical treatment. Tension development on activations by Ca2+ and Sr2+ was found to be nearly fully blocked in such TnC extracted preparations. Troponin C contents and the ability to develop tension on activations by Ca2+ and Sr2+ was permanently restored after incubation with 2-6 mg/ml purified TnC from either rabbit fast-twitch skeletal muscle (STnC) or the heart (CTnC, cardiac troponin C). The native (skinned) cardiac muscle is characteristically about 5 times more sensitive to activation by Sr2+ than fast muscle, but the STnC-loaded trabeculae gave response like fast muscle. Attempts were also made to exchange the TnC in psoas (fast-twitch muscle) fibers, but unlike cardiac muscle tension response of the maximally extracted psoas fibers could be restored only with homologous STnC. CTnC was effective in partially extracted fibers, even though the uptake of CTnC was complete in the maximally extracted fibers. The results in this study establish that troponin C subunit is the key in setting the characteristic sensitivity for tension control in the myocardium above that in the skeletal muscle. Since a major difference between skeletal and cardiac TnCs is that one of the trigger sites (site I, residues 28-40 from the N terminus) is modified in CTnC and has reduced affinity for Ca2+ binding, the possibility is raised that this site has a modulatory effect on activation in different tissues and limits the effectiveness of CTnC in skeletal fibers.

Animals↗
PubMed1986

[Effect of preliminary administration of prostaglandin E2 and the prostaglandin synthesis inhibitor indomethacin on disturbances of myocardial contraction during stress].

The effect of preliminary administration of indometacin and prostaglandin E2 on right atrial myocardial distensibility and contractility disturbances was studied in male Wistar rats after 6-hour immobilization stress. Indometacin administration (5 mg/kg) increased stress-related atrial distensibility and contractility disturbances, while prostaglandin E2 administration (5 mg/kg) significantly limited these stress-induced responses.

Animals↗
PubMed1997

Dynamic interaction between myocardial contraction and coronary flow.

Phasic coronary flow is determined by the dynamic interaction between central hemodynamics and myocardial and ventricular mechanics. Various models, including the waterfall, intramyocardial pump and myocardial structural models, have been proposed for the coronary circulation. Concepts such as intramyocardial pressure, local elastance and others have been proposed to help explain the coronary compression by the myocardium. Yet some questions remain unresolved, and a new model has recently been proposed, linking a muscle collagen fibrous model to a physiologically based coronary model, and accounting for transport of fluids across the capillaries and lymphatic flow between the interstitial space and the venous system. One of the unique features of this model is that the intramyocardial pressure (IMP) in the interstitial space is calculated from the balance of forces and fluid transport in the system, and is therefore dependent on the coronary pressure conditions, the myocardial function and the transport properties of the system. The model predicts a wide range of experimentally observed phenomena associated with coronary compression.

Animals↗
PubMed1985

[Characteristics of the action of strophanthin on central hemodynamics, pulmonary and intrahepatic blood circulation and myocardial contraction].

The effects of strophanthin treatment given in courses on the central hemodynamics, pulmonary, intrahepatic circulation and myocardial contractility were studied in 97 patients with decompensated chronic cor pulmonale depending on the hemodynamic type of circulation. In patients with CNPD and circulatory failure having the hypokinetic circulation, the treatment with strophanthin brought about improvement of the pulmonary and hepatic hemodynamics, increase in myocardial contractility, reduction of congestion. This may be accounted for by an elevation of the MOS, removal of the peripheral spasm on the part of the vascular system, elimination of prolonged venous congestion in the lungs and liver, and improvement of arterial blood flow in these organs. It was shown that in patients with hyperkinetic circulation, administration of strophanthin has an untoward effect on the hemodynamics in the lungs, liver and heart, thereby maintaining and increasing myocardial hyperfunction and venous hypervolemia. The data obtained indicate that it is inadvisable to prescribe strophanthin at early stages of the decompensated chronic cor pulmonale in patients with hyperkinetic circulation.

Adult↗
PubMed1986

[Effect of geomagnetic storms on the state of heart mitochondria and their role in providing energy for myocardial contraction].

The experiments on intact rabbits have shown that geomagnetic storm breaks the relationship between the size of myocardial mitochondria and the degree of cardiac contractility, causes swelling and further destruction of mitochondria. Geomagnetic storm leads to a decline in the left ventricular contractility. The development of geomagnetic storm is associated with a significant strong positive correlation between the size of mitochondria and the blood level of free fatty acids.

Animals↗