Disease relevance of Myocardial Contraction

• To investigate whether mechanical forces applied to the vascular wall by the myocardial contraction cycle were also a stimulus for EDRF release, cardiac arrest was induced by a continuous infusion of mepivacaine (final concentration, 0.02%) [1].
• Late gadolinium-enhanced magnetic resonance imaging in acute and chronic myocardial infarction. Improved prediction of regional myocardial contraction in the chronic state by measuring thickness of nonenhanced myocardium [2].
• We hypothesized that Lzm-S binds to or cleaves a cardiac membrane glycoprotein, thereby interfering with myocardial contraction in sepsis [3].
• Cardiac performance and left ventricular end-diastolic pressure were not affected and this lack of change in cardiac inotropism may confer and advantage to diltiazem over other calcium antagonistic drugs in patients with coronary heart disease [4].
• In acute spinal rats (C2-C3) application of capsaicin (0.2 and 2 micrograms in 25 microliters) on the urinary bladder induced a transient hypertension, tachycardia and positive cardiac inotropism [5].

Psychiatry related information on Myocardial Contraction

• New methylxanthine thio-derivatives inducing marked tracheal relaxation without increasing cardiac inotropism or motor activity [6].

High impact information on Myocardial Contraction

• Accordingly, the assessment of left ventricular function by echocardiography revealed severely impaired myocardial contraction in the CTSL-deficient mice [7].
• However, whether bFGF has any effects on myocardial contraction is unknown [8].
• There is much evidence to support the favorable effects of the phosphocreatine shuttle on myocardial contraction and relaxation [9].
• Suppression of myocardial contraction with lidocaine (3 dogs) and vasodilation with adenosine partly improved the distance-correlation coefficient relation under reduced coronary perfusion pressure [10].
• L-methionine augments mammalian myocardial contraction by sensitizing the myofilament to Ca2+ [11].

Chemical compound and disease context of Myocardial Contraction

• The comparative effects of dopamine and isoproterenol on local myocardial contraction and ischemic injury after coronary occlusion were evaluated in 10 dogs [12].
• Effect of verapamil on regional myocardial contraction during graded ischemia in the dog [13].
• Cocaine also induces a variety of pathological changes in the heart, including myocardial contraction band necrosis and ventricular hypertrophy [14].
• BACKGROUND: Nitric oxide (NO) is known to modulate myocardial contraction and coronary tone, and its inhalation reduces pulmonary vascular resistance in patients with pulmonary hypertension [15].
• Histopathologic investigation revealed that aluminum acetylacetonate caused unambiguous myocardial infarcts, characterized by myocardial contraction bands [16].

Biological context of Myocardial Contraction

• The height of the plateau of the action potential was increased by histamine and this seems to explain, at least, part of the drug action on heart contractility [17].
• This study has assessed the direct effects of verapamil on regional myocardial contraction during graded coronary flow reductions while blood pressure and heart rate were held constant [13].
• The economy of myocardial contraction as calculated by the ratio of systolic stress-time integral to myocardial oxygen consumption per beat was 675 +/- 192 before and 370 +/- 128 dyn.s.100 g/cm2.microliter O2 after administration of enoximone [18].
• In surgically prepared (open-chest) baboons, neomycin consistently induced a dose-related depression of myocardial contractile force, maximum dF/dt of myocardial contraction, cardiac output, heart rate, and systolic and diastolic blood pressures [19].
• The effects of bupivacaine on myocardial contraction and membrane potential were examined in isolated canine right ventricular papillary muscles [20].

Anatomical context of Myocardial Contraction

• CONCLUSIONS: Constitutive eNOS expression in murine LV myocytes is not essential for the muscarinic-mediated inhibition of beta-adrenergic signalling and does not appear to play a significant role in the regulation of basal and beta-adrenergic myocardial contraction [21].
• In contrast, felodipine has high vascular selectivity in such preparations, and drug concentrations required to depress myocardial contraction are more than 100 times greater than those required to relax vascular smooth muscle [22].
• Differential effects of cocaine and cocaethylene on intracellular Ca2+ and myocardial contraction in cardiac myocytes [23].
• T lymphocytes from T. cruzi-infected mice alter heart contractility: participation of arachidonic acid metabolites [24].
• As an alternative, acceptable surgical conditions have been created in patients undergoing coronary artery bypass operations with esmolol-induced minimal myocardial contraction [25].

Associations of Myocardial Contraction with chemical compounds

• However, since angiotensin II (Ang II) directly increases the strength of myocardial contraction, suppression of Ang II formation by ACE inhibitors could potentially reduce the beneficial effects of Ang II on the failing heart [26].
• BACKGROUND: Although tissue Doppler imaging (TDI) has recently emerged to quantify regional myocardial contraction, increased translational motion during a dobutamine challenge may affect the measurements [27].
• Diltiazem does not appear to cause significant increases in coronary blood flow or bring about improvement in ejectional and isovolumic indices of myocardial contraction - evidence of its intrinsic negative inotropic effect [28].
• Transmembrane voltage-gated Ca2+ channels play a central role in the development and control of heart contractility which is modulated by the concentration of free cytosolic calcium ions (Ca2+) [29].
• Interleukin-1 beta modulates myocardial contraction via dexamethasone sensitive production of nitric oxide [30].

Gene context of Myocardial Contraction

• No MLC3F protein can be detected in the adult or embryonic mouse heart, suggesting that post-transcriptional regulation prevents this fast myosin isoform contributing to myocardial contraction [31].
• The Ca(2+)-binding S100A1 protein displays a specific and high expression level in the human myocardium and is considered to be an important regulator of heart contractility [32].
• OBJECTIVE: The positive inotropic effect of endothelin-1 (ET-1) on normal myocardial contraction may be altered in pathological states [33].
• Moreover, Ucn has much more potent effects on the cardiovascular system than CRF, including enhanced cardiac contractility/heart rate and enhanced resistance of cardiac cells to injury induced, for example, by ischaemia/reperfusion [34].
• The findings support the hypothesis that thin filament heterogeneity due to the co-expression of alternatively spliced cTnT variants may desynchronize myocardial contraction and contribute to the pathogenesis and pathophysiology of cardiomyopathy and heart failure [35].

Analytical, diagnostic and therapeutic context of Myocardial Contraction

• The enhancement of cardiac inotropism induced by electrical stimulation of acutely decentralized efferent preganglionic sympathetic axons was reduced, but still present, following intravenous hexamethonium administration (10 mg/kg) [36].
• Longitudinal myocardial contraction improves early during titration with metoprolol CR/XL in patients with heart failure [37].
• Intravenous infusions of dobutamine (DT), angiotensin II (AII) and dextran (DN) were used to alter the cardiac inotropism, afterload and preload, respectively [38].

References