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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cardiovascular drugs and therapy 8 (1994), S. 437-446 
    ISSN: 1573-7241
    Keywords: endothelium ; endocardium ; heart failure ; nitric oxide ; endothelin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of vascular endothelium, endocardium, and coronary endothelium on vascular tone and myocardial contraction-relaxation sequence in heart failure is discussed. Vascular endothelium affects underlying vascular smooth muscle through paracrine secretion of relaxing and constricting factors. In heart failure, systemic vasoconstriction results not only from neuroendocrine activation, but also from disturbed local endothelial control of vascular tone because of impaired endothelial-dependent vasodilation and because of increased plasma concentration of endothelin. Experimental evidence obtained in isolated cardiac muscle strips established the influence of endocardial endothelium on the duration of myocardial contraction and on the onset of myocardial relaxation. By analogy to vascular endothelium, both diffusible agents that abbreviate (endothelial-derived relaxation factor-like substance) and those that prolong (endocardin) myocardial contraction have been shown to be released from the endocardium. Similar agents are released from the coronary endothelium and, because of the close proximity of capillaries and myocytes, could exert a major effect on myocardial performance. Endothelial dysfunction and concomitant lack of release of myocardial relaxant factors could explain left ventricular relaxation abnormalities observed in the cardiac allograft or in arterial hypertension. Since endothelial-derived relaxation factor or nitric oxide mediates the coronary reactive hyperemic response, a negative inotropic action of nitric oxide could contribute to left ventricular failure when left ventricular wall stress is elevated, as occurs after myocardial infarction in the noninfarcted zone and during left ventricular volume or pressure overload in the absence of adequate hypertrophy.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Heart failure reviews 5 (2000), S. 337-344 
    ISSN: 1573-7322
    Keywords: nitric oxide ; diastole ; myocardium ; nitric oxide synthase ; cytokines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Modulation by NO of systolic myocardial function received widespread attention but most studies focused on potential negative inotropic properties of NO. The very original observations on the effects of NO on myocardial contraction already provided evidence that NO modified myocardial contractile performance mainly through a relaxation-hastening effect (i.e. earlier onset of relaxation) and through an increase in myocardial distensibility. The present review discusses the relaxation hastening and distensibility-increasing effects of NO in experimental preparations, in the normal human heart, in left ventricular hypertrophy of aortic stenosis, in the human allograft and in dilated nonischemic cardiomyopathy. This 'diastolic flip side' of the myocardial effects of NO appears to be beneficial especially for patients who are dependent on the LV Frank-Starling response to maintain cardiac output.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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