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Coronary Perfusion (coronary + perfusion)

Distribution by Scientific Domains
Medical Sciences100%

Terms modified by Coronary Perfusion

  • coronary perfusion pressure
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    Selected Abstracts

    Arterial structural and functional alterations in uraemia

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2005
    A. P. Guérin
    Abstract Epidemiological and clinical studies have shown that cardiovascular disease in patients with end-stage renal disease (ESRD) is frequently related to damage of large conduit arteries. Arterial disease is responsible for the high incidence of ischaemic heart disease, peripheral artery diseases, left ventricular hypertrophy and congestive heart failure. The vascular complications in ESRD are ascribed to two different but associated mechanisms, namely atherosclerosis and arteriosclerosis. Whereas the former principally affects the conduit function with ischaemic lesions being the most characteristic consequence, the latter primarily disturbs the dampening function of large arteries. Arteriosclerosis in ESRD patients is characterized by diffuse dilation and wall hypertrophy of large conduit arteries and stiffening of arterial walls. These changes represent a clinical form of an accelerated ageing process. The main clinical characteristics due to arterial stiffening are isolated increase in systolic blood pressure with normal or lower diastolic pressure resulting in an increased pulse pressure. The consequences of these alterations are: (i) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand; and (ii) altered coronary perfusion and subendocardial blood flow distribution. Epidemiological studies have identified arterial remodelling and stiffening as independent predictors of overall and cardiac mortality in ESRD patients. [source]

    Coronary Hemodynamics and Myocardial Oxygen Consumption During Support With Rotary Blood Pumps

    ARTIFICIAL ORGANS, Issue 1 2009
    Peter Voitl
    Abstract Mechanical support offered by rotary pumps is increasingly used to assist the failing heart, although several questions concerning physiology remain. In this study, we sought to evaluate the effect of left-ventricular assist device (VAD) therapy on coronary hemodynamics, myocardial oxygen consumption, and pulmonary blood flow in sheep. We performed an acute experiment in 10 sheep to obtain invasively measured coronary perfusion data, as well as pressure and flow conditions under cardiovascular assistance. A DeBakey VAD (MicroMed Cardiovascular, Inc., Houston, TX, USA) was implanted, and systemic and coronary hemodynamic measurements were performed at defined baseline conditions and at five levels of assistance. Data were measured when the pump was clamped, as well as under minimum, maximum, and moderate levels of assistance, and in a pump-off condition where backflow occurs. Coronary flow at the different levels of support showed no significant impact of pump activity. The change from baseline ranged from ,10.8% to +4.6% (not significant [n.s.]). In the pulmonary artery, we observed a consistent increase in flow up to +4.5% (n.s.) and a decrease in the pulmonary artery pressure down to ,14.4% (P = 0.004). Myocardial oxygen consumption fell with increasing pump support down to ,34.6% (P = 0.008). Left-ventricular pressure fell about 52.2% (P = 0.016) as support was increased. These results show that blood flow in the coronary arteries is not affected by flow changes imposed by rotary blood pumps. An undiminished coronary perfusion at falling oxygen consumption might contribute to cardiac recovery. [source]

    Endothelin-1-mediated coronary vasoconstriction deteriorates myocardial depression in hearts isolated from lipopolysaccharide,treated rats: Interaction with nitric oxide

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2004
    Jie Tu
    Summary 1.,The aim of the present study was to evaluate the contribution of disturbance of coronary perfusion to myocardial depression in hearts isolated from lipopolysaccharide (LPS)-treated rats and to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO). 2.,Rats were treated with LPS (10 mg/kg, i.p.) and, 4 h later, plasma ET-1 concentrations were measured by radioimmunoassay and hearts were excised for perfusion at a constant perfusion flow. The selective ETA receptor antagonist BQ-123, in the absence or presence of aminoguanidine, a specific inhibitor of inducible NO synthase, was given 15 min before LPS challenge. Coronary perfusion pressure (CPP) and measures of myocardial contractile function were recorded. 3.,In hearts isolated from LPS-treated rats, there was a marked increase in CPP that was abolished by pretreatment with BQ-123. In parallel, an increase in plasma ET-1 concentrations was seen in these rats. Lipopolysaccharide also induced decreases in left ventricular developed pressure (LVDP), the product of LVDP and heart rate and maximal rate of rise/fall of left ventricular pressure (+/, dP/dtmax). Single treatment with BQ-123 or aminoguanidine attenuated LPS-induced myocardial depression. However, when these two drugs were given simultaneously, myocardial depression elicited by LPS was blocked significantly. 4.,Endothelin-1-mediated coronary vasoconstriction, together with NO, contributes to myocardial depression in hearts isolated from LPS-treated rats. [source]

    Large Artery Stiffness: Implications For Exercise Capacity And Cardiovascular Risk

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2002
    Bronwyn A Kingwell
    SUMMARY 1. Large artery stiffness, or its inverse, compliance, determines pulse pressure, which, in turn, influences myocardial work capacity and coronary perfusion, both of which impact on exercise capacity and cardiovascular risk. 2. In support of a role for arterial properties in exercise performance, aerobically trained athletes (aged 30,59 years) have lower arterial stiffness than their sedentary counterparts. Furthermore, in healthy older subjects (aged 57,80 years), time to exhaustion on treadmill testing correlated positively with arterial compliance. 3. Arterial stiffness is more closely linked to exercise capacity and myocardial risk in patients with coronary disease where, independently of degree of coronary disease, those with stiffer proximal arteries have a lower exercise-induced ischaemic threshold. 4. Moderate aerobic training elevates resting arterial compliance by approximately 30%, independently of mean pressure reduction, in young healthy individuals but not in isolated systolic hypertensive patients. Rat training studies support a role for exercise training in structural remodelling of the large arteries. 5. High-resistance strength training is associated with stiffer large arteries and higher pulse pressure than matched controls. 6. Large artery stiffness is an important modulator of the myocardial blood supply and demand equation, with significant ramifications for athletic performance and ischaemic threshold in coronary disease patients. Moderate aerobic training, but not high-resistance strength training, reduces large artery stiffness in young individuals whereas older subjects with established isolated systolic hypertension are resistant to such adaptation. [source]