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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 12 (2001), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Conduction and Left Ventricular Hypertrophy. Introduction: The aim of this study was to determine if anisotropic action potential conduction was altered during development of left ventricular hypertrophy (LVH). Methods and Results: Isolated guinea pig left ventricular preparations from hearts that had developed LVH were used to measure conduction velocity in longitudinal and transverse orientations to the fiber direction. A variable degree of LVH was induced by placing a ring around the ascending aorta for 50 to 250 days. Results were compared with an age-matched control group that underwent a similar operation but with no ring placement. LVH was measured as the heart-to-body-weight ratio (HBR), which correlated with an increase of mean myocyte cross-sectional area. Longitudinal conduction velocity (LCV) declined progressively as HBR increased (mean ± SD: sham vs LVH: HBR 3.74 ± 0.30 g/kg vs 4.53 ± 0.52 g/kg; LCV 72.8 ± 15.5 vs 63.6 ± 11.1 cm/sec). Mean transverse conduction velocity (TCV) was greater in LVH compared with control (20.5 ± 4.7 cm/sec vs 25.4 ± 8.1 cm/sec), but there was no significance in the trend as a function of HBR. The anisotropic ratio (LCV/TCV) significantly declined as HBR increased. The time constant of the foot of the action potential was smaller in the transverse compared with the longitudinal dimension. There was no influence of hypertrophy. Conclusion: The decrease of LCV and reduction of the anisotropic conduction ratio suggest remodeling of the tissue in LVH. The consequences for the generation of arrhythmias are discussed.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1912
    Keywords: Alpha- and beta-adrenoceptor sensitivity ; Reserpine ; [3H]-dihydroalprenolol binding ; [3H]Prazosin binding ; Positive inotropy and chronotropy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cardiac alpha- and beta-adrenoceptor sensitivities were examined after chronic pretreatment of rats with reserpine. Increases in sensitivity would indicate that the receptor is under the influence of the sympathetic innervation, removal by catecholamine depletion with reserpine of the tonic effect of neurotransmitter release would permit receptor upregulation. The positive inotropic responses of paced left atria and papillary muscles and the positive chronotropic responses of spontaneously beating right atria were recorded. A concentration-response curve to isoprenaline (beta-adrenoceptor-mediated) was followed, in the presence of beta-blockade, by one to methoxamine (alpha-adrenoceptor-mediated). Methoxamine exerted positive inotropy of left atria and papillary muscles, the maxima being 43.2 ± 2.7 and 26.8 ± 4.4% of the isoprenaline maxima. A small positive chronotropy (16.5 ± 5.6% maximum) of right atria occurred. After pretreatment with reserpine (1.0 mg kg−1 i.p. daily) for 7 days, the three preparations displayed supersensitivity to isoprenaline, revealed as a significant displacement (P 〈 0.05) of the concentration-response curves to the left of those for control rats. Reserpine pretreatment, however, had no effect on the sensitivity to methoxamine. The increase in beta-adrenoceptor sensitivity to isoprenaline after reserpine pretreatment was accompanied by a significant 41.3% increase (P 〈 0.05) in the number of [3H]-dihydroalprenolol ([3H]-DHA) binding sites (B max) in ventricular membranes, although the dissociation constant (K D) was unaffected. There were more alpha-adrenoceptor [3H]-prazosin binding sites in ventricular than atrial membranes. However, there was no difference in K D or B max between reserpine-pretreated and control tissues. It is proposed that the increase in beta-adrenoceptor sensitivity and binding sites arises from the depletion-induced loss of neuronal noradrenaline release onto the beta-adrenoceptors which are therefore directly under the influence of the neurotransmitter. The failure of cardiac alpha-adrenoceptors to exhibit supersensitivity and increased numbers suggests that they are not directly affected by the sympathetic innervation.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1615-2573
    Keywords: L-Selectin ; E-Selectin ; ICAM-1 ; Unstable angina
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Myocardial ischemia leads to the activation of neutrophils as well as endothelial cells. The interaction between these cells is dependent on certain adhesion glycoproteins which are expressed on their surface. Adhesion of neutrophils to endothelium, mediated by adhesion molecules, has been shown to result in coronary capillary plugging and impairment of coronary blood flow. In certain conditions, upon cell activation, adhesion proteins may be released in soluble form into the circulating blood. The purpose of our study was to verify whether myocardial ischemia occurring during angina episodes results in the release of the soluble adhesion molecules, L-selectin, E-selectin, and intracellular adhesion molecule-1 (ICAM-1), into the circulation. Plasma samples were collected by venepuncture from 15 patients admitted to the emergency room with chest pain caused by attacks of angina pectoris and 15 patients with noncardiac chest pain. To confirm the diagnosis, all patients underwent an exercise stress test and, if not conclusive,99mTc MIBI SPECT or coronary arteriography. Another set of plasma samples were taken from each patient in the absence of chest pain. In addition, blood for analysis was obtained from 15 sexand age-matched healthy subjects. Soluble adhesion molecules plasma levels were measured by standard enzyme-linked immunosorbent assay. In patients with angina pectoris, plasma levels of soluble L-selectin estimated during chest pain were significantly higher than in the control group and decreased in the absence of chest pain. Similarly, the mean concentration of soluble ICAM-1 at the time of angina onset was significantly elevated in the patients in comparison with the control group and remained higher, although not significantly, in the absence of chest pain. In patients with noncardiac chest pain, plasma levels of soluble L-selectin did not differ significantly from those observed in control subjects. In this group of patients, the plasma levels of soluble ICAM-1 estimated during pain onset and in the absence of this symptom were not significantly elevated. On the contrary, the mean values of soluble E-selectin in the patients with ischemic cardiac pain during chest pain and in the absence of this symptom, as well as those in the patients with noncardiac chest pain during or without symptoms, remained unchanged in comparison with the control group. During attacks of angina pectoris an increase in the plasma levels of the soluble adhesion molecules, ICAM-1 and L-selectin, was noted, possibly reflecting activation of neutrophils and endothelial cells during myocardial ischemia. However, Eselectin plasma levels remained unchanged in response to myocardial ischemia.
    Type of Medium: Electronic Resource
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