Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 10 (1999), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: I*, and Quinidine in Healed Infarction. Introduction: Mechanisms and drug treatment of serious ventricular arrhythmias in patients with healed myocardial infarction (HMI) are incompletely understood, in part because the electrophysiology and pharmacology of myocytes from noninfarcted regions of HMI hearts are not well characterized. Methods and Results: We studied the delayed rectifier potassium current (IK) and quinidine responsiveness of single left ventricular subendocardial myocytes isolated from the region remote to the border zone of healed infarct myocardium (4 to 6 mm from scar edge) in cat hearts 2 months after coronary artery occlusion. Subendocardial cells isolated from corresponding regions of normal cat hearts provided controls. IK activation and tail currents were recorded using whole cell, voltage clamp techniques. Membrane capacitance of cells remote to HMI (187 ± 7 pF) was significantly greater than normal (155 ± 6 pF; P 〈 0.001). Action potential durations (APDs) recorded from myocytes in remote regions were prolonged (APD90= 247 ± 10 msec) compared to normal (214 ± 11 msec; P 〈 0.05). Quinidine (1 μM) significantly prolonged APD90 in normal cells but not in remote cells. Density of IK, (tail current) was significantly decreased in remote cells (3.1 ± 0.3 pA/pF) compared to normal (3.9 ± 0.3 pA/pF; P 〈 0.05). and voltage-dependent activation of IK was shifted in the positive direction. Quinidine had significantly less incremental blocking effect on IK already blunted by regional hypertrophy compared to its effect on normal cells in remote cells. IC550 shifted to 0.95 μM in remote cells compared with 0.50 μM in normal cells. Conclusion: Cells in noninfarct region remote from the scar are hypertrophied and display altered electrophysiology. Their reduced IK responsiveness to quinidine may explain, in part, failure of quinidine to prolong APD in such cells. Moreover, dispersion of repolarization may be decreased by the effect of quinidine on normal cells.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 8 (1997), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: ICa in Healed Myocardial Infarction. Introduction: Abnormal action potentials in myocytes adjacent to 〉 2-month-uld feline LV myocardial infarcts (MI) may reflect alterations in Ca2+ currents (ICa). Methods and Results: We compared ICa, at 36°C, in subendocardial myocytes isolated from areas adjacent to MI and to ICa in cells from remote areas (〉 4 mm away; REM) and control cells from similar regions in normal hearts. Control (CON) myocytes had membrane capacitance of 234 ± 10 pF (n = 81 cells) compared to 305 ± 14 pF in REM (71 cells; P 〈 0.05 from CON) and 237 ± 11 pF (n = 55 cells) in MI (not different from CON). From Vh=−40 mV, peak ICa elicited by test potentials (−35 to +70 mV) were significantly larger in CON (−1746 ± 123 pA) and REM (−1795 ± 142 pA) compared to Ml (−1352 ± 129 pA) (P 〈 0.05). Peak 1(11 density was significantly reduced in REM (−6.0 ± 0.4 pA/pF) or MI (−5.7 ± 0.4 pA/pF, P 〈 0.05) compared to CON (−7.5 ± 0.4 pA/pF). Double exponential ICa decay was similar among groups. Half-inactivation potential (V0.5) was significantly shifted (hyperpolarizing direction) for MI (−29.1 ± 2.6 mV) and REM (−24.6 ± 1.2 mV) myocytes compared to −20.3 ± 1.0 mV in CON. MI slope factor (k; 9.0 ± 0.5) was significantly different from CON (6.8 ± 0.3) and RKM (7.3 ± 0.4). No differences in time course of recovery from inactivation were noted. Five millimolar Ba2+0 produced significant increases in ICa in CON and REM but an attenuated response in MI. Bay k8644 (1 μM) produced similar ICa increase in all groups. ICa increase due to isoproterenol (1 ICaM) in MI and REM was half that in CON, but there were no differences in increased ICa responses among groups following phenylephrine (10 μM). Conclusion: Reduced ICa density in REM reflects cell hypertrophy, whereas altered ICa of MI may reflect altered channel structure and/or function.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 1. Histamine (10−3 M) increased the spontaneous rate similarly in isolated preparations of normal left ventricular tissue from control, i.e. normal and sham-operated, dogs (control preparations) and in preparations consisting of normaland contiguous infarcted left ventricular tissue from dogs with subacute, i.e. 24 hours after left coronary artery ligation, myocardial infarction (infarcted preparations). 2. Histamine (10−3 M) markedly enhanced the irregular rhythm of infarcted preparations. 3. The H1-receptor antagonist, chlorpheniramine (10−4 M), and the H2-receptor antagonist, cimetidine (10−3 M), antagonized the effects of histamine (10−3 M) on the spontaneous rate of both control and infarcted preparations. 4. The H1-receptor agonist, 2-pyridyl ethylamine (PEA, 10−4 M), increased the spontaneous rate of control and infarcted preparations; these effects were antagonized by chlorpheniramine (10−4 M). The H2-receptor agonist, dimaprit, had no effect. 5. Similar to histamine (10−3 M), PEA (10−4 M) enhanced the irregular rhythm of infarcted preparations; dimaprit had no effect. 6. High local concentrations of histamine may occur in poorly perfused ischemic tissue. The enhancement of irregular rhythm produced by histamine, and the specific H1-receptor agonist, PEA, leads us to suggest its involvement in arrhythmias associated with subacute myocardial infarction.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 405 (1985), S. 37-45 
    ISSN: 1432-2013
    Keywords: Canine ventricular muscle ; Ca2+ movements ; Isoproterenol ; Excitation-contraction coupling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 45Ca2+ exchange was studied in small pieces of canine left ventricular free wall. The loss of45Ca2+ from45Ca2+ equilibrated tissue into ice-cold (4°C) “wash” medium could be best fitted with a model containing a minimum of 3 compartments.45Ca2+ uptake into and45Ca2+ efflux from the most slowly exchanging compartment (compartment 3) at 37°C allowed it to be subdivided into two fractions; a rapidly exchanging fraction (t 1/2∼1.25 min) and a slowly exchanging fraction (t 1/2∼50 min). The total Ca2+ content of compartment 3 was enhanced by isoproterenol but little affected by caffeine. The slowt 1/2 for exchange of the Ca2+ in compartment 3 at 4°C and its increased Ca2+ content following isoproterenol treatment suggest that this compartment contains some Ca2+ of intracellular origin. In addition, the finding that the rapidly exchanging part of compartment 3 could be preserved by cooling the tissue to 4°C shows that rapidly exchanging Ca2+ compartments can be studied in superfused cardiac preparations using this technique. Action potentials, elicited by electrical stimulation of the tissue, caused large changes in the Ca2+ content of compartment 3 (up to 170 μM/kg) indicating that this postulated intracellular compartment may play a significant role in the normal contraction-relaxation cycle.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1432-1424
    Keywords: triadin ; rat dyads ; excitation-contraction coupling ; transverse tubule ; junctional sarcoplasmic reticulum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Dyads (transverse tubule—junctional sarcoplasmic reticulum complexes) were enriched from rat ventricle microsomes by continuous sucrose gradients. The major vesicle peak at 36% sucrose contained up to 90% of those membranes which possessed dihydropyridine (DHP) binding sites (markers for transverse tubules) and all membranes which possessed ryanodine receptors and the putative junctional foot protein (markers for junctional sarcoplasmic reticulum). In addition, the 36% sucrose peak contained half of the vesicles with muscarine receptors. Vesicles derived from the nonjunctional plasma membrane as defined by a low content of dihydropyridine binding sites per muscarine receptor and from the free sarcoplasmic reticulum as defined by the Mr 102K Ca2+ ATPase were associated with a diffuse protein band (22–30% sucrose) in the lighter region of the gradient. These organelles were recovered in low yield. Putative dyads were not broken by French press treatment at 8,000 psi and only partially disrupted at 14,000 psi. The monoclonal antibody GE4.90 against skeletal muscle triadin, a protein which links the DHP receptor to the junctional foot protein in skeletal muscle triad junctions, cross-reacted with a protein in rat dyads of the same Mr as triadin. Western blots of muscle microsomes from preparations which had been treated with 100mm iodoacetamide throughout the isolation procedure showed that cardiac triadin consisted predominantly of a band of Mr 95 kD. Higher molecular weight polymers were detectable but low in content, in contrast with the ladder of oligomeric forms in rat psoas muscle microsomes. Cardiac triadin was not dissolved from the microsomes by hypertonic salt or Triton X-100, indicating that it, as well as skeletal muscle triadin, was an integral protein of the junctional SR. The cardiac epitope was localized to the junctional SR by comparison of its distribution with that of organelle markers in both total microsome and in French press disrupted dyad preparations. Immunofluorescence localization of triadin using mAb GE4.90 revealed that intact rat ventricular muscle tissue was stained following a well-defined pattern of bands every sarcomere. This spacing of bands was consistent with the interpretation that triadin was present in the dyadic junctional regions.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Cardiovascular drugs and therapy 7 (1993), S. 611-619 
    ISSN: 1573-7241
    Keywords: transient outward current ; cardiac hypertrophy ; whole-cell voltage clamp ; cardiac myocytes ; right ventricular hypertrophy ; Ito regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cardiac hypertrophy can decrease myocardial contractility and alter the electrophysiological activity of the heart. It is well documented that action potentials recorded from hypertrophied feline ventricular cells can exhibit depressed plateau voltages and prolonged durations. Similar findings have been made by others in rabbit, rat, guinea pig, and human heart. Whole-cell patch voltage-clamp studies designed to explain these changes in the action potential suggest that the only component of the membrane current recorded from feline right ventricular (RV) myocytes found to be substantially different from normal is the 4-aminopyridine-sensitive transient outward current (Ito). However, it was not clear if the change in Ito could explain the changes in the action potential of hypertrophied cardiocytes, nor was it clear if these changes reflect an alteration in the electrophysiological character of the channels underlying Ito. A kinetic comparison of Ito elicited by hypertrophied RV myocytes with that elicited by comparable normal RV myocytes previously revealed no differences, suggesting that the increased magnitude of the peak Ito recorded from hypertrophied myocytes arises because the current density increases and not because of any alteration in the kinetic parameters governing the current. This finding suggests that in hypertrophy additional normal channels are expressed rather than a kinetically different channel subtype emerging. Investigations designed to determine if enhancement of Ito could explain the hypertrophy-induced changes in plateau voltage and action potential duration suggest that a change in Ito density can indeed explain the entire effect of hypertrophy on RV action potentials. If this notion is correct, the likelihood of “sudden death” in patients with myocardial hypertrophy might be decreased by a blocker selective for cardiac Ito.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...