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  • 1
    ISSN: 1432-2013
    Keywords: Na+, K+-ATPase ; Ouabain ; Rubidium ; Vasodilation ; Autoregulation ; Reactive hyperemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Changes of coronary flow in the isolated perfused spontaneously beating guinea pig heart were induced by elevation of potassium concentration in the perfusion medium (4–16 meq/l). Potassium caused a dose-dependent transient increase of diastolic coronary inflow. The response was inhibited by ouabain (1.4×10−7 M) or reduced temperature. Rubidium ions elicited almost identical vasodilator effects which were also inhibited by ouabain. Autoregulation of coronary flow, reactive hyperemia, and hypoxic coronary dilation were not significantly altered in the presence of ouabain. The results support the hypothesis that potassium as well as rubidium cause vasodilation by activating a Na+, K+-ATPase. On the other hand, they do not favour the view of an essential involvement of potassium ions in local regulation of coronary flow under the conditions studied.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2013
    Keywords: 14C-adenine ; Coronary flow ; Adenosine ; Inosine ; Hypoxanthine ; Hypoxia ; Autoregulation ; Reactive hyperemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In an attempt to test the hypothesis whether adenosine is involved in the regulation of coronary flow, adenosine, inosine and hypoxanthine were measured in the effluent perfusate and in the tissue of isolated guinea pig hearts under various experimental conditions. In addition, the release of14C-adenosine,14C-inosine and14C-hypoxanthine was determined after prelabeling cardiac adenine nucleotides with14C-adenine. The decrease in coronary resistance induced by hypoxic perfusion (30% and 20% in the gas phase) and during autoregulation was associated with a considerable increase in the release of adenosine, inosine and hypoxanthine. Under both conditions the concentrations of adenosine in the effluent perfusate were clearly within the coronary vasodilating range of exogenously administered adenosine. The tissue content of adenosine also increased significantly when the perfusion pressure was reduced. The release of14C-adenosine closely paralleled the changes in coronary resistance during hypoxic perfusion, autoregulation and during reactive hyperemia. The specific activity of adenosine in the effluent perfusate, however, decreased substantially upon reduction of the oxygen supply to the heart, indicating that the release of14C-adenosine does not provide an absolute measure of total adenosine release by the heart. Our data indicate that the greater part of the adaptive changes of vascular resistance during hypoxia and autoregulation can be attributed to adenosine which is formed at an enhanced rate under these conditions. However, other factors might be involved as well.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 353 (1975), S. 317-326 
    ISSN: 1432-2013
    Keywords: Myocardial Energy Metabolism ; Reactive Hyperemia ; Autoregulation ; Pyruvate ; Adenosine ; Papaverine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hemodynamic and metabolic characteristics of an isolated guinea pig heart preparation perfused with a pyruvate fortified Krebs-Ringer-bicarbonate solution are described. The preparation is stable for more than 90 min with respect to coronary flow, heart rate, left ventricular pressure,dP/dt, oxygen consumption, and myocardial high energy phosphate levels. The changes in coronary flow induced by alterations of perfusion pressure, ischemia, and hypoxia resemble those seen under in vivo conditions. The preparation also exhibits concentration dependent and reproducible changes in coronary resistance upon administration of adenosine and papaverine. The in vivo like features of this preparation can be mainly attributed to the use of pyruvate as additional and preferentially utilized substrate. The preparation appears to be suitable for quantitative studies of myocardial metabolism and heart function as well as for investigations of the coronary system.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0878
    Keywords: Key words: Growth factors ; Cardiogenesis ; Cardiac mutant ; Myocardium ; Axolotl ; Ambystoma mexicanum (Urodela)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. In the Mexican axolotl (salamander), Ambystoma mexicanum, a recessive cardiac lethal mutation causes an incomplete differentiation of the myocardium. Mutant hearts lack organized sarcomeric myofibrils and do not contract throughout their lengths. We have previously shown that RNA purified from normal anterior endoderm or from juvenile heart tissue is able to rescue mutant embryonic hearts in an in vitro organ culture system. Under these conditions as many as 55% of formerly quiescent mutant hearts initiate regular contractions within 48 hours. After earlier reports that transforming growth factor-β1 and, to a lesser extent, platelet-derived growth factor-BB could substitute for anterior endoderm as a promoter of cardiac mesodermal differentiation in normal axolotl embryos, we decided to examine the effect of growth factors in the cardiac mutant axolotl system. In one type of experiment, stage 35 mutant hearts were incubated in activin A, transforming growth factors-β1 or β2, platelet-derived growth factor, or epidermal growth factor, but no rescue of mutant hearts was achieved. Considering the possibility that growth factors would only be effective at earlier stages of development, we tested transforming growth factors-β1 and β5, and activin A on normal and mutant precardiac mesoderm explanted in the absence of endoderm at neurula stage 14. We found that, although these growth factors stimulated heart tube formation in both normal and mutant mesodermal explants, only normal explants contained contractile myocardial tissue. We hypothesize that transforming growth factor-β superfamily peptides initiate a cascade of responses in mesoderm that result in both changes in cell shape (the basis for heart morphogenesis) and terminal myocardial cytodifferentiation. The cardiac lethal mutation appears to be deficient only in the latter process.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0878
    Keywords: Growth factors ; Cardiogenesis ; Cardiac mutant ; Myocardium ; Axolotl, Ambystoma mexicanum (Urodela)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In the Mexican axolotl (salamander), Ambystoma mexicanum, a recessive cardiac lethal mutation causes an incomplete differentiation of the myocardium. Mutant hearts lack organized sarcomeric myofibrils and do not contract throughout their lengths. We have previously shown that RNA purified from normal anterior endoderm or from juvenile heart tissue is able to rescue mutant embryonic hearts in an in vitro organ culture system. Under these conditions as many as 55% of formerly quiescent mutant hearts initiate regular contractions within 48 hours. After earlier reports that transforming growth factor-β1 and, to a lesser extent, platelet-derived growth factor-BB could substitute for anterior endoderm as a promoter of cardiac mesodermal differentiation in normal axolotl embryos, we decided to examine the effect of growth factors in the cardiac mutant axolotl system. In one type of experiment, stage 35 mutant hearts were incubated in activin A, transforming growth factors-β1 or β2, platelet-derived growth factor, or epidermal growth factor, but no rescue of mutant hearts was achieved. Considering the possibility that growth factors would only be effective at earlier stages of development, we tested transforming growth factors-β1 and β5, and activin A on normal and mutant precardiac mesoderm explanted in the absence of endoderm at neurula stage 14. We found that, although these growth factors stimulated heart tube formation in both normal and mutant mesodermal explants, only normal explants contained contractile myocardial tissue. We hypothesize that transforming growth factor-β superfamily peptides initiate a cascade of responses in mesoderm that result in both changes in cell shape (the basis for heart morphogenesis) and terminal myocardial cytodifferentiation. The cardiac lethal mutation appears to be deficient only in the latter process.
    Type of Medium: Electronic Resource
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