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  • 1
    Electronic Resource
    Electronic Resource
    On the mechanism and possible therapeutic application of delayed adaptation of the heart to stress situations (1995)
    Springer
    Molecular and cellular biochemistry 147 (1995), S. 115-122 
    Details
    ISSN: 1573-4919
    Keywords: cardioprotection ; delayed adaptation ; cAMP ; PDE-isoenzymes ; prolongation of protection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Mild (not harmful) stress may initiate anadaptive mechanism, protecting the heart from harmful consequences of a more severe stress. There are at least three known types of cardiac adaptation to stress such as: a) the gradually developing long lasting adaptation to chronic mechanical overload, leading to cardiac hypertrophy, later to cardiomyopathy and heart failure, b) the rapidly developing adaptation to moderate stress initiated by ‘preconditioning’ brief coronary occlusion(s) or brief periods of rapid cardiac pacing, protecting for less than 1 h against consequences of a subsequent, severe stress, c) the later appearing, more prolonged cardio-protective adaptation, described by us in 1983, induced by various forms of more severe but not injurious stimuli, such as an optimal dose of prostacyclin or its stable analogues; or a series of brief periods of rapid pacings. This form of cardiac adaptation to stress protects for 24–48 h against consequences of a more severe stress such as: 1. myocardial ischaemia; 2. early and late postocclusion and reperfusion arrhythmias; 3. early morphologic changes secondary to ischaemia and reperfusion; 4. ischaemia induced myocadial loss of K+ and accumulation of Na+ and Ca++; 5. it may increase the tolerance to the toxic effects of cardiac glycosides. A reduced response to beta-adrenergic stimuli and a concomitant increase in activity and amount of PDE I and IV was shown by us earlier. The hypothesis that these factors may play a role in the mechanism of delayed protection was confirmed by our present findings according to which 7-oxo-PgI2-treatment greatly attenuated the dose dependent isoprenaline-induced increase in contractility, relaxation and myocardial cAMP level in rat hearts isolated 48h after 7-oxo-PgI2. In addition all these values are in close correlation with each other. The endogenous ‘self-defence’ of the heart based on adaptation represents anew therapeutic concept, different from the classical drug-receptor interaction produced protection. Its possible exploitation to therapeutic use requires that the adaptation inducing stress should beapplicable topatients, furthermore prolongation of duration of protection should be possible. As a first step in testing applicability to therapy we had to show that drug induced adaptive protection is existing in the conscious animal. In our present study we found an attenuation of rapid pacing induced elevation of the ST-segment in the endocardial electrogram and in the left ventricular end diastolic pressure in conscious rabbits 24–48 h after treatment with Iloprost. Besides we found an attenuation of tachycardia and arrhythmias due to two stage coronary artery ligation in conscious dog 48 h after pretreatment with 7-oxo-PgI2. Finally we were able to demonstrate that protection against coronary artery occlusion-induced ST segment elevation and arrhythmias can be prolonged at will by periodically repeated maintenance doses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00944791
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  • 2
    Electronic Resource
    Electronic Resource
    Differentiation-dependent expression of cardiac δ-CaMKII isoforms (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 259-268 
    Details
    ISSN: 0730-2312
    Keywords: multifunctional Ca2+/calmodulin-dependent protein kinase ; cardiac isoforms ; muscle differentiation ; cell line Hgc2 ; adult rat heart ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Despite their important role in controlling the cardiac Ca2+ homeostasis, presence and functions of individual isoforms of the multifunctional Ca2+/calmodulin-dependent protein kinase in the heart are not well studied. Here we report on expression of isoforms of the δ class in two differentiation states of the embryonic rat heart-derived cell line H9c2 compared to adult rat heart. Reverse transcription coupled polymerase chain reaction analysis revealed specific expression patterns of four variants of the δ class (δB, δC, δ4, δ9) in adult rat heart, H9c2 myoblasts, and skeletal muscle-like H9c2 myotubes. δC was identified as a common isoform with higher amounts in H9c2 cells and the prominent one in myoblasts. In contrast, expression of δ9 accompanied cardiac as well as skeletal muscle differentiation. Expression of δB, however, was representative for differentiated cardiac muscle, whereas δ4 expression coincided with differentiation into the skeletal muscle-like state. Our results demonstrate differentiation-dependent isoform expression of the δ class of the multifunctional Ca2+/calmodulin-dependent protein kinase of muscle. The identification of cardiac target proteins for this kinase, e.g. the α1-subunit of the L-type Ca2+ channel, the sarcoplasmic reticulum Ca2+-ATPase, phospholamban and the ryanodine receptor define H9c2 myoblasts as a suitable model system for further functional characterization of the identified cardiac δ isoforms. J. Cell. Biochem. 68:259-268, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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