Physiological adaptation of the heart to pathological overloading.
Chronic overloading of the rat heart induces a cascade of adaptational events that compensate for the increase in work. At the myocardial level there are two types of adaptational mechanisms: qualitative, represented by the isomyosin changes leading to an improved efficiency; and quantitative, the hypertrophy. We present new approaches exploring possible adaptational changes at other levels within the myocardial cell. Studies of heart overload were performed either in young rats with experimental aortic stenosis or in humans with chronic compensatory hypertrophy. By means of double immunofluorescence labeling of isolated myocytes with anti-V1 and anti-V3 myosin immunoglobulins, we showed that the shift from high- to low-ATPase isomyosins occurs rapidly after aortic stenosis (2-3 days). Cardiac myocytes were shown to be poor in tubulin but a microtubule pattern was clearly visualized by an immunofluorescence approach. Their role in the onset of adaptational processes after aortic stenosis in not yet clear. On the other hand, we showed that in humans, contrary to small rodents, the adaptational process at the isomyosin level is very small or nonexistent.
D000818:Animals; D001024:Aortic Valve Stenosis / Q000378:metabolism / Q000503:physiopathology*; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D006706:Homeostasis; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D009218:Myosins / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D007527:Isoenzymes; D009218:Myosins; D000252:Calcium-Transporting ATPases