[Recovery of the isolated mammalian heart contractions after heart cooling to > or = 0 degrees C].
During rapid cooling of the isolated heart in vitro, heart standstill occurs in consequence of the cessation of the conductivity from pacemaker to working myocardium. During long slow cooling heart arrest occurs on account of the overloading of cytoplasm by Ca2+ in consequence of disturbance of the permeability of the cell membrane and sarcoplasmic reticulum membranes. These disturbances are the outcome of the energy deficit of the ionic pumps and the system of ATP synthesis in consequence of higher temperature dependence on chemical energetic mechanisms in comparison with physical-chemical mechanisms of membrane ionic percolation into cytoplasm due to concentration gradients. Perfusing heart which was rapidly cooled up to arrest in a very short time preserves its work capacity and quickly restores its contractions in heating. Isolated heart after cold arrest in vitro preserves a relatively high work capacity without use of the protective solutions (chemical cardioplegia) in the course of 2.0 +/- 2.5 hours. With the aid of cold cardioplegia at slow perfusion through the rat heart myocardium (during asystolic state of the heart at 11 degrees or below) it preserved its work capacity for up to 24 hours. With the aid of some methods (lowering the [K+]0 in perfusate, action of norepinephrine or acetylcholine, etc.) the heart action can be restored after cold arrest without heating (at the temperature of heart arrest or below).
Aliukhin
Iu S
IuS
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002463:Cell Membrane Permeability; D003080:Cold Temperature; D007036:Hypothermia, Induced; D016623:Ion Pumps / Q000378:metabolism; D009200:Myocardial Contraction; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D051381:Rats
D016623:Ion Pumps; D000255:Adenosine Triphosphate; D002118:Calcium