[Pathogenesis of the low cardiac output syndrome in postreanimation states].
Functional reserves of the cardiovascular system during sharp depression of the cardiac output  in the postreanimation period after 15-minute cardiac arrest were studied in experiments on dogs (by loading with different fluid volumes). Acute hypervolemia did not produce any circulatory decompensation. Reinforcement of venous return and changes in the peripheral circulation due to polyglucine loading augmented the CVP temporarily, and produced a stable increase of the AP, of the cardiac output, systolic volume, the work of the left cardiac ventricle and of the total oxygen consumption by the organism. Meanwhile there was a decrease of the peripheral vascular resistance. In model experiments on dogs, which sustained 20-minute isolated compression ischemia the syndrome of low cardiac output developed too. This indicated the relation of this phenomenon to the disorders in the neuro-humoral regulation of blood circulation.
D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000098:blood supply / Q000503:physiopathology; D002302:Cardiac Output; D002496:Central Venous Pressure; D004285:Dogs; D006331:Heart Diseases / Q000209:etiology*; D007511:Ischemia / Q000503:physiopathology; D009200:Myocardial Contraction; D010101:Oxygen Consumption; D012151:Resuscitation; D013577:Syndrome; D014655:Vascular Resistance
K patogenezu sindroma nizkogo serdechnogo vybrosa v postreanimatsionnykh sostoianiiakh