[The Contractile Function of the Surviving Heart Muscle Following Coronary Occlusion (author's transl)].
Following acute myocardial infarction the functional load of the surviving heart muscle does increase considerably, leading to an increased release of adrenergic neurotransmitters with a consequent decrease in endogenous catecholamine stores. Within the first 24 h following infarction, a temporary decline in the high-energy phosphate content is observed in the surviving heart muscle; futhermore, a reduction in lactate extraction is noted. In the intact organism an increased shortening of the surviving heart muscle is noted as a consequence of the altered ventricular geometry and the increased release of catecholamines. If these effects are excluded by means of isolation and analysis in vitro, a decrease in contractile function could be demonstrated in the surviving heart muscle in the early phase following infarction; the response to positive inotropic interventions was depressed as well. These changes are reversible; six weeks following infarction a normal contractile behaviour is observed.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D066298:In Vitro Techniques; D007773:Lactates / Q000378:metabolism; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000032:analysis / Q000378:metabolism*; D009638:Norepinephrine / Q000032:analysis; D010725:Phosphocreatine / Q000378:metabolism; D013997:Time Factors
D002395:Catecholamines; D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D009638:Norepinephrine
Die kontraktile Funktion des überlebenden Herzmuskels nach Koronarverschluss.