@entity2224 ( @entity2224 ) in conscious @entity35 with coronary artery ligation occurs in two phases, before (phase 1) and after (phase 2) 90 min of ischaemia respectively. The mechanisms of phase 2 @entity2224 are not established. Interestingly, phase 2 @entity2224 is absent in isolated (denervated) buffer-perfused @entity35 hearts. We investigated whether @entity2922 supplementation (to mimic sympathetic drive) was sufficient to restore phase 2 @entity2224 in such hearts. Isolated @entity35 hearts (n=10 per group) underwent coronary ligation for 240 min. At 90 min, during a period of relative electrical stability, the perfusion solution was switched from standard (Krebs) to identical solution or Krebs containing @entity2661 (313 nM @entity1063 and 75 nM @entity1425 ) with or without 10 microM @entity69565 (an alpha(1)-adrenoceptor antagonist) or 10 microM @entity2165 (a beta(1)-adrenoceptor antagonist). Although in all groups the incidence of phase 1 @entity2224 was high (80 - 100%), the temporal distribution of @entity2224 was monophasic, i.e. only one heart in one group developed phase 2 @entity2224 (P=NS). Other @entity943 (e.g., @entity591 ; VT) exhibited a similar temporal distribution. Nevertheless, haemodynamic changes confirmed sympathomimetic effects of @entity2661 , e.g., heart rate was increased from 278+/-7 beats min(-1) in controls to 335+/-8 beats min(-1) (P<0.05) by @entity2661 , an effect that could be blocked by @entity2165 (285+/-7 beats min(-1)) but not by @entity69565 (342+/-12 beats min(-1)). Coronary flow was correspondingly increased from 7.7+/-0.7 ml min(-1) g(-1) to 16.5+/-1.3 ml min(-1) g(-1) (P<0.05); this effect could be blocked by @entity2165 (8.1+/-0.6 ml min(-1) g(-1)) and was enhanced by @entity69565 (20.7+/-2.4 ml min(-1) g(-1)). In conclusion, despite evidence of adequate alpha- and beta-adrenoceptor activation, @entity2922 supplementation to isolated buffer-perfused @entity35 hearts was insufficient to restore phase 2 @entity2224 . It therefore appears unlikely that @entity2661 alone mediate phase 2 @entity2224 .

Independent contribution of XXXX to arrhythmogenesis during evolving infarction in the isolated @entity35 heart.

@entity69565 :: ('MESH:C005185', 'Chemical') :: ['trimazosin'] @entity943 :: ('MESH:D001145', 'Disease') :: ['ventricular arrhythmias'] @entity1425 :: ('MESH:D004837', 'Chemical') :: ['adrenaline'] @entity591 :: ('MESH:D013610', 'Disease') :: ['tachycardia'] @entity2224 :: ('MESH:D014693', 'Disease') :: ['VF', 'Ventricular fibrillation'] @entity2922 :: ('CHEBI:33567', 'Chemical') :: ['catecholamine'] @entity2165 :: ('MESH:D001262', 'Chemical') :: ['atenolol'] @entity35 :: ('10116', 'Species') :: ['rat', 'rats'] @entity2661 :: ('MESH:D002395', 'Chemical') :: ['catecholamines'] @entity1063 :: ('MESH:D009638', 'Chemical') :: ['noradrenaline']
@entity2661 :: (MESH:D002395,Chemical) :: ['catecholamines']
