Local noradrenaline release in acute myocardial ischemia: influence of catecholamine synthesis inhibition and beta-adrenoceptor blockade on ischemic injury.
Left coronary artery ligations or sham operations were performed on pentobarbitone-anesthetized rats. The rats were sacrificed at various times after artery occlusion or sham operation and the creatine kinase (CK), potassium (K+), and noradrenaline (NA) content was determined in the left and right ventricular myocardium and in the interventricular septum. One group of rats was pretreated with the NA synthesis inhibitor alpha-methyl-p-tyrosine methyl ester (alpha-MT), another group with d,l-propranolol, and a third group with saline. The NA level of the ischemic left ventricle fell rapidly after the onset of ischemia. This early NA reduction was attenuated after alpha-MT treatment, probably due to reduced transmitter release. Both CK and K+ decreased in a time-dependent manner in the ischemic area of the heart. The early reduction of CK tended to be attenuated after alpha-MT as well as after propranolol. The results support the theory of a detrimental effect of locally released NA. However, in this model the injury produced by the extensive and nearly total ischemia seems so severe that the additional effect of myocardial adrenoceptor activation may well be only marginal.
D000818:Animals; D001834:Body Water / Q000378:metabolism; D002395:Catecholamines / Q000096:biosynthesis*; D003327:Coronary Disease / Q000503:physiopathology*; D003402:Creatine Kinase / Q000378:metabolism; D006352:Heart Ventricles; D006439:Hemodynamics; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011941:Receptors, Adrenergic / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
D002395:Catecholamines; D011941:Receptors, Adrenergic; D011943:Receptors, Adrenergic, beta; D003402:Creatine Kinase; D011188:Potassium; D009638:Norepinephrine