[Effects of zatebradine on the course of experimental myocardial infarction under long-term treatment conditions in rats].
A long-term (21 days) administration of the specific bradycardic agent zatebradine to rats with experimental myocardial infarction led to a decrease in the intensity of necrotic changes in the cardiac muscle as evaluated from the ECG-recorded QS complex incidence rate. Morphological studies provided evidence for reduced intensity of the dystrophic processes in myocardium. Under these conditions, the drug did not affect the pump and contractile heart functions. At the same time, zatebradine normalized the reaction of mean aorta blood flow acceleration to volume load (which was inhibited at myocardial infarction), that is, prevented the development of latent heart failure. Zatebradine restored the infarction-decreased norepinephrine (NE) level in cardiac muscle and increased NE content in hypothalamus and brainstem. Along with that, the ratios of deoxyphenylacetic acid/dopamine and homovanillic acid/dopamine were reduced.
Tsorin
I B
IB
Palka
I P
IP
Chichkanov
G G
GG
Kudrin
V S
VS
Klodt
P M
PM
Sorokina
A V
AV
Miroshkina
I A
IA
D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001552:Benzazepines / Q000494:pharmacology*; D001783:Blood Flow Velocity / Q000187:drug effects; D001933:Brain Stem / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002316:Cardiotonic Agents / Q000494:pharmacology*; D004195:Disease Models, Animal; D004562:Electrocardiography; D007031:Hypothalamus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D013997:Time Factors
D001552:Benzazepines; D002316:Cardiotonic Agents; C043636:zatebradine; D009638:Norepinephrine