title: The treatment with pyridostigmine improves the cardiocirculatory function in rats with chronic heart failure.
abstract: Sympathetic hyperactivity and its outcome in heart failure have been thoroughly investigated to determine the focus of pharmacologic approaches targeting the sympathetic nervous system in the treatment of this pathophysiological condition. On the other hand, therapeutic approaches aiming to protect the reduced cardiac parasympathetic function have not received much attention. The present study evaluated rats with chronic heart failure (six to seven weeks after coronary artery ligation) and the effects of an increased parasympathetic function by pyridostigmine (an acetylcholinesterase inhibitor) on the following aspects: arterial pressure (AP), heart rate (HR), baroreceptor and Bezold-Jarisch reflex, pulse interval (PI) and AP variability, cardiac sympathetic and parasympathetic tonus, intrinsic heart rate (i-HR) and cardiac function. Conscious rats with heart failure exhibited no change in HR, Bezold-Jarisch reflex, PI variability and cardiac sympathetic tonus. On the other hand, these animals presented hypotension and reduced baroreflex sensitivity, power in the low frequency (LF) band of the systolic AP spectrum, cardiac parasympathetic tonus and i-HR, while anesthetized rats exhibited reduced cardiac performance. Pyridostigmine prevented the attenuation of all the parameters examined, except basal AP and cardiac performance. In conclusion, the blockade of acetylcholinesterase with pyridostigmine was revealed to be an important pharmacological approach, which could be used to increase parasympathetic function and to improve a number of cardiocirculatory parameters in rats with heart failure.
authors.affiliation: Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Av. Bandeirantes 3900, Ribeirão Preto, SP, Brazil.
authors.forename: João Paulo J
authors.initials: JP
authors.lastname: Sabino
authors.forename: Carlos Alberto Aguiar
authors.initials: CA
authors.lastname: da Silva
authors.forename: Rubens Fernando
authors.initials: RF
authors.lastname: de Melo
authors.forename: Rubens
authors.initials: R
authors.lastname: Fazan
authors.forename: Helio C
authors.initials: HC
authors.lastname: Salgado
mesh_terms: D000818:Animals; D017704:Baroreflex / Q000187:drug effects; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use*; D003326:Coronary Circulation / Q000187:drug effects*; D023921:Coronary Stenosis / Q000209:etiology / Q000503:physiopathology; D003331:Coronary Vessels / Q000601:surgery; D005071:Evoked Potentials / Q000187:drug effects; D006321:Heart / Q000187:drug effects* / Q000294:innervation / Q000503:physiopathology; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D008026:Ligation; D008297:Male; D009206:Myocardium / Q000473:pathology; D010275:Parasympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology; D011729:Pyridostigmine Bromide / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology
chemical_list: D002316:Cardiotonic Agents; D002800:Cholinesterase Inhibitors; D011729:Pyridostigmine Bromide