The increase in acetylcholine yielded by pyridostigmine (PYR), an acetylcholinesterase inhibitor, was evaluated for its effect on the haemodynamic responses-mean arterial pressure (MAP) and heart rate (HR)-and their nycthemeral oscillation in mice before and one week after myocardial infarction (MI). Mice were anesthetized (isoflurane), and a telemetry transmitter was implanted into the carotid artery. After 5 days of recovery, the MAP and HR were recorded for 48 h (10 s every 10 min). Following this procedure, mice were submitted to surgery for sham or coronary artery ligation and received drinking water (VEHICLE) with or without PYR. Five days after surgery, the haemodynamic recordings were recommenced. Sham surgery combined with VEHICLE did not affect basal MAP and HR; nevertheless, these haemodynamic parameters were higher during the night, before and after surgery. MI combined with VEHICLE displayed decreased MAP and increased HR; these haemodynamic parameters were also higher during the night, before and after surgery. Sham surgery combined with PYR displayed similar results for MAP as sham combined with VEHICLE; however, PYR produced bradycardia. Nevertheless, MI combined with PYR exhibited no change in MAP and HR, but these haemodynamic parameters were also higher during the night, before and after surgery. Therefore, MI decreased MAP and increased HR, while PYR prevented these alterations. Neither MI nor PYR affected nycthemeral oscillations of MAP and HR. These findings indicate that the increase in acetylcholine yielded by PYR protected the haemodynamic alterations caused by MI in mice, without affecting the nycthemeral haemodynamic oscillations.

The benefit of pyridostigmine (PYR), an acetylcholinesterase inhibitor, on mean arterial pressure (MAP), heart rate (HR) and intrinsic heart rate (IHR) was evaluated in mice (C57Bl/6J) submitted to myocardial infarction (MI). Mice were anesthetized (isoflurane) and telemetry transmitters (DSI) were implanted into the left carotid artery. After 5–7 days of recovery, basal MAP (mmHg) and HR (bpm) were recorded for 48 hours (10s every 10min). Further, basal MAP and HR were recorded continuously followed by methylatropine and propranolol administration. After basal recordings, mice were submitted to sham surgery or left anterior descending (LAD) coronary occlusion and received drinking water with or without PYR (3 mg/kg p.o. for 7 days). Five days after LAD occlusion, or sham surgery, recordings were repeated. Sham surgery did not affect MAP, HR and IHR (n=6). LAD occlusion (n= 3) promoted a MI of 11±1 %, decreased MAP (91±1 vs 106±1 before), increased HR (555±11 vs. 481±18 before) and did not affect the IHR (481±11 vs. 466±7 before). LAD occlusion combined with PYR (n=6) did not show any alteration in MAP (101±6 vs. 100±2 before), HR (489±20 vs. 469±15 before) and IHR (448±41 vs. 453±27 before). The results demonstrate that MI caused a decrease in MAP and an increase in HR combined with no alteration in IHR. In addition, PYR prevented the alterations in MAP and HR caused by MI, and did not change the IHR.