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Bridge amp fe221

Manufactured by ADInstruments
Sourced in Australia

The Bridge Amp FE221 is a laboratory instrument designed to amplify and condition physiological signals. It features four independent signal conditioning channels with configurable gain and filter settings. The device is intended for use in research and clinical applications that require precise measurement and analysis of biological signals.

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7 protocols using bridge amp fe221

1

Arterial Pressure and Respiratory Monitoring

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In order to record the arterial pressure, the arterial catheter was connected to a pressure transducer which is coupled to an amplifier (Bridge Amp FE221; ADInstruments, Colorado Springs, CO, USA). The pulsatile pressure was recorded continuously with a data acquisition system (PowerLab; ADInstruments, Colorado Springs, CO, USA). The MAP was calculated from the pulsatile signal using the LabChart software (v.7.3.7, ADInstruments, Colorado Springs, CO, USA). Analogical signals of the electrocardiogram (ECG), obtained through electrodes positioned in the forelimbs, were amplified 1000 times and filtered between 100 and 1000 Hz (Bridge Amp; ADInstruments, Colorado Springs, CO, USA). The heart rate (HR) was calculated as instantaneous frequency of the ECG signal (LabChart v.7.3.7, ADInstruments, Colorado Springs, CO, USA). The DIA motor activity signals was amplified 10,000 times (Bridge Amp; ADInstruments, Colorado Springs, CO, USA) and band-pass filtered (100–2000 Hz). The signal were rectified and integrated in 50 ms intervals using LabChart software (v.7.3.7; ADInstruments, Colorado Springs, CO, USA). The DIA motor activity was evaluated by burst amplitude (expressed as percentage difference from baseline) and frequency (considered as respiratory frequency, fR, and expressed in cycles per minute, cpm).
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2

Autonomic Function Evaluation in Stroke

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All biosignals derived from autonomic testing of neurocardiac, sudomotor and vasomotor function signals were processed by an artifact-filter and signal amplifier (Bridge Amp® FE221, ADInstruments, Castle Hill, Australia) and were converted using a four-channel-digitizing polygraph (Power-Lab®, ADInstruments, Castle Hill, Australia). Analyses were carried out using the software package LabChart® for Windows (ADInstruments, Castle Hill, Australia). In order not to interfere with stroke unit care all measurements took place in the patient's room of our stroke unit with a controlled room temperature of 21–25°C. Autonomic testing was performed in a semi-recumbent position after a 10-min lasting rest.
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3

Invasive Pressure Monitoring Protocol

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A signal acquisition system (PowerLab 8/35 Pro, AD Instruments, Australia) was connected to a signal amplifier (Bridge Amp FE221, AD Instruments) to record arterial and ventricular pressures. Data were recorded at 1000 points per second. The setting parameters were as follows: 1) Channel 1 for ECG: with sample rate at 1 k/s, range at 5 mV, connected to Bio Amplifier, and units in mV; 2) Channel 2 for pressure measurements: with sample rate at 1 k/s, range at 50 mV, connected to Bridge Amplifier, and units in mmHg; and 3) Channel 3 with a derivation of Channel 2 for HR: with sample rate at 1 k/s, range at 2 mV. A pressure transducer (MLT844; AD Instruments) was connected with one of its ends to the signal amplifier and the other end was coupled to an intermediate pressurized water seal system. The latter was necessary for system calibration and adequate pressure recording. The pressure calibration for the transducer was performed using a pressure gauge, where the pressures were recorded, from 0 to 250 mmHg.
Central arterial pressure was recorded for 5 min through the cannula in the right carotid. Then, the cannula was introduced and positioned in the left ventricle (LV), recording for 5 min more. The position of the cannula was determined by observing the ventricular pressure wave characteristic (15 (link)).
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4

Pulsatile Arterial Pressure Measurement

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The pulsatile arterial pressure (PAP) signal was obtained by connecting the femoral artery catheter to a pressure transducer (MLT0699, ADInstruments Bella Vista, Australia) coupled to an amplifier (Bridge Amp, FE 221, ADInstruments, Bella Vista, Australia). Data were digitized at a frequency of 2000 samples·s−1 using a digital analog converter (PowerLab 4/25, ML845, ADInstruments, Bella Vista, Australia). The MAP was calculated from the PAP signal integral (LabChart 7, v7.3.7, ADInstruments, Bella Vista, Australia). Heart rate (HR) was calculated as the instantaneous frequency of the PAP signal (LabChart 7, v7.3.7, ADInstruments, Bella Vista, Australia).
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5

Cardiac Function Assessment Protocol

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After the final of training period, the animals were anesthetized with ketamine (50 mg/kg) and xylazine (10 mg/kg) for left ventricle catheterization. Briefly, the right common carotid artery was separated from connective tissue and catheterized with a fluid-filled polyethylene catheter (PE50). The catheter was connected to a pressure transducer (FE221 Bridge amp, ADInstruments, Australia) and a digital system (Powerlab 4/35, ADInstruments, Australia). After arterial systolic and diastolic blood pressures were recorded, the catheter was advanced into the left ventricle to obtain the following measurements: heart rate (HR), left ventricular systolic pressure (LVSP), end-diastolic pressure (LVEDP), and the maximum rate of pressure rise (+dP/dt) and fall (-dP/dt). It was not possible to measure other parameters related to cardiac function such as cardiac output and ejection fraction because we not evaluate the ventricular volume. However, other studies have been demonstrated that LVEDP presents as an important parameter for the assessment of ventricular function, and his increase is associated with ventricular dysfunction. [21] The heart, soleus muscle, abdominal fat, uterus and a lung were removed immediately after hemodynamic evaluation and weighed.
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6

Dose-Dependent Effects of DL on Hemodynamics

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Rats were anesthetized with ketamine and xylazine (80 mg/Kg and 10 mg/Kg; i.p., respectively), and polyethylene catheters were implanted in the abdominal aorta and inferior vena cava via left femoral artery and vein, respectively. After insertion and fixation by cotton threads, the catheters were tunneled subcutaneously and exteriorized through an incision in the posterior cervical region of the animal. The incisions were closed and the animals were allowed a 24-hour post-operative recovery period. Mean arterial pressure (MAP) and heart rate (HR) were recorded through a pressure transducer (Edwards LifeSciences, Irvine, CA, EUA) coupled to an amplifier (FE221, Bridge Amp; ADInstruments, Bella Vista, NSW, Australia)
After post-operative recovery period, MAP and HR were recorded before (baseline values) and after IV bolus administration of DL (1, 5, 10, 20, and 40 mg/kg, i.v.) or vehicle to obtain dose-response curves. The DL curve (n = 6) was compared with the vehicle curve (n = 6).
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7

Cardiovascular Function Assessment in Rats

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Forty-eight hours after the last training day, the animals were anesthetized with ketamine and xylazine (50 and 10 mg/kg i.p., respectively) for measurement of the blood pressure and LV function. A polyethylene catheter (PE50) with heparinised saline (50 U/mL Ariston sodium heparin, São Paulo, Brazil) was introduced into the left carotid artery, followed by connection to a pressure transducer (FE221 Bridge Amp, ADInstruments, Australia), which was coupled to a data acquisition system (Powerlab 4/35). The catheter was carefully guided to the LV, where the LV systolic pressure (LVSD) and LV end-diastolic pressure (LVEDP) were measured, as was the maximum LV contraction and relaxation derivatives (dP/dt+ and dP/dt−, respectively). The isovolumic relaxation time (Tau) was also measured.
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