动物造模,急性心功能不全动物模型 z-bio 2023-10-16 596

　　1. Animal modeling material: Healthy hybrid dog, male and female, with a body weight of (18.54 ± 2.0) kg; Medication: pentobarbital.

　　2. Method of modeling: Animals were anesthetized by intravenous injection of 3% pentobarbital (30mg/kg), followed by tracheal intubation and assisted breathing with a ventilator. Place a sheath tube into the femoral artery and vein, monitor electrocardiogram, and monitor SaO in the anterior part of the animal tongue.

　　The femoral vein sheath sends a floating catheter (7F) to the distal end of the pulmonary artery. Record the average pulmonary capillary wedge pressure, average right atrial pressure and cardiac output, arterial systolic pressure, arterial diastolic pressure, and arterial mean pressure.

　　Open the fourth intercostal space on the left side of the dog, separate the beginning of the aorta, and place the Doppler flow meter probe at the root of the aorta to measure CO.

　　Adjust the clinical pacemaker perception to 0.75-1.0mV, output current 1-2mV, and under the guidance of electrocardiogram, shape the pacing electrode and send it to the right ventricle through the left femoral vein and right atrium. After the pacing threshold is below 1mV, the perception function is good, and there is a continuous and stable electrocardiogram pacing waveform, fix the electrode position, and turn off the power supply of the pacing pulse generator for use.

　　Separate and ligate the left anterior descending branch (LAD) of the coronary artery at a distance of about 2cm from the bifurcation of the main coronary artery, using silk thread to block its distal blood flow.

　　Turn on the power supply of the pacing pulse generator and perform right ventricular pacing at a slightly faster rate than the experimental dog's heart rate. Gradually increase the pacing frequency, starting with an increase of 10 times/min each time, and gradually decreasing in amplitude until CO stabilizes by 25% and 50%.

　　3. Modeling principle: After ligating the anterior descending branch of the coronary artery to cause acute myocardial infarction, rapid pacing is more likely to cause acute coronary insufficiency (ACI).

　　4. After modeling, the measured CO in the basic state of the experimental dog was (1.46 ± 0.16) L/min. After ligation of LAD, the electrocardiogram showed acute myocardial infarction ST-T changes in the precordial leads, but the changes in blood pressure and CO were not significant. After observing for 15 minutes, right ventricular pacing was performed, resulting in a 25% and 50% decrease in CO compared to the baseline state for (2.14 ± 0.43) and (3.18 ± 0.56) hours, respectively.

　　After the reduction of CO, the blood pressure of dogs significantly decreased, and a 50% decrease in CO was more significant than a 25% decrease; MRAP and mPCWP significantly increased, with a 50% decrease in CO and a more significant increase compared to a 25% decrease; Blood oxygen saturation also showed a similar decrease in change.

　　Take the apical four chamber section of the heart using echocardiography, measure the maximum transverse diameters of the left atrium, left ventricle, right atrium, and right ventricle, measure the left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV), and the ultrasound automatically gives the values based on LVEF=(LVEDV - LVESV) ÷ LVEDV