动物造模,急性肺水肿,药效评价 z-bio 2024-06-03 579

　　1. Animal modeling materials: SD rats, weighing 250-300g, with half male and half female; Medications: Epinephrine hydrochloride, pentobarbital.

　　2. Method of modeling: Model group animals were anesthetized intraperitoneally with pentobarbital 30mg/kg body weight, femoral artery was separated, intubation was performed, and blood pressure was measured; Separate the jugular vein, intubate, monitor with an oscilloscope, insert the hose into the pulmonary artery, measure pulmonary artery pressure, and record normal blood pressure and pulmonary artery pressure. A rat model of acute pulmonary edema was established by injecting 0.05mg/kg adrenaline hydrochloride through a jugular vein catheter.

　　3. The principle of modeling is that adrenaline causes pulmonary edema in animals.

　　4. Changes after modeling After modeling with adrenaline, within 10 minutes, due to the increase of pulmonary circulation resistance and pulmonary artery pressure, foam like substances appeared in the lungs and trachea, which caused acute pulmonary edema, decreased blood pressure, and arrhythmia, leading to death.

　　The pulmonary arterial pressure in the model group was significantly higher than that in the control group, and the rats in the model group died gradually within about 10 minutes. Therefore, the complete data of pulmonary artery pressure and blood pressure in the model group were only recorded up to 5 minutes. The pulmonary artery pressure in the model group was (2.20 ± 0.24) kPa before modeling, (4.49 ± 0.68) kPa at 1 minute of modeling, with a change rate of 104.8%, (3.59 ± 0.65) kPa at 3 minutes of modeling, with a change rate of 63.63%, and (2.97 ± 0.61) kPa at 5 minutes of modeling, with a change rate of 35.15%. The pulmonary artery pressure in the control group was (2.17 ± 0.29) kPa before modeling, (2.25 ± 0.39) kPa at 1 minute of modeling, with a change rate of 3.7%, (2.21 ± 0.28) kPa at 3 minutes of modeling, with a change rate of 1.84%, and (2.22 ± 0.24) kPa at 5 minutes of modeling, with a change rate of 2.45%.

　　The lungs of the experimental animals were dissected and observed immediately after death. The naked eye showed that the lung volume increased, the lung surface was wet, there were foam like substances, pulmonary edema was obvious, and there were scattered or patchy bleeding points. Pathological examination revealed edema fluid and red blood cells in the alveoli and interstitium under the microscope.