1. Animal modeling materials: SD rats, half male and half female, with a body weight of (200g ± 20) g; Medication: pentobarbital.
2. Method of modeling: sham surgery group: Except for not using silk thread to ligate the abdominal aorta, all other steps were the same as the surgery group; Operation group: the model of pressure overload myocardial hypertrophy was prepared according to the abdominal aorta constriction method: after pentobarbital (40mg/kg) intraperitoneal injection anesthesia, the left upper abdominal straight incision exposed the abdominal aorta and left and right renal arteries, the abdominal aorta was separated between the left and right renal arteries and threaded, a 0.45mm diameter acupuncture and moxibustion needle segment was placed along its long axis, the abdominal aorta was ligated with the acupuncture and moxibustion needle segment, and then the acupuncture and moxibustion needle segment was extracted, which caused the abdominal aorta constriction.
3. Principle of modeling: When left heart failure occurs due to pressure overload, the main determining physiological factors of lung function include mechanical properties, ventilation, blood flow, fluid exchange, gas exchange, and respiratory control, all of which are damaged to a certain extent, leading to functional abnormalities.
4. Changes after modeling: The average abdominal main artery pressure (MAP) of the surgical group was significantly higher than that of the sham group on the first day after surgery and continued to rise thereafter.
The pulmonary arterioles of sham operated rats have thin walls and large lumens, with regular arrangement of endothelial and smooth muscle cells. The surgical group of rats showed significant infiltration of inflammatory cells near the pulmonary arterioles, followed by interstitial pulmonary edema and/or alveolar pulmonary edema. The lumen around the pulmonary bronchiolar artery is significantly enlarged, some of which are replaced by significant proliferation of collagen fibers; The alveoli expand and fuse with each other to form larger alveoli, and pink homogeneous edema accumulates in the alveoli; The smooth muscle cells in the middle membrane of pulmonary arterioles gradually become enlarged and proliferated, the blood vessel wall thickens, the lumen becomes smaller, and some lumens even approach closure.