Animal model of hypoperfused acute renal failure

Summary

The establishment of human-like hypoperfusion acute ischemic renal failure animal models (animal models of hypoperfusion acute renal failure) is of great significance in exploring the pathogenesis and prevention of acute ischemic renal failure.

Principle

According to the different experimental methods, the corresponding principles are also different:

The basic principle of the animal model of low perfusion acute renal failure is to establish an animal model of low perfusion acute ischemic renal failure by partially ligating the abdominal aorta, which is more in line with the clinical reality than the traditional method of clamping the renal artery.

Appliance

This animal model of hypoperfused acute ischemic renal failure can be used to study the pathogenesis of acute ischemic renal failure and preventive measures.

Operation method

Animal model of hypoperfused acute renal failure

Principle

An animal model of hypoperfused acute ischemic renal failure was established by partial ligation of the abdominal aorta, which was more in line with the clinical reality than the traditional method of clamping the renal artery.

Materials and Instruments

Subject: Rats.
Experimental reagent: 3% pentobarbital sodium (60 mg/kg.

Move

(I) Procedure 1

Female SD rats, weighing 250-300 g, were anesthetized with 3% sodium pentobarbital (60 mg/kg) by intraperitoneal injection in the experimental group (n=30), and then blood was taken from the tail vein to measure blood creatinine concentration. A PE-50 catheter was inserted into the right femoral artery to monitor blood pressure.

The abdominal cavity was opened along the midline, and the right kidney was resected and the stump of the renal hilum was ligated. The superior mesenteric artery and the left renal artery were separated and exposed, and a suture was passed under the abdominal aorta in between, the ends of the two threads were brought together and rotated in the same direction so that they gradually compressed the abdominal aorta until the blood pressure measured along the femoral artery cannulae reached 2.7~3.3kPa, so that the kidneys were under hypoperfusion for one hour, the compression was lifted, the abdominal wall was sutured, and the kidneys were put back into cages for free eating and drinking.

All cases with large fluctuation of blood pressure in the femoral artery during the operation, which could not be controlled quickly and satisfactorily by adjusting the degree of abdominal aortic compression, or those whose blood pressure in the femoral artery could not be returned to the basal level within 1 minute after decompression were considered as "failures" and were abandoned.

In the control group of 10 cases, the whole surgical procedure was the same as that in the experimental group, except that the location of abdominal aortic compression was below the opening of the left renal artery. The blood of 15 rats in the experimental group and 5 rats in the control group was collected from their tails every day after the operation, and the creatinine concentration was measured by an automatic biochemical analyzer.

After anesthesia with 3% sodium pentobarbital (60 mg/kg) by intraperitoneal injection, the abdominal cavity was opened, and the left kidney was perfused with 1.25% glutaraldehyde phosphate buffer and then removed, fixed, dehydrated, embedded in paraffin wax, and sliced and stained with PE.

Caveat

1. Twenty-four of the 30 rats in the experimental group and 10 rats in the control group could satisfactorily control the femoral artery blood pressure at 2.7~3.3 kPa.Among the 6 cases of failure, 2 cases could only lower the femoral artery blood pressure to 4.7~6.7 kPa by the above method, and the blood pressure did not decrease after further compression of the abdominal aorta; 3 cases caused intestinal ischemia due to the occlusion of the opening of the superior mesenteric artery during compression of the abdominal aorta because of the proximity of the opening of the left renal artery to the opening of the superior mesenteric artery; and another Ⅰ case could not return to the preoperative level of the blood pressure within 1 minute after the decompression was lifted, although saline was added. In another case, the blood pressure could not return to the preoperative level within 1 minute after the compression was lifted, and the blood pressure was still at 10 kPa despite the supplementation of saline, suggesting that it was not caused by insufficient blood volume.The blood creatinine concentration of normal rats was (44.4±7.0) pumolL, and that of the experimental group was (188.2±61.6) umolL, (143.4±46.6) umolL, and (105.1±41.4) u.mol/L at 24, 48, and 72 hours after the operation, respectively, which were significantly higher than the normal value (P＜0.001), and then gradually declined, and was reduced to (143.4±46.6) umolL and (105.1±41.4) u.mol/L by day 7 of the operation, except for 1 day in the experimental group, and the blood pressure was still at 10 kPa, suggesting that it was not caused by blood volume insufficiency. On the 7th postoperative day, the blood creatinine was normal except for one rat with 60.7 umolL.In the control group, the 24-hour postoperative blood creatinine concentration was (46.6 earth 7.0) pu.mol/L, which was not significantly different from the normal value ( P>0.05).Morphological examination: The left kidney of the experimental group was hypoperfused for 1 hour and restored to perfusion for 24 hours, the kidney was significantly enlarged, and the renal peritoneum was highly tense. Light microscopy showed diffuse swelling of renal tubular epithelial cells and occasional small focal necrosis. The tubular pattern and interstitial edema were obvious. The control rats did not show any abnormality under the light microscope.

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