Modeling experiments in animal models of pulmonary hypertension

Summary

Pulmonary hypertension (PH) is a common and serious condition in the cardiovascular field. Currently, there are four main methods used to model pulmonary hypertension in animal models: chronic hypoxia, monocrotaline (MCT) injection, simple left pneumonectomy (PE), and abdominal aortocaval fistula shunting (A-VF). VF).

Principle

The basic principle of low pressure hypoxia to construct an animal model of pulmonary hypertension is that hypoxic pulmonary vasoconstriction (HPV) and pulmonary vascular reconstruction are the most important pathophysiological features of hypoxic pulmonary hypertension. Chronic hypoxia causes HPV in the pulmonary vasculature, and when HPV repeatedly persists, it promotes pulmonary revascularization and causes right ventricular hypertrophy, which is a vicious cycle.

Chronic hypoxia or intermittent hypoxia can cause abnormal reconstruction of pulmonary arteries in animals, which can lead to pulmonary hypertension and even lung failure. The possible pathogenesis of highland pulmonary hypertension is that the initiating stimulus (e.g., hypoxia-low pressure, etc.) causes pulmonary vascular reconstruction, thickening of the pulmonary artery intima-media, and increased pulmonary vascular resistance, which leads to elevated pulmonary artery pressure and right ventricular failure.

Operation method

Hypobaric hypoxia constructs an animal model of pulmonary arterial hypertension

Principle

The basic principle of low pressure hypoxia to construct an animal model of pulmonary hypertension is that hypoxic pulmonary vasoconstriction (HPV) and pulmonary vascular reconstruction are the most important pathophysiological features of hypoxic pulmonary hypertension. Chronic hypoxia causes HPV in the pulmonary vasculature, and when HPV repeatedly persists, it promotes pulmonary revascularization and causes right ventricular hypertrophy, which is a vicious cycle. Chronic hypoxia or intermittent hypoxia can cause abnormal reconstruction of pulmonary arteries in animals, which can lead to pulmonary hypertension and even lung failure. The possible pathogenesis of highland pulmonary hypertension is that the initiating stimulus (e.g., hypoxia-low pressure, etc.) causes pulmonary vascular reconstruction, thickening of the pulmonary artery intima-media, and increased pulmonary vascular resistance, which leads to elevated pulmonary artery pressure and right ventricular failure.

Materials and Instruments

Equipment:
① Hypoxia chamber;
② RM-6200 four-guide physiological recorder;
③ Surgical tools;
Wistar rats, etc.
Reagents:
① 10% Ulatan.

Move

The basic process of constructing an animal model of pulmonary hypertension with low pressure and hypoxia can be divided into the following steps:
A. Healthy Wistar rats were placed in a hypoxic chamber, in which 5 g of sodium lime was placed in each rat, and then pumped and depressurized at a rate of 3 kPa/min to 51-54 kPa (1 kPa = 7.5 mmHg), at which time the oxygen content was 10% to 10.5%, and the oxygen level was lowered for 6 hours each day for 2 to 4 weeks. The oxygen level was 10% to 10.5% at this time, and the hypoxia was continued for 6 hours every day for 2 to 4 weeks.
B. Animals were anesthetized intraperitoneally with 10% ursodiol (1 mL/100 g) the day after the last hypoxia experiment.
C. Measurement of right ventricular and pulmonary artery pressures: The right external jugular vein of the rat was separated, and a plastic catheter (0.9 mm OD, 0.6 mm I.D.) was inserted into the right external jugular vein from a plastic tube (0.9 mm OD, 0.6 mm I.D.) connected to a pressure transducer on one side. A plastic catheter (0.9 mm OD, 0.6 mm ID) was connected to a pressure transducer at one end and inserted through the external jugular vein. Mean right ventricular pressure and mean pulmonary artery pressure were measured and recorded.
D. After measurement, the right external jugular vein was ligated and the left common carotid artery was immediately detached. One end of the plastic catheter (1 mm OD, 0.6 mm ID) was connected to the injection needle, the end of the needle was connected to the three-way valve switch, and the latter was connected to the syringe, which facilitated the rinsing of the catheter with heparinized saline to prevent coagulation, and the other end was inserted through the common carotid artery. The three-way valve was turned to connect the catheter to the syringe, and when there was blood return, the three-way valve was closed. The rats were placed in an airtight chamber with the same conditions of gas concentration as before.
E. After 30 minutes, blood was withdrawn from the catheter portion and discarded. Arterial blood was drawn with a syringe for blood gas analysis. The rats were removed from the chamber and the thoracic cavity of the animals was immediately cut open and the heart and lungs were removed for preparation of pathologic specimens.

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