What is the mechanism of action of narcotic drugs in animal experiments?

      In animal experiments, it may be necessary to anesthetize animals, but most of the references to anesthetics in the data are limited to effects, route of administration, side effects, etc. In addition to certain drugs for injection (such as barbiturates), the mechanism of action of anesthetics (such as diazepa and ketamine) also has a clear mechanism of action. In other words, the central nervous system is in a certain degree of depression because it stimulates or blocks certain receptors. Other anesthetics rarely mention pharmacological mechanisms. For some animal experiments involving the central nervous system, this has brought many problems, and it also makes it difficult to choose the right anesthetic and how to minimize the effect of the drug on the experiment. For example, in the preparation of animal models of stroke, sodium pentobarbital and ketamine are usually not used, but chloral hydrate is used. Why can chloral be hydrated, because the GABA receptor agonism of sodium pentobarbital and the NMDA receptor blockade of ketamine can protect ischemic neurons, thereby affecting the actual results of the model preparation? What are its pharmacological goals? As another example, inhalation anesthesia such as ether cannot be used in a stroke model because it will aggravate penumbra damage and expand the range of ischemic penumbra. So what is the mechanism of action?

   What other commonly used anesthetics, such as inhaled anesthetics that can fall asleep, such as halothane, chloralose, carbamate and their mechanism of action? What is your pharmacological goal? First, the anesthetic effect of urethane is applied to ganglion cells, and its ion channel spectrum is different from other anesthetics. Gas anesthetics, volatile anesthetics or injection anesthetics may play a major role, stimulating GABAergic nerves, or inhibiting glutamatergic nerve transmission, but have no effect on urethane. Increasingly affect agonists and agonist systems. It is reversible in the concentration range of 10 to 300 mmol/L. Depending on the concentration, it can greatly enhance the current response of GABAA and glycine receptors (increase the apparent affinity of agonists) and the function of nACh receptors. Enhance, reversibly and non-competitively inhibit the response of NMDA and AMPA receptors, but uranoxane (up to 300 mmol/L) by itself cannot generate currents and anesthetics (such as ketamine and NMDA receptors) on any of the studied receptors Compared with propofol and GABAA receptors, receptors with only one system can also be selected. Carbamate will cause smaller changes and the ion channel has a wider range of action. I will. The only compound with a spectrum of action similar to carbamates is ethanol. It is speculated that the side effects of carbamate are related to various ion channel effects.

   Side effects: The immune system is severely damaged. Smooth muscle cells and ganglion cells in the muscle layer degenerate. The cells in each layer of the small intestine have varying degrees of degeneration and disintegration. Different organelles also have different degrees of malignant changes.

   Personal experience (more use):

   1. Polyurethane is not easy to wake up after anesthesia. If you only need a short period of anesthesia and still need to maintain the animal's state, it is not recommended to use this anesthetic, as it usually dies the next day. When studying the contents of the cardiovascular system, do not use this anesthetic because

   2 Ulandra has a great cardiovascular effect and a strong destructive effect. I treated spontaneously hypertensive rats, but after taking dozens of carbamates, their blood pressure in the carotid artery quickly returned to normal. After a long period of analysis, the cause was investigated and the cause of the heartache caused by data distortion was determined. Diethyl ether is a commonly used anesthetic, but ether anesthesia takes a short time and must be replenished continuously during the operation. Its dosage is not easy to control and requires special equipment for monitoring and management. This saves the operator from having to perform all operations.

   Its pharmacological effects are unclear. It is now believed that the drug binds to a specific site on the GABAA receptor to make the GABAA receptor sensitive to GABA, increase the opening of chloride channels, and cause neuronal membrane hyperpolarization to play a central role.