Aminoglycoside antibiotics have antibacterial effects on most Enterobacteriaceae, Pseudomonas aeruginosa, some other Pseudomonas, Acinetobacter, Alcaligenes, meningococci, gonococci, influenza bacilli, Yersinia, Campylobacter fetus, Mycobacterium tuberculosis and some Mycobacterium. The mechanism of action is to act on the 30S subunit of bacterial ribosomes and inhibit bacterial protein synthesis. Combination with semi-synthetic penicillins or cephalosporins often produces synergistic antibacterial effects.

This product mainly acts on alpha-receptors, directly stimulating alpha-receptors. Its effect is weaker than that of norepinephrine but more persistent. Its cardiovascular effect is similar to that of norepinephrine. It can constrict blood vessels, continuously increase systolic and diastolic blood pressure, and enhance myocardial contractility. The cardiac output of normal people does not change much, but it can increase the cardiac output of patients with shock. The excitement of heart rate is not very significant, rarely causes arrhythmia, and has no central nervous system excitation effect. Because its pressor effect is reliable and lasts for a long time, it rarely causes reactions such as palpitations or decreased urine volume. When administered continuously, because this product indirectly replaces the transmitter in the adrenergic nerve vesicles, it can reduce the transmitter and weaken the intrinsic effect, so it should not be stopped suddenly to avoid rebound hypotension.

This product is a β-receptor agonist, which has a strong stimulatory effect on both β1 and β2 receptors, and has almost no effect on α receptors. Main effects: It acts on the heart β1 receptors to enhance cardiac contractility, increase heart rate, accelerate conduction, increase cardiac output and myocardial oxygen consumption. It acts on the vascular smooth muscle β2 receptors to significantly dilate skeletal muscle blood vessels, and the kidneys, mesenteric blood vessels and coronary arteries also dilate to varying degrees, and the total vascular resistance is reduced. Its cardiovascular effects lead to increased systolic blood pressure, decreased diastolic blood pressure, and increased pulse pressure difference. It acts on the bronchial smooth muscle β2 receptors to relax bronchial smooth muscle. It promotes the decomposition of glycogen and fat and increases tissue oxygen consumption.

It stimulates the adrenaline receptors of the sympathetic nervous system and the dopamine receptors located in the kidneys, mesentery, coronary arteries, and cerebral arteries. Its effect is dose-dependent: at low doses, it mainly acts on dopamine receptors, dilating the blood vessels of the kidneys and mesentery; at low to medium doses, it can directly stimulate β1 receptors and indirectly promote the release of norepinephrine, increasing myocardial contractility and cardiac output; at high doses, it stimulates α receptors, leading to increased peripheral vascular resistance. In addition, it has a strong stimulating effect on cardiac β1 receptors, which can prevent the malignant development of shock caused by renal and mesenteric ischemia.

Acetylglutamine is the acetyl compound of glutamine. After passing through the blood-cerebrospinal fluid barrier, it is decomposed into glutamate and gamma-aminobutyric acid (GABA). Glutamate is involved in the information transmission of the central nervous system. GABA can antagonize the excitability of glutamate, improve nerve cell metabolism, maintain nerve stress resistance, reduce the effect of blood ammonia, and improve brain function.