HE BEI YI PIN Pharmaceutical Co., Ltd.

Induction and recovery with isoflurane are very rapid. After inhalation of isoflurane, the pharyngeal and laryngeal reflexes weaken rapidly. The depth of anesthesia changes rapidly, and the heart rhythm remains stable during the process. As anesthesia deepens, spontaneous breathing will be suppressed and should be closely monitored. A drop in blood pressure may occur during isoflurane induction and return to normal with the start of surgical stimulation. During the maintenance of anesthesia, blood pressure tends to decrease with the depth of anesthesia due to the dilation of peripheral blood vessels, and the heart rhythm remains stable at this time. Under mechanical ventilation and maintaining normal carbon dioxide partial pressure (PaCO2), cardiac output can be maintained even if the depth of anesthesia is increased, generally by compensating for it by increasing the heart rate. In the case of spontaneous breathing, the heart rate increases with the increase in carbon dioxide concentration, and cardiac output can also increase to above the level of the awake state. Cerebral blood flow does not change under mild isoflurane anesthesia, but increases as anesthesia deepens. Excessive cerebrospinal fluid pressure can be prevented or corrected by hyperventilating the patient before or during anesthesia. Isoflurane can cause increased sensitivity of the myocardium to adrenaline, but the degree is weaker than enflurane.

After entering the blood, most of it binds to plasma proteins and accumulates in tissues, with the largest accumulation in skeletal muscle. When the concentration in plasma decreases, it is released again. Most of it is hydrolyzed and converted by plasma cholinesterase, metabolized by the liver into p-aminobenzoic acid and dimethylaminoethanol, and then degraded or combined and excreted in the urine.

Anti-platelet aggregation and disaggregation, dilation of arterioles, improvement of microcirculation, improvement of cerebral blood flow and blood circulation and stasis-removing effects

Anti-platelet aggregation and disaggregation, dilation of arterioles, improvement of microcirculation, improvement of cerebral blood flow and blood circulation and stasis-removing effects

This product is an amide local anesthetic. After blood absorption or intravenous administration, it has obvious biphasic effects of excitation and inhibition on the central nervous system, and there may be no precursor excitation. When the blood concentration is low, analgesia and drowsiness occur, and the pain threshold increases; with increasing doses, the effect or toxicity increases, and it has an anticonvulsant effect at sub-toxic blood concentrations; convulsions may occur when the blood concentration exceeds 5μg·ml-1. At low doses, this product can promote the outflow of K in myocardial cells, reduce myocardial autonomy, and have an anti-ventricular arrhythmia effect; at therapeutic doses, it has no obvious effect on the electrical activity of myocardial cells, atrioventricular conduction, and myocardial contraction; further increases in blood concentrations can cause a slowing of heart conduction velocity, atrioventricular conduction block, inhibition of myocardial contractility, and a decrease in cardiac output.