| 英文摘要 |
In 1860, Niemann was successful in isolating an alkaloid from the leaves of Erythroxylon coca and named it 'cocaine'. In 1884, Koller applied this alkaloid as topical anesthetic in an ophthalmological surgery and Halsted used it for a nerve block. Since then cocaine was widely applied in clinical practice. In 1904, procaine, the first synethetic local anesthetic, was introduced by Einbom. From the time on, many synthetic local anesthetics have been synthesized and introduced into clinical practice. Many of them have been discarded due to some of the side effects. Until now, more than 10 of these drugs remain, e.g., bupivacaine, cocaine, procaine, tetracaine, lidocaine, ropivacaine, etc. Despite their somewhat physic or chemical differences, they can generally be divided into 2 groups: amide and ester. The former is metabolized through the liver and the latter mainly through hydrolysis by esterase in the blood. They both are almost the same in other aspects. For example, they all demonstrate an effect of neural blockade through sodium channel blocking effects. Additionally, they all have CNS toxicity and cardiovascular toxicity. Although some of them are emphasized for their having less toxicity on CNS or CV system, in fact, the differences are minor. This result may be explained by the fact that they all have similar structures. They all are derived from the framework of cocaine. In the basic structure, a lipophilic benzene ring is on one end; an ester linkage or amide linkage, in the middle; a hydrophilic tertiary amine, on the other end. Thus, a newly-developed local anesthetic that contain the said structure has similar pharmacologic effects. Consequently, the new local anesthetic-- ropivacaine-- still has CNS toxicity. |
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