摘要
研究了血管紧张素转换酶抑制药卡托普利（ｃａｐｔｏｐｒｉｌ）对大鼠痛阈与吗啡镇痛作用的影响，探讨了其与中枢神经系统内血管紧张素Ⅱ（Ａ Ⅱ）与内源性阿片祥物质（ＯＬＳ）之间的关系。结果显示，脑室和鞘内注射卡托普利可显著提高大鼠痛阈，产生明显的镇痛效应，并呈一定的量效关系。若与吗啡合用，可明显加强吗啡的镇痛效应。阿片受体拮抗药纳络酮可部分阻断卡托普利的镇痛效应。给药后３０分钟测定脑和脊髓内ＡⅡ含量的变化，其含量明显降低。提示卡托普利的镇痛效应可能与中枢神经系统内ＡⅡ含量的变化以及ＯＬＳ的作用有密切关系。
Angiotensin I is considered as an endogenous antiopioid sllbstance of CNS. We studied the effects of captopril on the content of angiotensin Ⅱ in CNS and the pain threshold in rats. The results showed that both intracere broventrlcular and intrathecal injections of captopril (50μg/μl ) significantly elevated the pain threshold by observing the screaming response to noxious stimulation to the tall skin and obvious analgesia were produced,which can he partly blocked by intracerebroventricular injection of naloxone. Central administration of captopril also significantly increased morphine analgesic effects administered by peripheral injections. At 30 min after central captopril administration, the contents of angiotensin Ⅱ in some brain regions,such as, hypothalamus, mid brain, medulla oblon gata, and the thoracic spinal cord (T.4~12) were significantly decreased. These results suggest that captopril anal gesic effects may be mediated by decreasing central angiotensin contents,and central opiate receptors may partly participated in the captopril effects.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
1995年第7期318-320,共3页
Chinese Journal of Anesthesiology
