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目的：观察急性不完全性脑缺血对左室功能的影响及 Ｌ精氨酸的保护作用。方法：家兔乌拉坦麻醉，结扎双侧颈总动脉和右侧椎动脉，观察结扎后３０ ～２４０ ｍｉｎ 左室功能和心肌的病理变化。结果：在结扎后６０ ｍｉｎ ，＋ Ｄ Ｐ／ Ｄ Ｔｍａｘ 、 Ｖｃｅ ４０ 和 Ｌｏ降低（ Ｐ＜ ０ ．０５） ，－ Ｄ Ｐ／ Ｄ Ｔｍａｘ 显著降低（ Ｐ＜ ０ ．０１） ；结扎后１２０ ～２４０ ｍｉｎ ， Ｈ Ｒ、 Ｌ Ｖ Ｓ Ｐ± Ｄ Ｐ／ Ｄ Ｔｍａｘ 、 Ｖｃｅ ４０ 、 Ｖｍｐ 、 Ｖｍａｘ 和 Ｌｏ显著降低（ Ｐ＜ ０ ．０１） ，心肌出现损害。 Ｌ精氨酸组在结扎后１８０ ｍｉｎ ，＋ Ｄ Ｐ／ Ｄ Ｔｍａｘ 降低（ Ｐ＜ ０ ．０５） 。结扎后２４０ ｍｉｎ ，± Ｄ Ｐ／ Ｄ Ｔｍａｘ 、 Ｖｍｐ 、 Ｖｍａｘ 及 Ｌｏ 均降低（ Ｐ＜ ０ ．０５） ；而－ Ｄ Ｐ／ Ｄ Ｔｍａｘ 显著降低（ Ｐ＜ ０ ．０１） 。与结扎组比较， Ｌ精氨酸组在结扎后３０ ｍｉｎ ， Ｌ Ｖ Ｓ Ｐ 显著增高（ Ｐ＜ ０ ．０５） ；结扎后６０ ｍｉｎ ， Ｌ Ｖ Ｓ Ｐ、－ Ｄ Ｐ／ Ｄ Ｔｍａｘ 与 Ｌｏ 显著增加（ Ｐ＜ ０ ．０１） ；结扎后１２０ 、１８０ 和２４０ｍｉｎ ，全部左室功能指标均有显著增加（ Ｐ＜ ０ ．０１）
Objective: To observe the effect of acute incomplete cerebral ischemia on left ventricular function and the protective effect of L-arginine. Methods: Rabbits were anesthetized with urethane, bilateral common carotid arteries and right vertebral artery were ligated. The left ventricular function and myocardial pathological changes were observed at 30 ~ 240 min after ligation. RESULTS: The levels of + D P / D Tmax, Vce 40 and Lo decreased (P <0.05) and D P / D Tmax decreased significantly at 60 min after ligation (P <0.01) , H R, L V S P ± D P / D Tmax, Vce 40, Vmp, Vmax and Lo significantly decreased (P <0.01), and myocardial damage occurred. L-arginine group 180 min after ligation, + D P / D Tmax decreased (P <0 .05). ± D P / D Tmax, Vmp, Vmax and Lo decreased at 240 min after ligation (P <0.05), while - D P / D Tmax decreased significantly (P <0.01). Compared with the ligation group, L V S P was significantly increased in L-arginine group at 30 min after ligation (P <0.05); L V S P, - D P / D Tmax and Lo significantly at 60 min after ligation (P <0.01); all the indexes of left ventricular function increased significantly at 120, 180 and 240min after ligation (P <0.01)