The Effect of U-74389G and MK-801 on the Size of Brain Infarction in the Transient Focal Ischemia-Reperfusion Rat Model

BACKGROUND: There has been considerable progression in laboratory investigations of novel therapeutic approaches aimed at protecting the brain parenchyma in the setting of the acute ischemia. The zone of ischemia surrounding an area of infarction provides a target for neuroprotective agents. MK-801 is a well known non-competitive NMDA receptor antagonist and has a neuroprotective effect to ischemic penumbra zone. U-74389G is a compound of Lazaroid(21-Aminosteroid) and a free radical scavenger which has been investigated to a neuroprotective effect to ischemic penumbra zone. METHODS: The protective effects of single or combined pretreatment of U-74389G and MK-801 on the focal cerebral ischemia in the Sprague-Dawley rats were evaluated. The size of infarction after 2 hours occlusion-4 hours reperfusion of the left middle cerebral artery with modified Longa method was measured. The rats were given 3mg/Kg I.v. of MK-801 and U-74389G or 0.5ml of normal saline 30 minutes before middle cerebral artery occlusion. The size of infarction was described as the volume. RESULTS: U-74389G, MK-801, and combined U-74389G and MK-801 pretreatment reduced significantly the volume of infarction 55%, 64%, 24%, respectively compared with saline pretreatment (p0.05). CONCLUSIONS: These results show that single or combined pretreatment of U-74389G and MK-801 before 30 minutes of occlusion significantly reduced the volume of infarction compared with the control group in the focal cerebral occlusion-reperfusion of rats. And the combined pretreatment of U-74389G and MK-801 before 30 minutes of occlusion significantly reduced the volume of infarction compared with the single pretreatment of MK-801 or U-74389G in the focal cerebral occlusion- reperfusion of rats.

Hemichorea Associated with Hyperglycemia: A Case Showing Increased Blood Flow in the Contralateral Striatum

We report a diabetic woman who developed paroxysmal hemichorea during an episode of non-ketotic hyper-glycemia. A MRI showed a high signal intensity on T1-weighted images and a low signal intensity on T2-weighted images in the contralateral putamen. SPECT on the 30th day after the onset revealed an increased blood flow in the contralateral striatum. Although these abnormalities in the left putamen are considered to be the cause of her involuntary movement, the exact pathophysiological mechanisms of these abnormalities are not yet clear and further investigations are needed.

Thyrotoxic Periodic Paralysis: Electrophysiologic Studies During Paralytic Attack in Two Patients

The precise nature of the underlying disturbance responsible for TTP is unknown, but recent work suggests that abnormalities of sodium channels play an important role. There are only a few electrophysiologic studies reported during an attack of paralysis of TTP and the electrophysiologic studies during paralytic attack in our two patients showed the following results, different only in severity. 1.Nerve conduction studies were normal in all the tested sensory nerves. Motor nerves showed normal conduction velocities, but low amplitudes of CMAPs except for median nerve. 2.Needle EMG showed markedly decreased insertional activities, and lowamplitude, short-duration, and polyphasic MUAPS, The recruitment patterns on maximal efforts were markedly reduced. There were no spontaneous activities. 3.Repetitive nerve stimulation of ulnar nerve showed significant incremental responses on digiti quinti muscle, marked during the early phase of stimulation. The degree of incremental responses was proportional to the frequency of stimulation.