Hitoshi Fukasawa

Therapeutic effects of hyperbaric oxygenation on acute focal cerebral ischemia in rats

The effects of hyperbaric oxygenation on acute focal cerebral ischemia in rats were investigated. All rats suffered 4-hour middle cerebral artery occlusion. Nontreated controls had a 27.9% +/- 5.5% infarct volume, and a left/right hemispheric volume ratio of 109% +/- 3%. Animals treated between 2.5 and 3.5 hours following occlusion had an 18.1% +/- 9.7% infarct volume (p less than 0.01), and a 105% +/- 3% left/right hemispheric volume ratio (p less than 0.001). In conclusion, at least until 4 hours following an ischemic insult, hyperbaric oxygenation reduces ischemic neuronal injury and brain edema following middle cerebral artery occlusion in rats treated between 2.5 and 3.5 hours following occlusion.

Reversible middle cerebral artery occlusion in rats using an intraluminal thread technique.

We investigated the temporal profile for neuropathologic outcomes after cerebral ischemia using a rat model of reversible middle cerebral artery occlusion, where reperfusion can be introduced in nonanesthetized rats. Reperfusion was performed 1 hour to 5 hours after the occlusion. Control animals underwent permanent occlusion. The results indicate that the time window to reduce infarct volume is 2 hours, and that a > or = 3-hour duration of ischemia is sufficient to attain the maximal infarction observed after permanent ischemia. This suggests that any therapies that follow the therapeutic window will provide little benefit for transient cerebral ischemia and reperfusion injury.

EFFECTS OF A CA2+ ENTRY BLOCKER (NILVADIPINE) ON ACUTE FOCAL CEREBRAL ISCHEMIA IN RATS

SummaryThe effects of nilvadipine, a Ca2+ entry blocker, on focal cerebral ischemia were investigated in rats having unilateral middle cerebral artery occlusion. All rats had 24 h ischemia, and were divided into threegroups (ten rats per group). Groups 1 and 2 received 1.0 and 3.2 mg/kg nilvadipine s.c. respectively, just after the occlusion. Control rats received an equal volume of the vehicle. Control animals had a % infarct volume of 28.2 ± 11.4%,and a left/right hemispheric volume ratio of 112 ± 12 %. Group-1 and -2 rats had % infarct volumes of 25.5 ±11.6% and 13.9 ±9.2% (p<0.01) respectively, and left/right hemispheric volumeratios of 111 ± 9% and 103 ± 7% (p < 0.05), respectively. Thus, the drug reduced the infarct size and the brain edema in a dose-dependent manner. The significant decrease in the infarct volumewas observed in the periphery of the frontoparietal cortex. This study supports the hypothesis that nilvadipine may be a potential therapeutic agent for cerebral ischemia. Neuropathological findings suggest the possible therapeutic effects of the drug in the ischemic penumbra.

Therapeutic effects of nilvadipine on rat focal cerebral ischemia.

The present study was conducted to invetigate the therapeutic effects of nilvadipine, a Ca2+ entry blocker, on rat focal cerebral ischemia. Under halothane anesthesia, a 3-0 nylon thread was introduced into the neck internal carotid artery to occlude the left middle cerebral artery. Either nilvadipine (3.2 mg/kg) or vehicle was administered subcutaneously 1, 2, 3, 4, 5 and 6 h following the occlusion (groups 1–6, respectively). Twenty-four hours after the occlusion, the percentage infarct volumes in nilvadipine-treated animals in groups 1–3 (21±11%, 24±11%, and 26±7%, respectively) were smaller than those in the respective control groups (36±5%, 35±3%, and 35+3%; P<0.05). Compared with controls, the infarct size of the periphery of the fronto-parietal cortex decreased in nilvadipine-treated animals. The results indicate that nilvadipine decreases the size of infarction when administered up to 3 h after an ischemic insult. Thus, nilvadipine can be considered a potential therapeutic agent for acute focal cerebral ischemia, and may be clinically useful in stroke patients.

A Case of Pineocytoma Presenting with Symptoms like Normal Pressure Hydrocephalus

A pineocytoma in an old man, whose initial symptoms resembled a normal pressure hydrocephalus, is reported. This 67-year-old man gradually became uncommunicative and difficult to walk alone in three months. Just before visiting our clinic, his family also noticed his nocturnal urinary incontinence. CT scan on admission disclosed tumor in the posterior wall of the third ventricle, and subsequent hydrocephalus. This oval, isodense tumor was homogeneously enhanced after the injection of contrast medium on CT scan. The vertebral angiography showed a mass in the pineal region with no vascular staining. Ventricular drainage, the opening pressure of which was 100 mmH2O, could not offer cytological verification of the tumor. By the infratentorial supracerebellar approach, the tumor was successfully extirpated, and the post-operative course was uneventful. The microscopic study revealed the nature of this tumor to be well compatible with that of a pineocytoma.