The blood-brain barrier is continuously open for several weeks following transient focal cerebral ischemia.

The blood-brain barrier (BBB) is the principal regulator of blood-borne substance entry into the brain parenchyma. Therefore, BBB leakage, which leads to cerebral edema and influx of toxic substances, is common in pathological conditions such as cerebral ischemia, inflammation, trauma, and tumors. The leakage of BBB after ischemia-reperfusion injury has long been considered to be biphasic, although a considerable amount of discrepancies as for the timing of the second opening does exist among the studies. This led us to evaluate systematically and quantitatively the dynamics of BBB leakage in a rat model of 90-min ischemia-reperfusion, using gadolinium-enhanced (small molecule) magnetic resonance imaging and fluorescent dye Evans Blue (large molecule). BBB leakage was assessed at the following time points after reperfusion: 25 min, 2, 4, 6, 12, 18, 24, 36, 48, and 72 h, and 1, 2, 3, 4, and 5 weeks. We observed BBB leakage for both gadolinium and Evans Blue as early as 25 min after reperfusion. Thereafter, BBB remained open for up to 3 weeks for Evans Blue and up to 5 weeks for gadolinium. Our results show that BBB leakage after ischemia-reperfusion injury in the rat is continuous and long-lasting, without any closure up to several weeks. This is the first systematic and extensive study fully demonstrating BBB leakage dynamics following transient brain ischemia and the findings are of major clinical and experimental interest.

TIA model is attainable in Wistar rats by intraluminal occlusion of the MCA for 10min or shorter.

Transient ischemic attack (TIA) has received only little attention in the experimental research field. Recently, we introduced a TIA model for mice, and here we set similar principles for simulating this human condition in Wistar rats. In the model: 1) transient nature of the event is ensured, and 2) 24h after the event animals are free from any sensorimotor deficit and from any detectable lesion by magnetic resonance imaging (MRI). Animals experienced varying durations of ischemia (5, 10, 12.5, 15, 25, and 30min, n=6-8pergroup) by intraluminal middle cerebral artery occlusion (MCAO). Ischemia severity and reperfusion rates were controlled by cerebral blood flow measurements. Sensorimotor neurological evaluations and MRI at 24h differentiated between TIA and ischemic stroke. Hematoxylin and eosin staining and apoptotic cell counts revealed pathological correlates of the event. We found that already 12.5min of ischemia was long enough to induce ischemic stroke in Wistar rats. Ten min or shorter durations induced neither gross neurological deficits nor infarcts visible on MRI, but histologically caused selective neuronal necrosis. A separate group of animals with 10min of ischemia followed up to 1week after reperfusion remained free of infarction and any MRI signal change. Thus, 10min or shorter focal cerebral ischemia induced by intraluminal MCAO in Wistar rats provides a clinically relevant TIA the rat. This model is useful for studying molecular correlates of TIA.

The location of the obturator nerve: a three-dimensional description of the obturator canal.

Satisfactory analgesia cannot be achieved in every obturator nerve block. To attempt to improve the success rate of obturator nerve block, this study describes the detailed anatomy of the obturator region and canal. Eleven (5 female and 6 male) cadavers, totally 22 sides were dissected. Anatomical positions of the structures entering and leaving the canal were defined. The position of the obturator nerve and its branches and their relation with the obturator artery, vein, and with the internal iliac and femoral veins were investigated. A mould of the canal and a model were created. Detailed measurements were performed on the cadavers and models. The obturator canal was in the shape of a funnel compressed from superior to inferior, with anterior and posterior openings. At the entrance of the canal, the nerve lay superiorly; the artery was in the middle, and the vein lay inferiorly. The obturator nerve ran close to the lateral wall of the obturator canal. The distance of lateral wall of obturator canal to the median plane was 41.4 +/- 1.1 mm. After leaving the canal, the nerve lay laterally while the anterior branch of the artery was medial. A venous plexus lay between the two structures. The presence of the branches of the obturator artery and vein alongside the obturator nerve may increase the risk of injury to these structures during anaesthetic procedures. The anterior division of the obturator nerve has a close relationship with these vessels. To provide complete analgesia, the obturator nerve should be blocked in the obturator canal or at its external orifice.

WITHDRAWN: Temporal and spatial expression patterns of laminins in ischemic adult rat brain.

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