Exacerbation of cerebral injury in mice that express the P-selectin gene: identification of P-selectin blockade as a new target for the treatment of stroke.

There is currently a stark therapeutic void in the treatment of evolving stroke. Although P-selectin is rapidly expressed by hypoxic endothelial cells in vitro, the functional significance of P-selectin expression in stroke remains unexplored. In order to identify the pathophysiological consequences of P-selectin expression and to identify P-selectin blockade as a potential new approach for the treatment of stroke, experiments were performed using a murine model of focal cerebral ischemia and reperfusion.

Use of carotid ultrasound as a preoperative assessment of extracranial carotid artery blood flow and vascular anatomy.

Carotid ultrasound evaluation as a preoperative assessment of internal carotid artery blood flow and anatomic stenosis is efficacious and safe. The technique, although operator dependent, is both inexpensive and easily repeated with essentially no risk to the patient. Furthermore, when combined with MR angiography, it usually can obviate the need for angiography in most endarterectomy candidates.

Short-term perioperative anticonvulsant prophylaxis for the surgical treatment of low-risk patients with intracranial aneurysms.

The long-term use of anticonvulsant medication to prevent postoperative seizures in patients with aneurysms has been accepted medical practice for many years. The low incidence of seizures in more recent aneurysm series makes it appropriate to re-evaluate the use of prophylactic anticonvulsants to prevent postoperative epilepsy, especially in patients at low risk of seizure disorders. On the basis of preoperative presentation, we categorized 387 of the 420 craniotomies for aneurysms over a 4-year period to be at low risk of seizure.

Mild hypothermia and MK-801 have similar but not additive degrees of cerebroprotection in the rat permanent focal ischemia model.

Although not the sole factor, glutamate-mediated excitotoxicity is accepted as a major mechanism of ischemic neuronal damage. MK-801 and mild hypothermia, two cerebroprotective modalities, which have been documented to alter glutamatergic action, were tested in the rat middle cerebral artery occlusion (MCAO) model simulating permanent focal ischemia. We administered normothermic (37 degrees C) animals with either MK-801 (1.

Hypothermic protection following middle cerebral artery occlusion in the rat.

The effects of deep hypothermia on ischemic neuronal injury were examined using a permanent middle cerebral artery occlusion model in the rat. Animals were maintained at temporalis temperatures of either 24 degrees C or 36 degrees C and killed 6 hours after arterial occlusion. Normothermic rats displayed an average infarct volume of 25.