We here investigated endothelial nitric oxide synthase (eNOS) expression after 10 minutes of forebrain ischemia. Real-time polymerase chain reaction, immunoblots and immunohistochemical studies revealed up-regulation of eNOS expression in the hippocampal CA1 subfield of gerbil. Immunoreactivity of eNOS significantly increased in endothelium but neither in neurons nor astrocytes after 6 to 168 hours of reperfusion. An increased Akt activity preceded the postischemic eNOS up-regulation. Intracerebroventricular injection (i.c.v.) of wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI-3K), significantly inhibited the increases in both eNOS mRNA and its protein with concomitant inhibition of Akt activation. The significant increase in the eNOS expression was also evident following preconditioning 2-minute ischemia. Both eNOS up-regulation and acquisition of ischemic tolerance observed at 3 days after preconditioning ischemia were significantly inhibited by pretreatment with wortmannin. Administration (i.c.v.) of N-nitro-L-arginine methyl ester, but not 7-nitroindazole, 30 minutes prior to lethal 10-minute ischemia, significantly abolished the acquired tolerance. Intraperitoneal injections of aminoguanidine at immediately after, 24, and 48 hours after preconditioning had no effects on the tolerance. These results suggest that eNOS expression is up-regulated in the endothelium via PI-3K pathways after transient forebrain ischemia, and that preconditioning-induced eNOS expression plays an important role in neuroprotection in the ischemic tolerance.

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Although three-dimensional computed tomographic angiography (3D-CTA) is less complicated and time-consuming than conventional cerebral angiography (CCA) and represents a reliable alternative for evaluating cerebral aneurysms, some patients experience aneurysmal rerupture during 3D-CTA. Two women, 79 and 71 years old, who presented with severe subarachnoid hemorrhage (SAH) underwent 3D-CTA within 3 h after SAH onset. Their images clearly indicated extravasation from their aneurysms. Neither patient recovered from deep coma, and both died within 2 days. We reviewed the literature with special reference to the condition of SAH patients at admission and the interval between SAH onset and 3D-CTA, and discuss serious complications of 3D-CTA study. Although aneurysmal rerupture may reflect the natural course, rerupture during 3D-CTA, especially in SAH patients who are in poor clinical condition during the acute stage, should be recognized as a potentially fatal complication. Their blood pressure must be strictly controlled and factors such as their clinical condition and the interval from the ictus must be considered.

Cervical myelopathy at the C4-5 level is a potential risk for motor dominant C5 paralysis. Although it is merely a speculation, when C5 radiculopathy occurs after laminoplasty, C5 paralysis becomes clinically apparent because the deltoid muscle gets predominantly innervated by C5 root due to intramedullary spinal cord damage on the C6 segment in C4-5 myelopathy before surgery. It may represent the high signal intensity area on T2-weighted MRI at the C4-5 level.

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