The likelihood of rupture of unruptured intracranial aneurysms that were less than 10 mm in diameter was exceedingly low among patients in group 1 and was substantially higher among those in group 2. The risk of morbidity and mortality related to surgery greatly exceeded the 7.5-year risk of rupture among patients in group 1 with unruptured intracranial aneurysms smaller than 10 mm in diameter.

Summary: The hypothesis was tested that hyperbaric oxygen therapy (HBO) reduced brain infarction by preventing apoptotic death in ischemic cortex in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) and subsequently were exposed to HBO (2.5 atmospheres absolute) for 2 h, at 6 h after reperfusion. Rats were killed and brain samples were collected at 24, 48, 72 h, and 7 days after reperfusion. Neurologic deficits, infarction area, and apoptotic changes were evaluated by clinical scores, 2,3,7-triphenyltetrazolium chloride staining, caspase-3 expression, DNA fragmentation assay, and terminal deoxynucleotidyl transferase-mediated 2Ј-deoxyuridine 5Ј-triphosphate-biotin nick end labeling (TUNEL)-hematoxylin and eosin (H&E) costaining. In MCAO/R without HBO treatment animals, DNA fragmentation was observed in injured cortex at 24, 48, and 72 h but not in samples at 7 days after reperfusion. Double labeling of brain slides with NeuN and caspase-3 demonstrated neurons in the injured cortex labeled with caspase-3. TUNEL+H&E costaining revealed morphologic apoptotic changes at 24, 48, and 72 h after reperfusion. Hyperbaric oxygen therapy abolished DNA fragmentation and reduced the number of TUNEL-positive cells. Hyperbaric oxygen therapy reduced infarct area and improved neurologic scores at 7 days after reperfusion. One of the molecular mechanisms of HBO-induced brain protection is to prevent apoptosis, and this effect of HBO might preserve more brain tissues and promote neurologic functional recovery. Key Words: Cerebral ischemia-HBO-Apoptosis-Infarction.Cell death, either necrosis or apoptosis, occurred in the brain tissues during the first few days after cerebral ischemia (Johnson et al., 1995;Rink et al., 1995). Necrotic cell death is characterized by cellular swelling, nuclear pyknosis with karyorrhexis, and cytoplasmic eosinophilia (Searle et al., 1982;Dure et al., 1995). Apoptosis is characterized by morphologic and biochemical features, including cell shrinkage, formation of apoptotic bodies, and extensive internucleosomal fragmentation (Johnson Jr et al., 1995, 1996. Cerebral hypoxia/ischemia produces a cascade of interconnected pathologic processes, including changes in intracellular Ca 2+ , excitatory amino acid, oxidative stress, and inflammatory response, and leads to apoptosis in the ischemic penumbra (Okamoto et al., 1993;Johnson Jr et al., 1995;Rink et al., 1995;Leker et al., 1999). Prevention of apoptosis becomes a therapeutic strategy to preserve brain tissues and promote functional recovery (Graham and Chen, 2001).Hyperbaric oxygen therapy (HBO) is a potent mean to increase the amount of oxygen dissolved in blood plasma and thereby delivered to the ischemic brain. However, HBO is not currently used in acute stroke management, partially due to the insufficient information of its molecular mechanisms (Kawamura et al., 1990;Anderson et al., 1991;Mink and Dutka, 1995;Nighoghossian and Trouillas, 1997;Chuba et al., 1997;Ro...

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Background and Purpose-Endothelin-1 (ET-1) is suggested to be a major cause of cerebral vasospasm after subarachnoid hemorrhage. However, the mechanism of ET-1-induced contraction in cerebral arteries remains unclear. This study was undertaken to demonstrate the possible role of protein tyrosine kinase (PTK), mitogen-activated protein kinase (MAPK), and protein kinase C (PKC) in ET-1-induced contraction. Methods-PD-98059, damnacanthal, wortmannin, AG-490, genistein, calphostin C, and staurosporine were used to inhibit, or relax, the ET-1-induced contraction of basilar artery, studied with an isometric tension system. Immunoprecipitation of MAPK in ET-1-stimultated rings of basilar artery without or with the above inhibitors was studied with Western blot.