{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,9,8]],"date-time":"2024-09-08T10:15:39Z","timestamp":1725790539759},"reference-count":30,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1993,5]]},"abstract":"<jats:p content-type=\"fine-print\">\u2713 To investigate the pathogenetic significance of metabolic failure observed in spastic cerebral arteries after subarachnoid hemorrhage (SAH), the temporal profile of alterations in the arterial content of high-energy phosphates was studied. A canine model of double hemorrhage was used. Constriction of the basilar artery was measured angiographically on Days 3, 5, 7, and 14 after SAH in separate groups of animals. Adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), guanosine triphosphate (GTP), guanosine diphosphate, creatine phosphate (CrP), and creatine (Cr) levels in the arteries were assayed using high-performance liquid chromatography. A time-dependent development of angiographic spasm was confirmed. A mild vasospasm was seen in the group studied 3 days after SAH, progressed in the Day 5 group, remained comparably severe in the Day 7 group, and resolved partially in the Day 14 group. The content of high-energy phosphates (ATP, GTP, and CrP) declined rapidly over the course of the study, and a significant reduction in ATP, GTP, and CrP was observed in the Day 3 group. Levels of ATP and CrP decreased further in the Day 5 and 7 groups. The decrement in GTP was completed in the early phase; a significant reduction took place in the Day 3 group, with no progression thereafter and no recovery though Day 14. Total adenylate (ATP + ADP + AMP) and total creatine (Cr + CrP) content diminished markedly over the course of the study. These results indicate that metabolic failure and trophic disturbance in the cerebral artery occurs with a rapid onset following SAH and progresses in close association with the development of vasospasm, suggesting a significant causal relationship with the pathogenesis.<\/jats:p>","DOI":"10.3171\/jns.1993.78.5.0807","type":"journal-article","created":{"date-parts":[[2009,5,27]],"date-time":"2009-05-27T15:03:05Z","timestamp":1243436585000},"page":"807-812","source":"Crossref","is-referenced-by-count":25,"title":["Temporal profile and significance of metabolic failure and trophic changes in the canine cerebral arteries during chronic vasospasm after subarachnoid hemorrhage"],"prefix":"10.3171","volume":"78","author":[{"given":"Yuhei","family":"Yoshimoto","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Phyo","family":"Kim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomio","family":"Sasaki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kintomo","family":"Takakura","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1754","reference":[{"key":"b1","series-title":"Am J Physiol","first-page":"324","article-title":"Mechanics of guinea pig taenia coli smooth muscle during anoxia and rigor.","volume":"229","author":"Bose","year":"1975"},{"key":"b2","series-title":"Am J Physiol","first-page":"1509","article-title":"Rigor and resistance to stretch in vertebrate smooth muscle.","volume":"231","author":"Butler","year":"1976"},{"key":"b3","series-title":"J Neurosurg","first-page":"925","article-title":"Prevention of chronic experimental cerebral vasospasm with ibuprofen and high-dose methylprednisolone.","volume":"59","author":"Chyatte","year":"1983"},{"key":"b4","series-title":"J Neurosurg","first-page":"44","article-title":"Intracranial vessels lack vasa vasorum.","volume":"61","author":"Clower","year":"1984"},{"key":"b5","series-title":"J Neurosurg","first-page":"49","article-title":"Sequential changes of vascular ultrastructure in experimental cerebral vasospasm. 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