Ment L R, Stewart W B, Duncan C C, Cole J, Pitt B R
J Neurosurg. 1985 Dec;63(6):899-904. doi: 10.3171/jns.1985.63.6.0899.
Perinatal cerebral infarction is a not uncommon finding in newborn babies surviving intensive care. Asphyxia, with its attendant hypotension, is the most common cause of this problem and may result in neuropathological changes in the periventricular white matter. Previous studies have demonstrated uncoupling of cerebral blood flow and metabolism in the periventricular white matter regions of newborn beagle pups exposed to hemorrhagic hypotension. This work examines the effects of hypotension on serum and regional cerebral prostaglandin levels in the newborn beagle pup. The animals were anesthetized, tracheostomized, and paralyzed. Pups were randomly assigned to two groups: one was subjected to hemorrhagic hypotension and the other received no insult. Hypotension was induced by slow venous hemorrhage calculated to maintain a mean arterial blood pressure at 20 to 30 mm Hg. Serum prostaglandin determinations were made immediately before and 15 minutes after random assignment to hypotension or control groups. In addition, regional cerebral prostaglandin determinations were performed 15 minutes after randomization. Analysis of the serum prostaglandin data revealed that there were no significant differences in the values for thromboxane B2 or 6-keto-prostaglandin (PG) F1 alpha, which are the stable breakdown products of thromboxane A2 and prostacyclin, respectively. Prostaglandin E2 levels increased in response to hemorrhagic hypotension insult. Regional cerebral prostaglandin determinations demonstrated decreases in thromboxane B2 and 6-keto-PGF1 alpha in both gray and white matter. Although gray matter PGE2 was increased in pups exposed to hemorrhagic hypotension, this increase was not found in the periventricular white matter of injured pups. This regional difference in PGE2 synthesis in response to insult may explain the periventricular white matter neuropathological changes attributed to it.
围产期脑梗死在重症监护下存活的新生儿中并不少见。窒息及其伴随的低血压是导致这一问题的最常见原因，可能会导致脑室周围白质发生神经病理学改变。先前的研究表明，暴露于出血性低血压的新生比格幼犬脑室周围白质区域的脑血流与代谢出现解偶联。这项研究探讨了低血压对新生比格幼犬血清及局部脑前列腺素水平的影响。动物被麻醉、气管切开并麻痹。幼犬被随机分为两组：一组遭受出血性低血压，另一组未受损伤。通过缓慢静脉放血诱导低血压，使平均动脉血压维持在20至30毫米汞柱。在随机分组进入低血压组或对照组之前及之后15分钟立即测定血清前列腺素。此外，在随机分组后15分钟进行局部脑前列腺素测定。血清前列腺素数据分析显示，血栓素B2或6 - 酮 - 前列腺素（PG）F1α（分别是血栓素A2和前列环素的稳定降解产物）的值没有显著差异。前列腺素E2水平因出血性低血压损伤而升高。局部脑前列腺素测定表明，灰质和白质中的血栓素B2和6 - 酮 - PGF1α均降低。虽然暴露于出血性低血压的幼犬灰质中PGE2升高，但在受伤幼犬的脑室周围白质中未发现这种升高。这种对损伤反应中PGE2合成的区域差异可能解释了与之相关的脑室周围白质神经病理学改变。
