Takahashi S
No To Shinkei. 1978 Jul;30(7):777-87.
Cerebral vasospasm, cerebral metabolism and the acid-base-balance of blood and cerebrospinal fluid of dogs were studied during and after the experimental subarachnoid hemorrhage. Subarachnoid hemorrhage was induced by infusion of fresh blood into the basal cistern through a small sraniectomy in the base of the skull. Eighty adult mongrel dogs were used. Of these a complete recording was obtained in 32 cases under the constant controlled ventilation. The samples of the blood and cerebrospinal fluid (CSF) were obtained repeatedly at the inserted 1 to 3 hours from the Polyethylene tube inserted into the cisterna magna subarachnoid space, carotid artery and internal jugular vein. During these procedures, the luminal size of the intracranial basal artery was measured angiographically. Vasoconstriction of the cerebral arteries in response to experimental subarachnoid hemorrhage had a biphasic course, an acute phase (the vasoconstrictive phenomenon which lasts less than 6 hours) and chronic phase (the revasoconstriction occured and continued more than 24 hours after the hemorrhage). The former was named "Released Group" which consists of 16 dogs and the later was named "Prolonged Group" which consists of 20 dogs. In both group, pH and bicarbonate ion concentration of CSF were found to be reduced by twenty percent of the normal value on the aveaage about three hours after subarachnoid hemorrage, apparently reflecting occurence of early cerebral vasospasm. Remarkable metabolic acidosis was seen in CSF of the prolonged group as compared with in cerebral blood. The occurrence of A-V shunt was suggested in the cerebral circulation from the blood gas findings. The experimental results indicates that prolonged cerebral vasospams phenomenon causes persistent hypoxic state in the cerebral tissue. However, cellular metabolism of cerebral tissue will be probably maintained by oxygen supply necessary to cellular respiration through the blood-brain barrier from the cerebrospinal fluid.
在实验性蛛网膜下腔出血期间及之后,对犬的脑血管痉挛、脑代谢以及血液和脑脊液的酸碱平衡进行了研究。通过在颅骨底部进行小的硬脑膜切除术,将新鲜血液注入基底池来诱导蛛网膜下腔出血。使用了80只成年杂种犬。其中32例在持续控制通气下获得了完整记录。从插入枕大池蛛网膜下腔、颈动脉和颈内静脉的聚乙烯管中,在插入后1至3小时反复采集血液和脑脊液(CSF)样本。在这些操作过程中,通过血管造影测量颅内基底动脉的管腔大小。实验性蛛网膜下腔出血后,脑动脉的血管收缩有双相过程,急性期(血管收缩现象持续少于6小时)和慢性期(出血后24小时以上发生并持续的再收缩)。前者称为“释放组”,由16只犬组成,后者称为“延长组”,由20只犬组成。在两组中,蛛网膜下腔出血后约3小时,脑脊液的pH值和碳酸氢根离子浓度平均降低至正常值的20%,这显然反映了早期脑血管痉挛的发生。与脑血相比,延长组脑脊液中出现明显的代谢性酸中毒。从血气结果提示脑循环中存在动静脉分流。实验结果表明,延长的脑血管痉挛现象导致脑组织持续缺氧状态。然而,脑组织的细胞代谢可能通过脑脊液经血脑屏障为细胞呼吸提供所需的氧气供应来维持。