[Correlation of vasospasm and intracranial metabolism under experimental subarachnoid hemorrhage--Part 1. In reference with the acid-base-balance of cerebral blood and cerebrospinal fluid].
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.
[Correlation of vasospasm and intracranial metabolism under experimental subarachnoid hemorrhage--Part 1. In reference with the acid-base-balance of cerebral blood and cerebrospinal fluid]. 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.