In the previous papers, changes in CO
2 tension and H
+ concentration in the cerebrospinal fluid have been investigated with interest since those are known as stimulants on the central chemoreceptor. It has been thought that the changes in acid-base and gas tensions in the cerebrospinal fluid may be resulted from the alterations in those of arterial blood and the brain in relation to gas diffusion across the blood-brain barrier and blood-CSF barrier. In the present experiments, an investigation has been carried out to clarify the relationship between the changes of pH and gas composition of CSF and those of arterial blood and cerebral venous blood induced by inhalation of different gas mixtures.
Ten dogs (8-12kg) were anesthetized with chloralose (80mg/kg) one hour after recieving morphine (1mg/kg). Arterial blood samples were taken from the femoral artery, cerebral venous blood from the dorsal sagittal sinus and CSF from the cisterna magna. In the first series of the experiments, following a preliminary period of spontaneous breathing of room air, five dogs were made to breath a gas mixture containing 24%O
2, 10%CO
2 and 60%N
2 for twelve minutes, and then the samples were taken simultaneously at intervals of two minutes during the CO
2 inhalation. The sampling was continued until a recovery from the effect of CO
2 breathing had been reached after returned to room air breathing. In the second series of the experiments, five dogs were made to rebreath 100 liters of high O
2 mixture (40%O
2+60%N
2) and the samples were drown at intervals of ten minutes for two hours. All samples were taken with 0.1m
l heparinized glass microcapillary and analysed by the electrode method (IL-113, type S-1).
In both series of the experiment, similar patterns of alterations in CSF P
CO2, and in the cerebral venous blood P
CO2, were obtained. However, the CSF P
CO2, never equilibrated with the cerebral venous blood P
CO2. within the experimental period. These findings lead us to suspect that the alteration in CSF P
CO2, may be related to the metabolism of brain. There was some-what a similarity of the patterns of alterations in CSF P
O2 and cerebral venous blood P
O2 in the first series. However in the second series, CSF P
O2 increased following an abrupt rise in arterial P
O2 and kept that level in parallel to the arterial P
O2 throughout the high O
2 breathing, but the cereral venous P
O2 did not rise. One hour later from the beginning of the high O
2 inhalation, cerebral venous blood P
O2 began to rise gradually, probably in response to the increased cerebral blood flow, but the CSF P
O2 remained in the some range as it was, regardless of the increased cerebral venous P
O2.
From these findings, it appears that there are some differences in mechanisms of regulation for the cerebrospinal fluid P
CO2 and
O2. Alteration of pH in CSF also appeared to be similar to the change of cerebral venous blood pH, but further investigations are required.
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