The CBF-PaCO₂ relationship curves in chronic cerebrovascular disease

Abstract

The purpose of the present study was to know the correlation between cerebrovascular CO₂ reactivity and the hypertensive organ changes in cases of cerebrovascular disease.
The subjects of the present study were 45 patients with cerebral infarction confirmed by CT scan and cerebral angiogram. Of 45 patients, 31 cases (Group N) had no occlusion in the major cerebral arteries, and the other 14 cases (Group M) had occlusions in the stem of the middle cerebral artery. Measurements of cerebrovascular CO₂ reactivity were made at least more than a month after the attack.
The cerebral blood flow (CBF) was determined by using the Argon inhalation method. The changes of CBF during hyperventilation, 3% CO₂, 5% CO₂ and 7% CO₂ inhalations, were estimated by using the method of cerebral arteriovenous oxygen difference. The individual CBF-PaCO₂ relationship curves of the patients were calculated by the following equations by Olesen et al.
In CBF=K·PaCO₂+A
The cerebrovascular CO₂ reactivity was represented as K value which was a slope index of the In CBF-PaCO₂ relationship curve.
The severities of hypertensive and arteriosclerotic involvements in organs were estimated according to the classification of hypertension severity (IKEDA et al, 1984).
Results were summarized as follows :
1) There was a strong negative correlation between K values and the scores of the hypertension severity in Group N (r=-0.86, p<0.001). Although, no significant correlation was seen in Group M.
2) There was negative correlation between K values and the cerebrovascular resistance (CVR) in Group N (r=-0.46, p<0.01).
From these observations, it was suggested that the decline of cerebrovascular CO₂ reactivity in Group N was reflected in the arteriolosclerotic chages due to sustained hypertension. Then, the cerebrovascular CO₂ reactivity in Group M might be influenced by pathophysiological factors, such as. the quality of the collateral circulation, the changes of vascular beds or vascular tones and so on, in addition to arteriolosclerotic change.
Moreover, we discussed a propriety to use the K value as an index of a cerebrovascular CO₂ reactivity rather than a conventional 5% CO₂ reactivity.