Abstract
It is widely accepted that the autoregulation and chemical regulation of cerebral blood flow are impaired in the acute stage of stroke and that various vasoactive substances are also released in this stage. Therefore, the present study was aimed at investigating whether central endogenous prostaglandins, the potent vasoactive substances, contributed to the regulations of cerebral circulation in the acute stroke.
The study was carried out in 36 patients with acute stroke (within 7 days after the onset; mean ± S.D.=3.6 ± 1.9 days), ranging in age from 45 to 83 (64.8 ± 9.8 yr.) including 17 occlusive and 19 hemorrhagic lesions. Blood samples were taken from the brachial artery and from the internal jugular vein at the level of jugular bulb. Blood gases and pH were measured by using the Corning 168 pH/blood gas analyzer. Cerebral blood flow was estimated by means of the method of arterio-venous oxygen difference. Changes in cerebral perfusion pressure (CPP) were induced by head-up tilt method and changes in PaCO2 were induced by 7% CO2 + air inhalation. The cerebral vasomotor responses to changes in perfusion pressure and to changes in PaCO2 were quantitatively estimated by dysautoregulation index (|ΔCBF/ΔCPP|; %/mmHg) and chemical index (|ΔCBF/ΔPaCO2|; %/mmHg). Prostaglandins (PG E, PG F2α & 6-ketoPG F1α, the stable metabolite of PG I2) and catecholamines during the steady stage were measured by means of radioimmunoassay and high performance liquid chromatography methods.
The results were summarized as follows :
1) The levels of arterial and cerebral venous PG E had significant correlations with the dysautoregulation index, the degree of cerebral vasomotor response to changes in perfusion pressure (r=0.521·p<0.01, r=0.479·p<0.05, respectively).
2) No significant correlations were obtained between the level of arterial PG E and the chemical index, but the level of cerebral venous PG E had a significant reverse correlation with the chemical index (r=-0.536, p<0.05).
3) The levels of arterial and cerebral venous PG F2α did not have any significant correlation with either the dysautoregulation index or the chemical index.
4) No significant correlations were observed between the level of arterial 6-keto-PG F1α and the dysautoregulation index, but the level of cerebral venous 6-keto-PG F1α had a significant correlation with the dysautoregulation index. (r=0.688, p<0.05).
5) The level of arterial 6-keto-PG F1α had a significant reverse correlation with the chemical index (r=-0.957, p<0.01), but no significant correlations were observed between the level of cerebral venous 6-keto-PG F1α and the chemical index.
6) The levels of arterial and cerebral venous noradrenaline did not show any significant correlation with dysautoregulation index, chemical index or the level of PG E.
From the above data, it is suggested that the central endogenous PG E and PG I2 play important roles in the regulations of cerebral blood flow, cerebral vasomotor responses to changes in perfusion pressure and PaCO2.
