Experimental study of acute brain swelling under acute intracranial hypertension -Cerebral acid-base balance, gas metabolism and cerebral vasoparalysis-

Acid-base and gas parameters of CSF and sagittal sinus blood were examined to investigate the pathogenesis of acute brain swelling following elevation of ICP. Acute intracranial hypertension was produced in 26 adult mongrel dogs by means of unilateral epidural balloon inflation. ICP was monitored by a small epidural balloon connected to a pressure transducer and recorded by a strip recorder. Arterial blood pH, pCO(2) and pO(2) were measured every 10 min. during the course of the experiment, and were kept within normal range by artificial ventilation. Venous blood from the superior sagittal sinus and CSF from the cisterns magna were also sampled for pH, pCO(2) and pO(2) measurement. Cortical pH was measured using a microglass electrode placed on the brain surface. EEG was recorded in the bilateral frontoparietal cortical region. Changes of the ICP were recorded after 10% CO(2) inhalation in order to estimate CO(2) reactivity of the cerebral vessels under intracranial hypertension. Animals used were divided into two groups: Group A consisted of six animals in which the epidural balloon was inflated to 6 ml. resulting in increase of ICP to 50-100 mmHg. Group B included 20 animals in which the epidural balloon was inflated to the level where the so called Cushing's response was observed. In both groups, the balloon was abruptly deflated at the point where a desingated intracranial hypertension was obtained. In 9 out of 20 animals of Group B, ICP spontaneously increased again after deflation of the epidural balloon; this situation was called "acute brain swelling". In these animals with acute brain swelling, acid-base measurement revealed not only lowering of pH in cerebral venous blood, CSF and cerebral cortical surface, but also a significant increase in pCO(2) in both cerebral venous blood and CSF. Disappearance of CO(2) reactivity of cerebral vessels associated with isoelectric EEG was observed in these animals as well. On the other hand, acute brain swelling did not develop in the animals of Group A which did not lose CO(2) reactivity with EEG and remained normal. These animals showed no disorder of acid-base balance and gas metabolism in CSF and cerebral venous blood. In order to treat cerebral acidosis and hypercapnia in 9 animals which developed acute brain swelling, the alkalizing agent, tris hydroxy methyl amino methane (THAM) was administered and its beneficial effect on the acute brain swelling was examined. After drip infusion of 0.3 mole THAM (10 ml/kg), acidosis and hypercapnia of CSF and cerebral venous blood improved in 7 out of 9 animals. These results indicate that acute brain swelling following intracranial hypertension results from cerebral vasoparesis which is mainly caused by metabolic abnormalities such as cerebral acidosis and/or cerebral hypercapnia. Moreover it is suggested that THAM is an useful agent for combating acute brain swelling since it acts to restore cerebral vasomotor tone.