Experimental study of acute brain swelling under acute intracranial hypertension

Abstract

UNLABELLED There are many problems about the cause, pathophysiology and treatment of acute brain swelling under intracranial hypertension frequently encountered in the neurosurgical clinics. Generally, rapid increase of the cerebral vasoparesis caused by unknown etiology is thought to be the main cause of acute brain swelling under intracranial hypertension. Moreover, disturbance of the cerebral venous circulatory system is discussed recently by many authors. But, research from the point of systemic respiration and hemodynamics is necessary for resolving these problems. This experiment was designed to study the effects of respiration and hemodynamics on the cerebral vasoparesis. METHOD Using 22 adult dogs, acute intracranial hypertension was produced by epidural balloon inflation sustained at the level of 300 - 400 mmH2O. Simultaneously with measurement of intracranial pressure at the epidural space, superior sagittal sinus pressure, respirogram, systemic blood pressure (femoral artery), central venous pressure, common carotid blood flow, EKG and bipolar lead EEG were monitored continuously. The experimental group was divided by the respiratory loading into 5 groups as follows: control (6 cases), 10% CO2 hypercapnia (4 cases), 10% O2 hypoxia (4 cases), stenosis of airway (5 cases), 100% O2-controled respiration (3 cases). RESULTS AND CONCLUSIONS 1) Cerebral vasoparesis under acute intracranial hypertension took place earlier and showed more rapid progression in groups of stenosis of airway, hypercapnia and hypoxia than control group of spontaneous respiration in room air. No occurrence of cerebral vasoparesis was found out in a group of 100% O2 controlled respiration. It is proved that increased airway resistance or asphyxia, hypercapnia and hypoxia have strictly reference to the occurrence and progression of cerebral vasoparesis and for the prevention of cerebral vasoparesis, correct 100% O2 cont rolled respiration is effective. 2) From the hemodynamic change, the progression of rapid increase of cerebral blood volume with increase of blood volume in the superior sagitta sinus during cerebral vasoparesis under intracranial hypertension is presumed. It is suggested from the superior sagittal sinus pressure in various experimental groups that the site, reactivity and disturbed degree of the cerebral venous system are changed by the difference of respiratory or ventrilatory state and the cerebral venous circulatory disturbance has also reference to the occurrence of acute brain swelling. 3) During cerebral vasopareris under acute intracranial hypertension, remarkable supression of respiration, increased central venous pressure and increased common carotid blood flow were observed. It is concluded that the reaction of systemic hemodynamics following respiratory change effects on cerebral circulation markedly and they are being important factors to occurrence of acute brain swelling.