1977 Volume 17pt2 Issue 6 Pages 507-515
An intense intracranial hypertension plays a most important role for syndrome following subarachnoid hemorrhage. This work was made to characterize intracranial hypertension and identify the responsible components of blood. Continuous recording of ICP was made in dogs after intracisternal infusion of some amount of fresh blood, incubated blood, oxyhemoglobin, methemoglobin, heroin and bilirubin.
1. Infusion of whole blood in amount of 10 ml or red blood cells equivalent to 10 ml of whole blood produced increase of ICP 200 to 300 mm H2O which started 9 to 12 hours later and continued for about 8 to 16 hours. Infusion of RBC ghost produced a minor rise of ICP for a short period. Infusion of plasma did not produce a noticeable intracranial hypertension. Intense intracranial hypertension which reached the level of 600 to 1, 000mm H2O was found after infusion of incubated blood, oxyhemoglobin, heroin and bilirubin.
2. Spike-like elevations (pressure waves) were superimposed on elevated basal pressure. The pressure waves could be classified into three types. The first type of pressure waves were with durations of 30 seconds to 3 minutes and were accompanied with simultaneous decreases in systemic blood pressure (SBP). They were observed in the first or mild stage of increased ICP. The second type of pressure waves were with durations 10 to 30 seconds, and they accompained marked increases in SBP. The third type of pressure waves belonged to the first one as far as the durations are concerned, i.e. 30 to 40 seconds, but they were accompanied with little changes in SBP.
3. The histological examination revealed that intracisternal infusions of blood components invariably produced leptomeningitis. The changes increased in the following order; whole blood, incubated blood, hemoglobin and heme component of hemoglobin. Cell infiltration was most noticeable in the base of the brain. An irregular arrangement of ependymal layer and perivascular cell infiltration were also found in the floor of the fourth ventricle.
4. It is concluded that an intense rise in ICP in acute stage of subarachnoid hemorrhage is produced by instability or paralysis of cerebral vasomotor activity due to brain stem dysfunction, although brain edema and the accumulation of CSF by meningeal reaction are also responsible.
