In a retrospective study, pathological tissue enhancement was found in nearly two fifths of patients with acute SAH on contrast-enhanced cranial computed tomography. By means of absorption measurements with the region of interest technique over the basal ganglia, it was proved indirectly that pathological tissue enhancement should be brought about not only by hyperaemia, i.e., a blood volume increase, but also by extravasation of the contrast material, i.e., blood-brain barrier (BBB) disruption. A similar conclusion was drawn from the retrospective isotope brain scintigraphy study. It was further established that, although the pathological contrast enhancement was most obvious in the cortex, and particularly in the neighbourhood of the subarachnoid spaces, the phenomenon is probably widespread throughout the brain. Patients with abnormal enhancement are likely to be in less favourable clinical grades, have a high incidence of marked or diffuse spasm, have a poorer outcome independent of surgical or conservative treatment, and develop cerebral infarction more frequently. Systemic arterial hypertension was associated with an increased incidence of abnormal enhancement. Pathological tissue contrast enhancement or isotope accumulation in the first few days of SAH may serve as prognostic signs indicative of the late development of vasospasm and ischaemia. As ischaemic disruption of the capillary system is not prominent in the initial days following any stroke, vasoactive substances arising from the breakdown of the blood clot should play important part in the BBB damage in the acute stage of SAH. The "cortical SAH" model developed in the animal experiments ensured a constant subarachnoid blood volume with minimal local brain damage. The intracranial pressure and mean arterial blood pressure did not change significantly, and perfusion defects did not arise. Thus, this model proved suitable for studying the influence on the BBB of vasoactive blood breakdown products (responsible for arterial spasm) without the accompanying effects of pathological conditions such as raised intracranial pressure, systemic hypertension, non-reflow phenomena, which also disrupt the BBB. Measurements on the water, electrolyte, albumin contents of brain tissue, as well as the immunohistochemical localization of albumin, clearly indicated that the brain oedema developing at the acute stage of experimental SAH could be classified as having a primary vasogenic component in addition to the cytotoxic component. This increased capillary permeability was found to be brought about by opening of tight junctions and pinocytosis in the endothelial cells. The pathological capillary permeabilit

Brain water accumulation (1.2%) with an accompanying increase in the sodium content was observed in Wistar rats as early as 1 hour after experimental subarachnoid hemorrhage (SAH). After 6 and 24 hours, the water content was 1.3 and 1.4%, respectively, higher than that of control animals. In contrast, in Brattleboro diabetes insipidus rats the content of brain water and electrolytes had not changed significantly 1 hour after the administration of blood into the subarachnoid space. Increased brain water and sodium and a normal potassium content, indicative of a vasogenic type of brain edema, were seen at 6 hours after SAH. In these animals, known to be devoid of vasopressin, the increase in brain water 24 hours after SAH was 2.6%, compared with 1.4% for Wistar rats with SAH. It is suggested that the lack of vasopressin could alter the course of brain edema formation after experimental SAH in Brattleboro diabetes insipidus rats. It is hypothesized that vasopressin, by regulating the water permeability of the brain capillaries, the choroid plexus, and the cerebrospinal fluid absorption structures, plays an important role in controlling the brain fluid and electrolyte balance during the course of SAH.

The intraventricular administration of vasopressin or DDAVP (desmopressin acetate) increased the brain water content from 78.2% to 79.2-79.5%. This was achieved without an accompanying water load. The applied water load alone did not increase the water content of the brain. There was no significant difference in the water content of the brain between animals treated with intraventricular vasopressin and intravenous water load and animals receiving only intraventricular vasopressin. The water content of the olfactory bulbs of the control animals was 3.8% higher than that of the hemispheres. While the water content of the hemispheres increased by 1.3%, that of the olfactory bulbs did so by 1.7% subsequent to the intraventricular administration of DDAVP. Measurement of the brain electrolyte content was not conclusive as to the mechanism of water permeability changes. The possible mechanism is discussed. Although no tissue or cerebrospinal fluid concentrations of vasopressin enabling comparison with clinical pathological conditions have been measured, it is suggested that increased secretion of vasopressin into the cerebrospinal fluid in conditions such as subarachnoid hemorrhage or intracranial hypertension of various origins might play a role in edema formation.

No abstract

Radioisotope cisternography was performed and the erythrocyte and hemoglobin contents of the cerebrospinal fluid (CSF) were determined within the first 4 days after subarachnoid hemorrhage in 42 patients. The clinical condition of the patients was related to the severity of the CSF circulation disturbances. Thirty-five patients had some degree of disturbance of CSF flow, and only 2 of the 42 patients had normal flow. In 5 cases the cisternograms were inconclusive. The severity of CSF circulation disturbances correlated well with clinical condition. No relationship was found between the number of erythrocytes in the CSF and the development of CSF circulation disturbances. The CSF erythrocyte content did not correlate with the clinical condition. It is suggested that flow disturbances of the CSF during the acute stage of subarachnoid hemorrhage might play an important role in the pathomechanism of the disease.