Experimental intracerebral hemorrhage has been shown to cause extensive cerebral ischemia. This study was performed to ascertain the time course of these changes and also to examine the type of brain damage that may occur under such circumstances. Halothane anesthesia was induced in rats, and 25 microliter autologous blood was injected into the caudate nucleus; the effects were studied with autoradiographic measurement of local cerebral blood flow and capillary permeability, and also by light microscopy and histochemical techniques. Blood flow returned to normal or to slightly increased levels within the first 3 hours, and ischemic levels of flow were found to persist only to a marginal degree beyond 10 minutes after the lesions were made. Capillary permeability was maximum during the first 30 minutes after the hemorrhage and diminished with time. Structural evidence of ischemic damage was localized to the cortex overlying the hemorrhage, but was not seen in the caudate nucleus. Nevertheless, histochemical investigation did reveal an area of disturbed enzyme function in the striatum. This finding of biochemical disturbance without structural evidence of ischemic damage reveals that there is an area around the hematoma that, although demonstrating disturbed function, does not show structural damage, and the milieu of this partially injured brain may be implicated in the delayed development of the ischemic brain damage that follows intracerebral hemorrhage in man.
A model of experimental intracerebral hemorrhage is described in which carefully controlled volumes of autologous blood were injected at arterial pressure into the caudate nucleus of the rat. A comparison of intracranial pressure changes and local cerebral blood flow (CBF) was made between three groups of rats, each receiving different injection volumes, and sham-operated control rats by monitoring intraventricular pressure and by obtaining quantitative autoradiographic measurements of CBF within 1 minute of the experimental hemorrhage. Cerebral blood flow was reduced both around the hematoma and in the surrounding brain. This change was strongly volume-dependent and was not accompanied by significant alterations in cerebral perfusion pressure. This finding suggests that the degree of ischemia at the time of an intracerebral bleed depends on the size of the lesion, and implicates local squeezing of the microcirculation by the hematoma, rather than a generalized alteration in perfusion pressure, as the cause of ischemia.
The authors have studied the effect of a low-dose (0.28 gm/kg) bolus infusion of mannitol on brain water in man. In eight patients with severe head injury, small pieces of subcortical white matter were taken at craniotomy both before and after infusion of mannitol. The tissue specific gravity was measured using a graduated specific-gravity column, and from it the brain water content was calculated. White matter specific gravity rose from a mean (+/- standard error of the mean) of 1.0325 +/- 0.0012 before mannitol infusion to 1.0352 +/- 0.0011 after mannitol administration, and the brain water content fell from a mean of 80.94% +/- 2.5% to 75.28% +/- 2.3%. The differences were significant (p less than 0.01). This study shows that, after head injury in man, mannitol increases the white matter specific gravity and probably does so by reducing brain water.
In patients with intracerebral haematoma, ischaemic damage and final outcome are often more serious than the size of the lesion would suggest. The aetiology of the ischaemia in relation to space-occupying effects or specific factors present in blood is unclear. In a rat model of an intracerebral space-occupying lesion, the pathophysiological effects of a haematoma were compared with those of an equal volume of inert fluid (mock cerebrospinal fluid [CSF] or silicone oil). Cerebral blood flow was measured at 1 min by 14C iodoantipyrine autoradiography, and ischaemic cell damage was assessed by light microscopy at 4 h. In all animals, cerebral blood flow was reduced immediately adjacent to the lesion. In the group with a haematoma, blood flow was reduced (p less than 0.001) over a greater radius and also in the ipsilateral frontal and parietal cortex. Ischaemic damage was seen in animals lesioned with blood or oil of blood viscosity, but not in animals with CSF lesions. These data suggest that both tissue pressure and vasoactive substances are components of the immediate reduction in blood flow following intracranial haemorrhage. Tissue pressure may be the more important factor in later ischaemic neuronal damage.
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