Effects of experimental ischemia on electrolytes of cortical cerebrospinal fluid and on brain water.
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Biomedical subjects
Publications and source records attributed to C R West.
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A prospective 12-month survey in 272 United Kingdom hospitals was performed and data are presented on the incidence of adverse reactions following intravenous urography, contrast CT scanning, and intravenous cholangiography. Minor and intermediate reactions are commonest in young adults, but severe and fatal reactions predominate in the older age group. There is an increased risk of severe reactions in patients with a history of allergy or previous reaction to contrast media and in patients with heart disease. The risk of severe reaction is also increased in certain ethnic groups. There appears to be an association between the incidence of severe reactions and contrast medium dose. Etiology, prevention and treatment of reactions are briefly discussed.
Sixty-one patients of a population of 343 with cerebral arteriovenous malformations (AVMs) were diagnosed with seizures. Their AVMs were larger (p less than 0.02) and more frequently superficial (p less than 0.05) as compared with the AVMs of patients who were diagnosed with haemorrhage. The factors influencing the development of denovo seizures in patients with diagnosed AVMs were surgical treatment, a presentation with haemorrhage, and age at diagnosis.
Selective embolization of the internal carotid artery bifurcation (ICA bifurcation) was performed in monkeys (Macaca mulatta) to study acute regional cerebral ischemia in the middle cerebral artery (MCA) territory with minimum surgical intervention in the neck under sedated conditions. The anthropomorphic similarity in angio-anatomy of the carotid system of monkeys and the use of silastic spheres, as artificial emboli, of the critical diameter of 1.2 to 1.4 mm resulted in the overall success rate of 87% in localizing the site of embolization to the ICA bifurcation, producing ischemia in the whole middle cerebral artery territory. All the animals with ICA-bifurcation embolization had contralateral deep motor weakness and conjugate eye deviation with nystagmus toward the site of embolization. Simultaneous EEG recording showed flattening of the basic background activities over the affected MCA area and cerebral arteriograms showed definite retrograde filling of the proximally occluded MCA. Clinical recovery was observed in a few animals within two to five hours of embolization. Gross ischemic swelling in the affected MCA territory, particularly in the gray matter, became obvious in six of eight animals which were exposed to four to five hours of ischemia. The angio-anatomical study of the carotid system of this experimental animal as a background for this MCA stroke model confirmed the previous observations of other investigators that the extremely abundant leptomeningeal anastomoses would be one of the major factors leading to the variability in the clinicopathological pictures seen in the models of proximal MCA occlusion. In addition, the pre-parenchymal anastomoses in the base of brain between the medial striate arteries from the proximal anterior cerebral (ACA) and lateral lenticulostriate arteries from the MCA were observed and described as a possible functional collateral to the basal ganglia in case of proximal MCA occlusion.
Acute regional cerebral ischemia was produced in the middle cerebral artery (MCA) territory in monkeys (Macaca mulatta) by selective embolization of the internal carotid (ICA) bifurcation with minimum surgical intervention in the neck under sedated conditions. Two of five hours after embolization, brain water (measurement of dry weight) and tissue concentration of sodium and potassium were determined in the tissues of the sylvian cortex, putamen and subcortical white matter in the affected MCA territory. As early as three hours, initial increase in brain water was detected in the samples of the putament without noticeable change in tissue electrolytes in two of three animals. Gross ischemic swelling of the gray matter, in both the sylvian cortex and putamen, became obvious in six of eight animals after four to five hours. This swollen gray matter showed marked increase in brain water (up to 36% swelling), increase in tissue sodium (up to 100% of the control value), and decrease in tissue potassium (down to 55%). On the other hand, edema in the white matter, if present at all, was minimal without detectable change in tissue electrolytes and was always accompanied by much greater ( greater than two to seven times) edema in the gray matter. Thus, the gray matter edema, in both the deep subcortical structures and the cortex, appeared to play the major role in the development of hemispheric swelling of the brain which may begin within hours of the onset of the MCA stroke in monkeys. Microscopically, the swollen gray matter which showed more than 10% swelling with a definite shift of tissue sodium and potassium content appeared to be dead tissue. However, early edema in the gray matter which showed less than 10% swelling without detectable change in electrolytes might be caused by simple diffusion of water through the dysfunctional capillary wall or cell membrane with or without a permeability gradient between the intravascular cerebrospinal fluid and cerebral tissue compartment and might possibly be reversible.
Experimental regional cerebral ischemia was produced in the middle cerebral artery (MCA) territory in primates (M. mulatta) by macrosphere embolization. Determinations of percentage tissue dry weight and tissue sodium and potassium concentrations were obtained in samples from the ischemic and non-ischemic hemispheres at various time from 12 to 48 hours after the onset of cerebral ischemia. Samples from the cortex normally supplied by the occluded MCA showed maximal accumulation of edema fluid with fluxes in sodium and potassium in reciprocal directions at 12 hours and similar edematous changes in putamen at 24 hours after embolization By 48 hours after MCA occlusion and despite the presence of infarction, partial reversal was observed in the redistribution of water and electrolytes in these gray matter structures. In contrast to cerebral cortex and putamen, the adjacent subcortical white matter showed progressive increases in water content from 12 to 48 hours and definite increases in tissue sodium with decreases in potassium were not observed until 48 hours after MCA occlusion. This late severe white matter edema associated with cerebral infarction appears to be a major factor responsible for the hemispheric swelling observed at this state.
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