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F J Schuier

Publications and source records attributed to F J Schuier.

6 recordsLinked to original sources
PubMed1991

Effect of stable xenon on regional cerebral blood flow and the electroencephalogram in normal volunteers.

We evaluated the effects of breathing 35% stable xenon in 65% oxygen on regional cerebral blood flow and the electroencephalogram in 20 normal volunteers. We measured blood flow in 32 brain regions over both hemispheres with the xenon-133 intravenous injection technique in two protocols. In the first protocol (n = 10), a baseline study was followed by a second study during 5 minutes of breathing stable xenon; in the other protocol (n = 8), the baseline study was followed by a second study after 5 minutes of breathing stable xenon. Two volunteers were excluded due to excessive movements during the inhalation of stable xenon. Some of the remaining 18 volunteers had varying alterations of consciousness accompanied by electroencephalogram changes. After stable xenon inhalation the electroencephalogram returned to normal within 2-3 minutes. During stable xenon inhalation mean +/- SD PECO2 dropped significantly from 39.4 +/- 4.4 to 33.3 +/- 5.4 mm Hg in the first protocol and from 39.4 +/- 2.6 to 34.8 +/- 4.1 mm Hg in the second protocol due to hyperventilation in 13 volunteers. Mean regional cerebral blood flow increased significantly by 13.5-25.4% without correction for PECO2. In the first protocol regional cerebral blood flow increased by greater than 12% in 11-14 (depending on the flow parameter) of the 20 hemispheres. In the second protocol regional cerebral blood flow increased by greater than 12% in 9-13 of the 16 hemispheres. We conclude that cautious interpretation is necessary in the assessment of regional cerebral blood flow with 35% xenon-enhanced computed tomography.

Adult↗
PubMed1990

Cerebral blood flow and plasma volume during hyperglycemia in the conscious rat.

Cerebral blood flow (CBF) and cerebral plasma volume (CPV) were measured under steady-state hyperglycemic conditions in the hemispheres and brainstem-cerebellum of conscious rats. There groups of hyperglycemic animals each having a different level of plasma glucose concentration, 25, 33.3, 44.4 mmol/l, and a normoglycemic control group were studied. CBF was not affected at the hyperglycemic levels of 25 and 33.3 mmol/l. Mean hemispheric and brainstem-cerebellum CBF values appeared lower than in controls at the highest glycemic level although the differences were not statistically significant. CPV was found to be unchanged at the hyperglycemic level of 25 mmol/l, while it was found to be increased in the hemispheres of the animals whose plasma glucose concentration had been elevated to 33.3 and 44.4 mmol/l. The results of the study do not support the claim that hyperglycemia may enhance ischemic brain injury by reducing CBF.

Animals↗
PubMed1978

[Symmetric cerebral calcification associated with disturbed parathyroid function (author's transl)].

Alteration of the metabolism of calcium and phosphate may be associated with symmetric cerebral calcification. Detailed investigations of the function of parathyroid glands including computer tomography of the brain are so far missing. In 6 patients with clinical and biochemical signs of altered function of the parathyroid glands symmetric cerebral calcification could be demonstrated by computer tomography. They are also visible by X-ray examination in one patient. Consequently, functional disturbances of the brain, cerebellum and of the extrapyramidal system may occur. Moreover, the combination of hypoparathyroidism and hypothyroidism also appears to result in the development of symmetric cerebral calcification. The pathogenesis of the calcification as well as therapeutic approaches will be discussed.

Adult↗
PubMed1978

Cerebral microembolization. II. Morphological studies.

Cats underwent massive microembolization via carotid infusion of 10.5 million microspheres (15 +/- 5 mu in diameter), resulting in brain death within four hours; 87.4 +/- 10.2% of emboli reaching the brain were in the ipsilateral hemisphere; 87.9 +/- 4.4% were in the grey matter; and 12.1 +/- 4.4% were in the white matter. Evans blue and sodium fluorescein dyes were given intravascularly before and at different times after embolization. Fluorescence microscopy disclosed that embolization initially provoked a hyperemic engorgement of both the embolized and nonembolized hemispheres. Multifocal, blood-brain barrier extravasations occurred throughout the ipsilateral cortex and oral basal ganglia. Severe vasogenic brain edema ensued, with migration of extravasations from cortex into the white matter, which initially showed only minimal injury. Migration and accumulation of edema in white matter, with subsequent uptake and swelling of neuroglia and axons, may be related to secondary white matter damage following cortical embolic lesions. Degenerative foci developed throughout the embolized cortex over the one- to four-hour period of this study. These sites may correspond to those areas in which hyperemia and damage to the blood-brain barrier was present shortly after embolization.

Animals↗