PubMed Health⌕ Search

Biomedical subjects

L I Persson

Publications and source records attributed to L I Persson.

29 records · Page 2Linked to original sources
PubMed1981

Effect of ethanol, chlorpromazine and dexamethasone on blood-brain barrier dysfunction to albumin around large cerebral stab wounds.

Stab-wounded ethanol-intoxicated and non-intoxicated albino rats subjected to chlorpromazine or dexamethasone treatment were studied with respect to blood-brain barrier (BBB) dysfunction. Fifteen h after inflicting large cerebral stab wounds (diameter 400 microns), the animals were intoxicated with ethanol by ip injections or kept as non-intoxicated controls. One h later, the animals were either subjected to intravenous injections of chlorpromazine or dexamethasone or kept as non-treated controls. After intravenous injection of Evans blue-labelled albumin (EBA) or bovine serum albumin only, the rats were killed by intra-aortal perfusion and the BBB dysfunction was studied by fluorescence microscopy or measured by rocket immunoelectrophoresis. In the non-intoxicated group, fluorescence microscopy revealed a considerable decreased area showing extravasation of EBA around the stab wound in rats treated with chlorpromazine. In ethanol-intoxicated, compared to non-intoxicated rats, the area showing extravasation of EBA was not enhanced as studied by fluorescence microscopy. This extravasation was substantially decreased by chlorpromazine treatment, but not affected by dexamethasone. Immunoelectrophoretic assays of the amount of albumin extravasated around the stab wound confirmed the effect of chlorpromazine on the blood-brain barrier dysfunction to bovine albumin in both ethanol-intoxicated and non-intoxicated rats.

Alcoholic Intoxication↗
PubMed1980

Brain primary culture - a characterization.

Primary cultures from rat or mouse brain hemispheres contain predominantly glial cells. These cells accumulated [3H]GABA and showed a specific fluorescence with FITC-labeled anti-S-100 antiserum. Round or elongated cells which reacted positively with antimacrophage antiserum and exhibited phagocytotic activity, were considered mesodermal macrophages. Big flat cells, unreactive to S-100 antiserum or to any other antiserum tested, showed a morphology similar to mesenchymal cells of a low differentiation grade. These cells formed a monolayer upon which other cell types grew. Positive reaction for alkaline phosphatases was used as a criterion to identify endothelial cells, the number of which increased with increasing age of the cultures. Anti-14-3-2 antiserum gave no specific reaction, indicating the presence of very few or no differentiated neurons in the cultures.

Alkaline Phosphatase↗
PubMed1980

Albumin extravasation in bicuculline-induced blood-brain barrier dysfunction. A comparison between endogeneous and 125I-labeled exogeneous serum albumin.

The extravasation of endogeneous rat albumin and exogeneous 125I-labeled human serum albumin was compared in rats subjected to bicuculline-induced blood-brain barrier dysfunction. The correlation between rocket immunoelectrophoretic assays of endogeneous rat albumin and 125I-labeled human serum albumin, assayed by gamma scintillation counting, was good respective of whether 125I-labeled albumin was studies in whole brain tissue or in brain homogenates. The ratio of brain to serum albumin was similar with the two assay methods.

Albumins↗
PubMed1979

Chlorpromazine treatment of blood-brain barrier dysfunction. A quantitative and fluorescence microscopical study on small cerebral stab wounds in the rat.

The extravasation of albumin around small cerebral stab wounds in the rat frontal cortex was studied by fluorescence microscopy after i.v. injection of Evans blue-labeled albumin and by quantitative immunoelectrophoresis after i.v. injection of bovine albumin, in both nonintoxicated and ethanol-intoxicated rats. The extravasion of albumin was enhanced in ethanol-intoxicated compared to nonintoxicated rats, as studied both by immunoelectrophoresis and by fluorescence microscopy. Administration of chloropromazine (2 mg/kg body weight i.v.) 16 h after inflicting cerebral stab wounds decreased the area around the wound showing extravasation of Evans blue-labeled albumin as studied by fluorescence microscopy both in nonintoxicated and in ethanol-intoxicated rats. Quantitative studies showed a significanct decrease in the amount of extravasated albumin around cerebral stab wounds in ehtnaol-entoxicated rats, while the extravasation in nonintoxicated rats was not significantly changed by chlorpromizine treatment.

Albumins↗
PubMed1979

Blood-brain barrier dysfunction to peroxidase after air embolism, aggravated by acute ethanol intoxication.

Ethanol-intoxicated and non-intoxicated rats were injected with horseradish peroxidase and Evan's blue-labelled albumin and given a small air embolus in the right common carotid artery after ligation of the external carotid branch. In both ethanol-intoxicated and non-intoxicated rats, some endothelial cells, mainly in arteries and arterioles, showed a diffuse distribution of peroxidase in the cytoplasm. In some arterioles with a diffuse endothelial distribution of peroxidase there was a detachment of endothelial cells from the vessel wall, with an exposure of the adluminal basement membrane to blood elements. This endothelial detachment was mainly observed in ethanol-intoxicated rats. The vascular basement membranes underlying detached endothelial cells contained peroxidase, both in ethanol-intoxicated and in non-intoxicated rats. There was a considerable leakage of peroxidase via endothelial pinocytotic vesicles into the vascular basement membranes, mainly in arterioles, but also in capillaries and venules of the embolised hemisphere. This transendothelial pinocytotic transport of peroxidase was more prominent in ethanol-intoxicated than in non-intoxicated rats.

Alcoholic Intoxication↗
PubMed1979

Influence of ethanol and dexamethasone on blood-brain barrier dysfunction to albumin.

Stab-wounded ethanol-intoxicated and non-intoxicated rats were studied with respect to the effect of postoperative dexamethasone treatment on blood-brain barrier dysfunction to bovine albumin. In ethanol-intoxicated rats, fluorescence microscopy revealed an increased area of extravasation of fluorescent tracer, compared to non-intoxicated ones. No significant effect of dexamethasone treatment was observed in non-intoxicated rats. In ethanol-intoxicated rats, dexamethasone treatment resulted in a decreased area of extravasation. Quantitative immuno-electrophoretic measurements of exogeneous bovine albumin confirmed a significant decrease of blood-brain barrier dysfunction to albumin after dexamethasone treatment in ethanol-intoxicated rats, while no significant effect was observed in non-intoxicated ones.

Alcoholic Intoxication↗
PubMed1978

Ultrastructural studies on blood-brain barrier dysfunction after cerebral air embolism in the rat.

Male albino rats were anaesthetized with diazepam, injected with horseradish peroxidase and Evans blue-labeled albumin and given an embolus of 0.01 ml air in the right common carotid artery after ligation of the external carotid branch. The pial arteries of the right cerebral hemisphere were stained blue, particularly the middle cerebral artery and its main arterial branchlets. Ultrastructurally, some endothelial cells in the right middle cerebral artery, small arteries and arterioles showed a diffuse distribution of horseradish peroxidase in their cytoplasm, although these vessels only occasionally showed peroxidase in their basement membranes. Other endothelial cells in these arterial branchlets showed few if any signs of a diffuse distribution of peroxidase but displayed several pinocytotic vesicles and occasionally trans-endothelial channels filled with peroxidase, sometimes with a slight leakage of peroxidase into adjacent basement membranes and neuropil. Scattered pinocytotic vesicles were observed in capillaries and venules, but there was usually no extravasation of peroxidase around these vessels.

Animals↗
PubMed1978

Ultrastructural studies on blood-brain barrier dysfunction around cerebral stab wounds, aggravated by acute ethanol intoxication.

Ethanol-intoxicated and non-intoxicated albino rats subjected to cerebral stab wounds were injected with Evans blue-labelled albumin (EBA) and horseradish peroxidase (HRP) 24 hours after the injury. The tracers were injected 30 and 2 minutes before perfusion fixation with glutaraldehyde and then prepared for light microscopy and electron microscopy. There was prominent leakage of peroxidase through chains of pinocytotic vesicles and transendothelial channels from blood, through the endothelial cells, into the brain. There was no difference in the way of peroxidase leakage through the endothelial cells between ethanol-intoxicated and control rats, but the area containing leaking blood vessels was greater in intoxicated rats. Furthermore, the number of trans-endothelial channels, vesicles and caveolae per unit length of capillaries and venules was increased in ethanol-intoxicated rats. Injured neurons with a diffuse distribution of peroxidase in their cytoplasm were observed within a greater area around the stab wound in ethanol-intoxicated than in control rats.

Alcoholic Intoxication↗
PubMed1978

Hypertension-induced protein leakage in the brain in ethanol-intoxicated conscious and anesthetized rats.

Ethanol has been shown to aggravate the blood-brain barrier (BBB) dysfunction in cerebral trauma and in cerebral gas embolism, possibly by changing the endothelial cell membrane. No difference in protein extravasation was found between intoxicated and control rats under nitrous oxide anesthesia after the injection of bicuculline, a drug that hemodynamically gives rise to high blood pressure in combination with cerebral vasodilatation. In contrast there was a statistically significant increase in protein leakage in conscious intoxicated rats. The fact that ethanol increased the vulnerability only in conscious rats might indicate that nitrous oxide and ethanol have a common effect on the endothelial cell membranes or that nitrous oxide neutralizes an action of ethanol. Protein leakage induced by acute hypertension is more severe in rats anesthetized with nitrous oxide than in conscious rats, a difference that might to some extent be related to an effect of nitrous oxide on the endothelial cells. Further studies are needed to evaluate the influence of ethanol and nitrous oxide on the endothelial cell membrane.

Alcoholic Intoxication↗
PubMedDate not supplied

Effects of single doses of vigabatrin on CSF concentrations of GABA, homocarnosine, homovanillic acid and 5-hydroxyindoleacetic acid in patients with complex partial epilepsy.

Vigabatrin, as a single oral dose of 50 mg/kg, was administered to 11 patients with drug-refractory complex partial epilepsy. Serial lumbar punctures were performed prior to and 5 times within the first week following treatment. Cerebrospinal fluid (CSF) concentrations of total GABA, free GABA, homocarnosine, homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and vigabatrin were determined as well as blood vigabatrin levels. CSF GABA, homocarnosine, HVA and 5-HIAA concentrations increased by 6 h after the single dose and remained elevated for up to 5-7 days. In contrast, CSF and blood vigabatrin levels were maximal within the first 24 h and were no longer detectable thereafter. Hence, these results are consistent with vigabatrin acting as an irreversible inhibitor of GABA-transaminase and suggest that it may also increase biogenic amine turnover.

Administration, Oral↗