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Biomedical subjects

M Juhler

Publications and source records attributed to M Juhler.

49 records · Page 3Linked to original sources
PubMed1986

Regional cerebral blood flow in acute experimental allergic encephalomyelitis.

Regional cerebral blood flow was studied in Lewis rats with fulminant acute experimental allergic encephalomyelitis (EAE). [14C]iodoantipyrine was used as a tracer. By employing a short experimental time and an infusion schedule producing an increasing arterial tracer concentration, the spatial resolution of the method was fine enough to detect focal increases in blood flow in the small central nervous system lesions (lymphocytic accumulations). An increase of flow of 100% in the lesions and a decrease of 50% in the cerebral cortex of EAE animals was statistically significant. In all other regions studied (deep cerebral structures, cerebellum), blood flow in EAE animals did not differ from the control values. The flow increase corresponding to the lesions may be due to inflammatory hyperemia. The cortical decrease in flow may be secondary to sensory motor impairment.

Acute Disease↗
PubMed1986

The distribution of immunoglobulins and albumin in the central nervous system in acute experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis (EAE) was induced in young male Lewis rats. Immunohistochemical visualisation of albumin and IgG in the nervous tissue was performed at intervals after induction. The results were correlated to the histological appearance of the tissue. Albumin appeared in the tissue about day 10, 1-2 days before IgG. Within one day both proteins spread from sharply defined perivascular subpial locations to diffuse distribution throughout the tissue. Cellular inflammation was not seen until 3-4 days after extravasation of proteins. The cells also spread from perivascular locations to a diffuse infiltration of the tissue.

Acute Disease↗
PubMed1986

Decreased blood-brain barrier permeability to sodium in early experimental diabetes.

Blood-brain barrier (BBB) permeability to 24Na+, 36Cl-, and [3H]sucrose was studied in rats after 2 wk of streptozocin-induced diabetes. The PS (permeability-surface area product) for Na+ in the cortex of the frontal lobes was 5.4 +/- 0.6 (10(-5) cm3 X g-1 X s-1; +/- SD) in diabetic rats compared with 7.1 +/- 1.7 in control rats. In the occipital cortex, the values were 7.6 +/- 1.5 and 9.9 +/- 1.6, respectively. In contrast, BBB permeability to Cl- and sucrose remained unchanged. We conclude that a selective alteration in BBB permeability to Na+ unrelated to changes in brain capillary surface area is present in experimental diabetes.

Animals↗
PubMed1985

Role of extracellular proteins in the dynamics of vasogenic brain edema.

The relationship between extravasation of proteins into extracellular spaces of brain parenchyma and the water content of such regions were evaluated in an experimental model. In this model, a temporary opening of the blood-brain barrier (BBB) to proteins was produced without significant injury to the cellular elements of brain tissue. Rabbits were subjected to bolus injection of their own blood under 360-400 mm Hg pressure via the internal carotid artery. The opening of the barrier and its duration were evaluated with Evans blue (EB), horseradish peroxidase (HRP), and sodium fluorescein (NaFl) tracers. The water content of brain tissue was assessed by specific gravity (SG) measurements in 1-mm-diameter tissue samples. Quantitative evaluation of protein penetration into brain tissue was carried out using 125I bovine serum albumin (BSA). The opening of the BBB to proteins persisted up to 9 h, whereas the barrier remained permeable to small molecular NaFl for 24 h. The SG measurements indicated in the areas of EB extravasation a progressive increment in water content up to 9 h, i.e., the duration of BBB opening to proteins. Following this, there was a progressive clearance of edema in spite of the BBB remaining open for NaFl for 24 h. Quantitative evaluations of 125I-BSA and SG in the same tissue samples, supported by statistical analysis, indicated approximately linear relationship analysis, indicated approximately linear relationship between albumin and water, implying a strong correlation between the development of vasogenic edema and extravasation of proteins into extracellular spaces.

Animals↗
PubMed1985

A spatial analysis of the blood-brain barrier damage in experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis was induced in young male Lewis rats. Following the development of neurological signs, the local distribution of perivascular inflammatory cellular infiltrates and the local blood-to-tissue transfer constants (K1) of alpha-aminoisobutyric acid (AIB) were determined, and these results were compared. Perivascular infiltrative lesions were generally found near areas of the CNS that normally lack an effective blood-brain barrier (BBB) such as the choroid plexus and the entry zones of the cranial and spinal nerve roots. This distribution pattern indicates that the entry of the causative agent into CNS tissue may be by way of the permeable microvessels of these structures. In tissue around inflamed veins, the mean transfer constant was slightly but significantly increased (2.8 +/- 1.5 microliter g-1 min-1) compared with uninvolved regions (0.9 +/- 0.2 microliter g-1 min-1) and similar areas in control animals (0.9 +/- 0.3 microliter g-1 min-1). Analysis of the autoradiographic method of determining transfer constants suggested that the AIB influx rate in the lesion areas may actually be manyfold larger than measured, that BBB permeability may be greatly increased at such sites, and that the areas of lymphocytic infiltration and increased K values may be virtually identical.

Aminoisobutyric Acids↗
PubMed1984

Blood-brain and blood-spinal cord barrier permeability during the course of experimental allergic encephalomyelitis in the rat.

Experimental allergic encephalomyelitis (EAE) was induced in young male Lewis rats. Blood-brain barrier permeability to radiotracers of different molecular sizes was studied at intervals after induction using a tissue sampling technique. The results were correlated to the clinical picture and to the histological appearance of the central nervous system. Significant increase in blood-brain barrier permeability to small molecules was found to precede clinical symptoms by one day in the lumbar spinal cord and to coincide with the onset of clinical disease in other regions. In all regions, increased blood-brain barrier permeability preceded the occurrence of histological lesions (perivascular cellular infiltrates). No permeability increase to large molecules could be demonstrated.

Animals↗
PubMed1984

Effects of captopril on cerebral blood flow in normotensive and hypertensive rats.

Cerebrovascular effects of the angiotensin converting enzyme inhibitor captopril were examined in normotensive and hypertensive rats. Cerebral blood flow was measured with the intracarotid 133xenon injection method in halothane-anesthetized animals. The blood-brain barrier permeability of captopril (determined with an integral-uptake method) was negligible, the permeability-surface area product in most brain regions being 1 X 10(-5) cm3/g per second, that is, three to four times lower than that of sodium ion. When administered into the cerebral ventricles to bypass the blood-brain barrier, captopril had no effect on cerebral blood flow: furthermore, cerebral blood flow autoregulation (studied by raising and lowering blood pressure) was identical to that in controls. In contrast, when given intravenously, captopril had a marked effect on cerebral blood flow autoregulation--both the lower and upper limits of autoregulation being shifted to a lower pressure (by about 20 to 30 and 50 to 60 mm Hg, respectively), and the autoregulatory range was shortened by about 40 mm Hg. This effect may be ascribed to inhibition of converting enzyme in the cerebral blood vessels rather than within the brain.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Cerebrovascular aspects of converting-enzyme inhibition II: Blood-brain barrier permeability and effect of intracerebroventricular administration of captopril.

The blood-brain barrier permeability to captopril, and the cerebrovascular effects of intracerebroventricular administration of captopril, were studied in normotensive Wistar rats. The blood-brain barrier permeability-surface area product (PS), determined by an integral-uptake method, was about 1 X 10(-5) cm3/g/s in all brain regions studied. This was three to four times lower than the simultaneously determined PS of Na+ and Cl-, both of which are known to have very low blood-brain barrier permeability. Cerebral blood flow, determined by the intra-arterial 133xenon injection method, was unaffected by intracerebroventricular administration of 100 micrograms captopril. Furthermore the lower limit of cerebral blood flow autoregulation during haemorrhagic hypotension was also unaffected, being in the mean arterial pressure range (50-69 mmHg) in both controls and captopril-treated rats. It was concluded that the blood-brain barrier permeability of captopril was negligible and that inhibition of the brain renin-angiotensin system has no effect on global cerebral blood flow. The cerebrovascular effects of intravenously administered captopril (a resetting to lower pressure of the limits and range of cerebral blood flow autoregulation) are probably exerted via converting enzyme on the luminal surface of cerebral vessels.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

CT findings in acute MS.

In 5 patients with definite or highly probable MS, unusually large hypodense plaques are seen by computerized tomography (CT scan). The active plaques all show enhancement after i.v. contrast medium injection, suggestive of blood-brain-barrier-damage, and differ from the well-known CT findings in chronic MS patients, causing diagnostic difficulties between glioma and infarction.

Adult↗
PubMedDate not supplied

Torture: diagnosis and rehabilitation.

This article describes psychological and physical methods of torture, the general stress-related sequelae that are unrelated to the method used, and some examples of clinical effects that are related to specific methods. The approach to the rehabilitation of victims of torture practised at RCT is outlined. Two illustrative case histories are given.

Diagnosis↗