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Biomedical subjects

Y Olsson

Publications and source records attributed to Y Olsson.

At least 199 records · Page 11Linked to original sources
PubMed1979

Early influx of horseradish peroxidase into axons of the hypoglossal nerve during Wallerian degeneration.

Horseradish peroxidase (HRP) was applied around mouse hypoglossal nerves which were damaged by a crush or a ligature. HRP was then visualized distal to the lesions by light- and electron microscopic histochemistry. At the injury the enzyme entered axons and could also be detected several millimetres down in the distal segment. By 24 h reaction product (r.p.) was either diffusely distributed in the axoplasm or present in various vesicular organelles. Our results indicate that there is a rapid influx of macromolecules into axons after a lesion to a nerve. A similar uptake of 'wound substances' into axons distal to an injury might well have some relation to the process by which axonal breakdown is initiated during Wallerian degeneration.

Absorption↗
PubMed1979

Local anesthetics: importance of mode of application, concentration and adrenaline for the appearance of nerve lesions. An experimental study of axonal degeneration and barrier damage after intrafascicular injection or topical application of bupivacaine (Marcain).

Local anesthetics are designed for application in or close to nerve tissue. In spite of their wide clinical use, surprisingly few investigations deal with the neural toxicity of modern local anesthetics. In this experimental study, the effects were investigated of intrafascicular or topical application of the long-acting local anesthetic bupivacaine on the rabbit sciatic nerve. Axonal degeneration was histologically evaluated and a fluorescence-microscopic technique used to detect lesions in the blood-nerve barrier. Topical application of bupivacaine in clinically recommended concentrations around the nerve caused no detectable nerve injury, while intrafascicular injections caused considerable axonal degeneration and damaged the blood nerve barrier. Axonal degeneration was the same after injection of physiologic saline solution and bupivacaine 0.5%, but it increased with increasing bupivacaine concentration and especially with the addition of adrenaline. On the other hand, the acute effects of intrafascicular injection, as visualized in the barrier experiments, changed little with the addition of adrenaline, indicating that it is the injection trauma itself which is deleterious. It is concluded that intraneural injections should be avoided and that plain bupivacaine solutions should be routinely used.

Administration, Topical↗
PubMed1978

Uptake and retrograde axonal transport of various exogenous macromolecules in normal and crushed hypoglossal nerves.

Macromolecular tracers were injected into the tongue or around a crush in mouse hypoglossal nerves. At various times thereafter, the tracers were histochemically localized on the basis of peroxidase activity. The distribution of reaction product was then examined using light microscopy in order to study the influence of molecular charge and size on uptake and retrograde axonal transport from the periphery or from the crushed axon. Of various proteins with peroxidase activity, horseradish peroxidase and cytochrome-c showed the greatest penetration into axons proximal to the crush. Following injection into the tongue, intra-axonal cytochrome-c was detectable in some of the peripheral branches but not any of the other proteins. Retrograde transport to the nerve cell bodies was demonstrated for horseradish peroxidase and cytochrome-c, both from the tongue and from the axonal crush but not for microperoxidase, myoglobin, hemoglobin, lactoperoxidase and catalase. The number of neuronal cell bodies having detectable reaction product was higher for peroxidase-injected than for cytochrome-c-injected animals. Ferritin and iron-dextran (Imferon) also accumulated in hypoglossal neurons, but this could be detected only after repeated injections into the tongue. Uptake and retrograde transport from the tongue or from the crush occurred both for anionic and for cationic horseradish peroxidase. This is interpreted as evidence against absolute specificity in the uptake and transport of macromolecules on the basis of electrical charge.

Animals↗
PubMed1978

A sensitive method for histochemical demonstration of horseradish peroxidase in neurons following retrograde axonal transport.

A study was made on the effects of various fixatives and some other histochemical parameters used in the procedure for demonstrating labeled neurons following retrograde axonal transport of horseradish peroxidase (HRP). The enzyme was injected into the tongue of adult mice and the results were obtained by counting labeled hypoglossal neurons following certain variations in the procedure. Paraformaldehyde in the fixative should be avoided since it reduces the number of labeled neurons as compared to glutaraldehyde in a concentration of 1.5-2.5% Fixation for about 4 h is recommended followed by a wash in 5% sucrose buffer overnight. Variables in the histochemical procedure were systematically studied in order to determine optimal pH, buffer type, buffer concentration and substrate concentration. The effect of using a "preincubation" in buffer containing only diaminobenzidine tetrahydrochloride (DAB) was also examined. These results were used to develop a modified histochemical procedure which produced a substantial increase in the number of detectable HRP-labeled neurons as compared to equivalent sections that were reacted in the incubation medium described by Graham and Karnovsky. The modified histochemical procedure involves incubation (no preincubation with DAB only) of sections in the dark for 30 min in a solution consisting of 10 ml cacodylate buffer (pH 5.1;0.1 M), 20 mg DAB and 0.1 ml of 1% hydrogen peroxide. The Kodak Wratten no. 46 filter is recommended for light-microscopical identification of labeled neurons since it is closely matched to the absorption spectrum of the DAB reaction product and consequently greatly increases the contrast of HRP-labeled neurons.

Animals↗
PubMed1978

A sliver-gold impregnation technique for routine neuropathological use.

A silver-gold impregnation technique for routine neuropathological use is presented. It is easy to perform, gives reproducible results and the ingredients are chemically well characterized. It has been successfully applied to formalin-fixed paraffin-embedded material from human brain, where nerve cell processes, neurofibrillary changes and melanin-containing neurons are distinctly visualized. Axons in peripheral nerves are impregnated and cross striations in muscle cells can also be demonstrated.

Axons↗
PubMed1977

Macroglobulinemia Waldenström and motor neuron syndrome.

One patient suffering from macroglobulinemia Waldenström developed a neurological disease which may be a previously unrecognized paramalignant phenomenon in this disorder. The clinical symptoms and signs indicate a motor neuron syndrome and autopsy revealed degeneration of ventral and lateral funicles in the spinal cord, loss of ventral motor neurons, degeneration of ventral nerve roots and muscular atrophy. The rather low incidence of macroglobulinemia and motor neuron disease suggest some causal relationship rather than a sporadic occurrence of two disorders in the same patient.

Aged↗
PubMed1976

Retrograde transport of horseradish peroxidase in transected axons. 3. Entry into injured axons and subsequent localization in perikaryon.

Horseradish peroxidase (HRP) applied to crushed mouse sciatic nerves diffused through the damaged perineurium into the endoneurium. In the injured area, HRP passed into damaged myelinated and unmyelinated axons forming columns of reaction product, which extended for several millimeters proximally to the lesion. Ultrastructurally, HRP adhered to the inner surface of the axoplasm and to the surfaces of neurotubules and neurofilaments in such columns. At more proximal levels axons contained HRP in vesicular and tubular organelles and, later, nerve cell bodies of the corresponding spinal ganglia showed HRP, accumulation in cytoplasmic vesicles, cup-shaped bodies, multivesicular bodies and tubules of agranular endoplasmic reticulum. Markedly less HRP reached neurons in the spinal ganglia when applied to the nerve 30 or 60 min after the crush. After such time intervals solid HRP containing axons were also less frequently observed. Conceivably, HRP enters crushed axons momentarily after a crush as an injured cell reaction. Subsequently it is incorporated into organelles higher up in the axons, from where retrograde transport to the perikaryon will fellow. This phenomenon of a sudden non-specific influx of exogenous macromolecules into axotomized neurons and their subsequent transport to the perikaryon might be relevant for development of certain biochemical and morphological responses, e.g. lysosomal alterations, of the neuron to an axonal injury.

Animals↗
PubMed1975

Fluorescein labelled dextrans as tracers for vascular permeability studies in the nervous system.

Golden hamsters received i.v. injections of dextrans labelled with fluorescein isothiocyanate (FITC-Dextran). After 4 hrs samples from the cerebral hemispheres, Gasserian ganglia and sciatic nerves were fixed either by immersion in formalin or by cardiac perfusion with the same fixative. The distribution of the tracer was then studied by fluorescence microscopy of thin frozen sections. With this simple technique FITC-Dextrans could easily be detected in tissue sections. The tracers used (mol. w. 19000 and 154000) spread in the same way as fluorochrome-labelled albumin, remaining in the lumen of cerebral vessels but leaking extensively from vessels in the ganglia. FITC-Dextrans thus appear to be very useful tracers for vascular permeability studies of nervous tissue since dextrans can be obtained in a wide range of molecular weights. FITC-Dextrans can also be subjected to microscopic and quantitative studies.

Animals↗
PubMed1975

Retrograde transport of horseradish peroxidase in transected axons. II. Relations between rate of transfer from the site of injury to the perikaryon and onset of chromatolysis.

The sciatic nerves of 2--3 month-old mice, rats and rabbits were crushed and at the same time horseradish peroxidase (HRP) was applied around the crushed region at mid-thigh level. At varying time intervals thereafter, HRP was seen in neurons of the corresponding spinal ganglia and levels of the spinal cord. The rate of ascent of HRP appeared to be similar in the different animals and to be independent of the length of the nerve. The accumulation of HRP was more conspicuous in small than large neurons in the ganglia at early stages after the nerve crush. The arrival of HRP in the perikarya preceded the onset of early morphological changes in the neurons (chromatolysis). The rate of ascent of the signal for chromatolysis appeared to be within the same range as that of the retrograde transport of HRP in the crushed axons. The possibility therefore exists that these two phenomena are in some way interrelated.

Animals↗
PubMed1975

Experimental brain damage from fluid pressures due to impact acceleration. 3. Morphological observations.

"Contre-coup" lesions occurring particularly in the frontal and temporal lobes following head injury have been claimed to be caused by sudden negative pressure transients, as part of the "contre-coup" end pressures occurring in the brain tissue at an occipital impact. With a new experimental model such impact acceleration pressure (near-1 atm) could be generated in the rabbit brain through a parietal opening. Resulting morphological changes were evaluated with various microscopical methods, including Evan's blue-albumin technique for observations on vascular permeability changes. Regardless of the magnitude of the negative pressure transients no changes characteristic of "contre-coup" lesions were seen in temporal lobes, i.e. in areas where preparative artefacts are absent in control animals. Therefore such negative pressure transients per se do not appear to be of major importance for the development of contre-coup lesions. However, vascular permeability changes were frequently observed in the brain stem and upper cervical cord and are presumably related to the flow of tissue in the cranio-spinal junction.

Acceleration↗
PubMed1975

Experimental brain damage from fluid pressures due to impact acceleration. 4. comparative studies with acceleration-concussion.

In order to elucidate the cause of brain damage in head injuries experiments are often designed to cause impacts to the intact skull of animals. To study the injurious significance of the contre-coup part of the impact acceleration pressure pattern we have previously applied direct loading through a parietal opening to the rabbit skull cavity. In order to evaluate the effects of the acceleration, similar impacts were delivered with greater magnitudes of such movements of the intact reinforced rabbit skull with the same equipment attached but without trephine opening. Varied and predictable acceleration, velocity and displacement of the head, and minimized skull deformation were possible with this model. Threshold levels of such impact acceleration were studied with regard to changes in respiratory and vasomotor activities ("concussive response"). Vascular permeability changes in the brain and spinal cord were studied with Ean's blue-albumin injection before the impact. Morphological observations were also made at the end of the experiments. No significant pathophysiological or morphological effects were elicited below peak acceleration of 2000 gn (duration 0.7 ms), peak velocity of 5 m/s or total dislocation of the head of 30 mm. At higher levels of impact a "concussive response" was elicited without fractures of the skull bone or significant brain lesions. Thus, in impact tests resulting in acceleration magnitudes far below those levels the signs of brain damage induced might mainly be related to the mechanical effects added--i.e. the fluid pressure loading.

Acceleration↗
PubMed1975

Case report: injury of the spinal cord at birth.

Spinal cord injury may occur as a severe complication to delivery. In the vast majority of such cases the injury results from a traumatic breech delivery, but cases of injuries after cephalic presentation and fetal malposition have also been described. Two cases were reported. One of the infants died at the age of 8 months and neuropathological examination of the brain and spinal cord was performed. The other child, now 6 years old, is still alive. Incidence, mechanism of injury, clinical and morphological features, and treatment are briefly discussed.

Autopsy↗