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Biomedical subjects

C Nordborg

Publications and source records attributed to C Nordborg.

At least 73 records · Page 4Linked to original sources
PubMed1992

Giant cell arteritis.

Giant cell arteritis is a generalized inflammatory disorder involving large and medium-sized arteries. The etiology is unknown, although an autoimmune pathogenesis seems probable. In view of the clinical similarities between patients with positive biopsy findings for polymyalgia rheumatica and those with negative biopsy findings, many authors favor the concept that polymyalgia rheumatica is an expression of an underlying giant cell arteritis. There is, however, still controversy as to whether polymyalgia rheumatica and temporal arteritis are different expressions of one and the same disease or two separate, partly overlapping types of giant cell arteritis. A single etiologic factor may be responsible for the two conditions, sometimes expressing itself as polymyalgia rheumatica and sometimes as giant cell arteritis. Recent findings of morphologic similarities in terms of arterial wall atrophy, calcifications, and inflammatory reactions may indicate that polymyalgia rheumatica and temporal arteritis represent different degrees or stages of the same disease.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1991

Sensorimotor performance and rotation correlate to lesion size in right but not left hemisphere brain infarcts in the spontaneously hypertensive rat.

In order to correlate behavioural deficits to lesion size and to reveal possible functional asymmetries in the rat brain, locomotor activity, rotation and sensorimotor integration to touch were studied in spontaneously hypertensive rats (SHR) subjected to right or left middle cerebral artery occlusion. Control and infarcted rats showed no difference in locomotor activity. Infarcted rats tended to rotate towards the side of the lesion. A large sensorimotor deficit was found contralateral to the infarcted hemisphere. The absolute values of the side-biases for the rotation and sensorimotor tests were of the same degree irrespective of lesion side. Whereas the left hemisphere lesion size did not correlate to the behavioural outcome, the size of the right hemisphere lesion was highly correlated to the total sensorimotor deficit. Furthermore, the sensorimotor deficit of specific body parts was found to correlate to the damage of certain brain regions in a rostrocaudal fashion, reminiscent of a somatotopical organization. The extent of ipsilateral rotation correlated to brain tissue loss at the level of the posterior caudate-putamen. The present results indicate an asymmetrical organization for brain functions involved in the performance of the rotation and sensorimotor tests.

Animals↗
PubMed1991

The relationship between plasma protein extravasation and remote tissue changes after experimental brain infarction.

Extravasated endogenous serum albumin and fibrinogen were identified immunohistochemically in coronal brain sections from normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) after permanent ligation of the right middle cerebral artery. Infarcts were seen in all the SHR but only in 6 out of 14 WKY. Six hours after ligation, extravasated proteins were located primarily within the borders of the infarcts whereas after 24 h and later there was an increasing spread in the white matter. After 7 days, a protein immunoreactivity was seen far outside the infarcted areas, mainly in the white matter and occasionally extending somewhat into the contralateral side. Three weeks after permanent ligation, the immunoreactivity for plasma proteins had a similar extension but was less intense than after 7 days. A gliosis was noted within the protein-positive regions. From 72 h and onwards the immunoreactivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where marked, mainly cytolytic nerve cell damage and gliosis was found. The close spatial correlation with albumin immunopositivity and the histological features of the thalamic lesions indicate that the propagation of extravasated plasma constituents or degradation products from the infarct may influence the character, timing and extent of remote tissue changes after cerebral infarction.

Animals↗
PubMed1991

Effects of chondroitinase ABC on intrathecal and peripheral nerve tissue. An in vivo experimental study on rabbits.

The enzyme chondroitinase ABC has recently been suggested for use in chemonucleolysis. The effects of 200 U ml of chondroitinase ABC were studied on intrathecal and peripheral nerve tissue in rabbits. After the intrathecal (subarachnoid) application of 0.2 ml of either the diluent in the control group (N = 2) or chondroitinase in the study group (N = 4), no neurologic deficit was detected. Compared with the control group, no morphologic changes at the light microscopic level were induced in the spinal cord by chondroitinase. No neurophysiologic differences were detected between tibial nerves after exposure to 1 ml of the diluent (control, N = 8) or chondroitinase (the other leg) for 4 weeks, nor did the study group, compared with the control group, show any morphologic changes in the tibial nerves. Because the concentration of chondroitinase ABC tested was approximately 40 times higher than might be used clinically for chemonucleolysis, the present study indicates a wide margin of safety for unwanted side effects on nerve tissue.

Animals↗
PubMed1991

Temporal artery morphology and morphometry in giant cell arteritis.

Paraffin sections and more than 7,000 plastic cross-sections of temporal arteries from 27 patients with a clinical diagnosis of polymyalgia rheumatica (PMR), 16 patients with a clinical diagnosis of temporal arteritis (TA) and 18 age- and sex-matched postmortem controls were studied using light microscopy. A new method was developed to permit a morphometric comparison between biopsies and autopsy specimens. Two stages of inflammation were discerned in TA. In atrophic arterial segments there was a focal, foreign-body, giant-cell reaction to the calcified internal elastic membrane (IEM) with a spatially correlated, mononuclear cell infiltration. Isolated giant cells were also found to attack the IEM in these cases. The majority of the biopsies displayed a different picture with a diffuse macrophage attack on media and intima with numerous and apparently macrophage-derived giant cells, which did not attack calcifications. The latter arteries were significantly widened (p less than 0.02), which indicates that this phase is the later one. Non-inflamed segments of PMR vessels displayed a significant, non-reactive media atrophy compared with controls (p less than 0.03) and their IEM calcifications were significantly larger (p less than 0.02). The circumference was smaller in atrophic PMR arteries than in inflamed TA arteries (p less than 0.006), which contradicts post-inflammatory scarring.

Aged↗
PubMed1991

Nerve function and structure beneath and distal to a pneumatic tourniquet applied to rabbit hindlimbs.

Neurophysiologic and neuropathologic changes were studied in rabbit hindlimbs after 2 hours of pneumatic tourniquet application with either 350 mmHg (n = 18) or 1,000 mmHg (n = 6) cuff inflation pressure. The toe spread reflex was decreased in 66% and absent in 33% of limbs 2 days after 350 mmHg compression, and was absent in all limbs after 1,000 mmHg compression. Compound motor action potential amplitudes (CMAPs), recorded from the abductor hallucis muscle, were significantly decreased with sciatic nerve stimulation 1 hour after 350 mmHg compression. CMAPs returned to baseline values one and two days later, however nerve conduction velocity (NCV) was still significantly decreased in the compressed sciatic nerves of these groups. In contrast, complete nerve conduction block, localized beneath the cuff's distal border, was observed two days after 1,000 mmHg compression, and NCV was still significantly decreased distal to the tourniquet zone. Using light and electron microscopy, scattered axonal degeneration, mild myelin damage, and normal nodes of Ranvier were observed two days after 350 mmHg tourniquet compression. Severe fiber damage and nodal obliteration were noted after 1,000 mmHg tourniquet compression. Although nodal invagination is probably not a significant pathogenic mechanism at clinically relevant tourniquet pressures and durations, functional abnormalities were induced by 2 hour, 350 mmHg tourniquet compression. Such changes probably correlate with clinical electromyographic abnormalities and delayed post-operative recovery following 'routine' extremity surgery using pneumatic tourniquets.

Action Potentials↗
PubMed1991

Polyneuropathy possibly caused by 30 years of low exposure to n-hexane.

A slowly developing, mainly sensory, polyneuropathy was found in a 60-year-old man exposed to n-hexane (10-100 mg/m3) for 30 years in a mountain fuel stockpile. The nerve damage was verified by electromyography and sural nerve biopsy, and it is proposed that also a low-grade, but prolonged, exposure to n-hexane may cause polyneuropathy.

Biopsy↗
PubMed1990

Brain tumors in childhood and adolescence in west Sweden 1970-1984. Epidemiology and survival.

A population-based series of 198 children, aged 0 to 16.9 years, with primary brain tumors, diagnosed from 1970 to 1984, was retrieved from the Swedish Cancer Registry. After review of slides and reclassification of histology according to the American Cancer Society, the average annual incidence rate was estimated to be 34.9 per million, which is a very high incidence compared to other countries. The age distribution was not uniform as age group 0 to 4 included more children than age groups 5 to 9 and 10 to 14. The largest subgroups were astrocytomas (25%) and primitive neuroectodermal tumor (PNET)/medulloblastomas (MB) (21%). Associated diseases were neurofibromatosis and Rubinstein-Taybi syndrome. The overall male to female ratio was 1.08:1, the same as in the population at risk; but for PNET/MB, it was 1.8:1. The 5-year survival for all tumors was 54%, and the 15-year survival, 49%, with great variation between tumor subgroups.

Adolescent↗
PubMed1990

Evaluation of brain damage in a rat model of neonatal hypoxic-ischemia.

In spite of improvements in obstetric and neonatal care, hypoxic-ischemic brain damage with severe neurologic disability is still a clinical reality. A model in 7-day-old rats has been introduced to study the pathophysiology of perinatal hypoxic-ischemic brain damage. Unilateral brain damage is produced in the cerebral cortex, striatum and hippocampus, i.e. a similar distribution as is often seen in human asphyxiated neonates. In the present investigation the model was evaluated further by comparing three different methods to assess the brain damage: weighing the hemispheres, morphometry and somatosensory evoked potentials. Seven-day-old rats were subjected to unilateral carotid artery ligation followed by 2 h of hypoxia (7.7% O2 at 36 degrees C). After 2 h of hypoxic-ischemia pCO2 and pO2 decreased in mixed arterial/venous blood. The evaluation of the damage 2 weeks after the insult, demonstrated close correlation between morphometry and weighing (r = 0.836, P less than 0.01). The amplitude of evoked potentials correlated to the other parameters (r = 0.814, P less than 0.01 and r = 0.824, P less than 0.01 respectively) and displayed a greater relative attenuation than the other methods but with a more pronounced variability. These results indicate that the degree of brain damage can be assessed by weighing for screening purposes.

Aging↗
PubMed1989

[Risk of central pontine myelinolysis in the treatment of severe hyponatremia].

Central pontine myelinolysis is a life-threatening condition involving the demyelination of axons in certain areas of the brain. It has been shown almost invariably to occur in connection with hospital care. In recent years, a connection has been noted between the rapid restitution of low serum sodium and the development of the condition. In this review, the most recent scientific information is summarized. It is concluded that the risk should always be considered in treating a hyponatremic patient. The serum sodium level should be raised slowly and the acute treatment ended before normal serum sodium levels are reached, ie when the patient is still slightly hyponatremic.

Demyelinating Diseases↗
PubMed1989

The influence of antihypertensive treatment on the mesenteric arterial structure in spontaneously hypertensive rats. A morphometric study.

Spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SHRSP) were treated with a combination of a beta 1-blocker (metoprolol) and a calcium antagonist (felodipine) from 1 to 4 or from 4 to 6 months of age. The main trunk and peripheral branches of the mesenteric arterial tree were fixed by immersion and embedded in plastic. The total length of the internal elastic membrane and the media area were measured in cross-sectioned arteries. The ratio between media thickness (m) and luminal radius (ri) was then determined for a calculated, standardized condition, assuming a smooth and circular internal elastic membrane. The treatment caused a significant decrease in blood pressure and a reduction in m/ri ratios in the mesenteric arterial trunk as well as in mesenteric arterial branches when initiated in young as well as in adult SHR and SHRSP, i.e. the therapy efficiently prevents as well as reverses hypertensive arterial changes. The m/ri ratios in the superior mesenteric arterial trunks were significantly smaller in treated 4-month-old SHR and SHRSP than in WKY, although their blood pressures were not fully normalized. There was a marked increase in luminal radius in the young treated rats, possibly secondary to a therapy-induced increase in splanchnic blood flow.

Animals↗
PubMed1988

Cyst formation and glial response in the brain lesions of stroke-prone spontaneously hypertensive rats.

The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of larger lesions was due to swollen neuronal and astrocytic cell processes, i.e. at this stage the oedema was mainly intracellular. Cystic lesions were formed in the grey matter both by expansion of the extracellular space (ECS) containing protein-rich oedema fluid, and by rupture and subsequent loss of massively swollen cellular elements. In the white matter small slit-formed cysts along the fibre tracts were also formed by the expansion of ECS. In apparently recent lesions astrocytes displayed cyto-plasmic oedema but otherwise were still fairly normal. In more chronic lesions increased numbers of enlarged astrocytes with prominent staining for glial fibrillary acidic protein were present. Their distribution corresponded well to the spread of oedema, i.e. they were prominent around the leaky vessels in the grey matter, in the subpial zone and in the white matter. In the reparative phase the grey matter cysts became lined by astrocytic processes, a new glia limitans. Profuse sheets of glial processes in the neuropil around the cysts reestablished the compactness of the brain parenchyma.

Animals↗
PubMed1988

Nerve cell injury in the brain of stroke-prone spontaneously hypertensive rats.

The brain lesions in stroke-prone spontaneously hypertensive rats (SHRSP) are characterized by multifocal microvascular and spongy-cystic parenchymal alterations particularly in the gray matter. An essential feature of the lesions is the presence of edema with massive extravasation of plasma constituents as evidenced by specific gravity measurements, Evans blue technique and immunohistochemistry. The nerve cell injury occurring in the brain lesions in SHRSP is further characterized by light and electron microscopy in the present study. Two types of neuronal changes were seen within the blood-brain barrier (BBB) leakage sites. A small number of neurons with dark condensed nucleus and cytoplasm were found most often at the periphery of recent lesions. The majority of injured neurons were pale and showed intracellular edema confined to the dendrites and perikarya sparing axons and synapses. Their nuclei were well preserved with finely dispersed chromatin. The swollen and watery cell processes of neurons and astrocytes gave a spongy appearance to the neuropil. The intracellular edema seemed to result in cytolysis. The results suggest that primary anoxia-ischemia is not the major pathogenetic mechanism behind the nerve cell injury in severely hypertensive SHRSP, rather it is the massive BBB leakage and consequent brain edema that causes cytolytic destruction of neurons. Secondary focal ischemia as a consequence of occlusion in microvessels may, however, contribute to the nerve cell destruction.

Animals↗
PubMed1988

Cerebral microangiopathy in stroke-prone spontaneously hypertensive rats. An immunohistochemical and ultrastructural study.

The morphology of cerebral microvessels was studied immunohistochemically and ultrastructurally in 6- to 9-month-old normotensive Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP) with a systolic blood pressure of 138 +/- 15 mm Hg, 189 +/- 9 mm Hg, and 258 +/- 30 mm Hg respectively. Regions with major opening of the blood-brain barrier (BBB) were revealed by an i.v. injection of Evans Blue. Multifocal BBB opening with massive leakage of plasma constituents rich in fibrinogen-fibrin-related antigen occurred in SHRSP with a blood pressure above 210-220 mm Hg. BBB-leakage sites were found in the cerebral cortex and the basal ganglia, most frequently in the arterial border zones. The perivascular tissue spaces were dilated within the BBB-leakage sites, in particular around arterioles. Damaged endothelial and smooth muscle cells were replaced by fibrin-like material, multiple layers of basement membranes and bundles of collagen fibrils surrounded by proliferated fibroblasts. The degenerative-infiltrative-proliferative disease process transformed short segments of single arterioles into severely thickened, tortuous and stenotic vessels. Fibrinoid degeneration, formation of microaneurysms and fibrin-rich vascular occlusions were observed. In contrast, only minor or no vascular alterations were seen in regions with preserved BBB in SHRSP and SHR. A severely increased intraluminal pressure load appears to be of major pathogenetic importance for breakdown of the BBB and initiation of the vascular disease process in SHRSP. However, since only short segments of a limited number of widely separated vessels are severely affected, and the number of affected vessels increase towards arterial end and border zones, additional predisposing and aggravating factors may play significant roles in the development of fibrinoid vascular lesions in arterial hypertension.

Animals↗
PubMed1988

Atherosclerosis in rabbits identified as high and low responders to an atherogenic diet and the effect of treatment with a beta 1-blocker.

In order to investigate whether initial plasma lipid concentrations could be used to distinguish between high and low responders to an atherogenic diet, rabbits were divided into 3 groups according to their plasma concentrations of cholesterol and phospholipids after 4 weeks on a standard rabbit diet. Plasma cholesterol and phospholipid levels were less than 0.5 mM, less than 1.1 mM, respectively, in group 1 (n = 17), greater than 0.5 mM, less than 1.1 mM, in group 2 (n = 13), and greater than 0.5 mM, greater than or equal to 1.1 mM, in group 3 (n = 14). After 7 weeks on a diet containing 0.25% cholesterol and 3% coconut oil, animals in groups 1 and 2 had a lower increase in their plasma lipid levels compared with group 3. Half of each group was then treated with the beta 1-adrenoceptor antagonist metoprolol during the next 14 weeks on the atherogenic diet. At the end of the study, the extent of atherosclerosis both in the aortas and in the coronary arteries of the control animals showed a positive correlation to plasma cholesterol and to plasma phospholipid concentrations integrated over time. The metoprolol-treated animals in groups 1 and 2 had a reduction of atherosclerosis compared with their respective controls. We conclude that subpopulations of rabbits that react differently on an atherogenic diet can be identified by their initial plasma lipid levels, and that metoprolol treatment of low responders to an atherogenic diet significantly reduces atherosclerotic lesions of the aorta.

Animals↗
PubMed1988

Influence of antihypertensive treatment on basal cerebral arteries in spontaneously hypertensive rats. A morphometric study.

Spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SHRSP) were treated with a combination of a beta 1-blocker (metoprolol) and a calcium antagonist (felodipine) from 1 to 4 or from 4 to 6 months of age. Basal cerebral arteries were fixed by immersion and embedded in plastic. The ratio between media thickness and luminal radius was determined in cross-sectioned arteries for a standardized condition, assuming a smooth and circular internal elastic membrane. The treatment caused a significant decrease in blood pressure and a normalization of m/r ratios in basal cerebral arteries when initiated in young as well as in adult SHR and SHRSP, i.e. the therapy efficiently prevents as well as reverses hypertensive arterial changes. Even though 4-month-old treated rats were still significantly hypertensive, their m/r ratios did not differ from those of normotensive controls. The latter results may indicate that the treatment affects the vessel walls also through other mechanisms than by decreasing the pressure load.

Animals↗