Biomedical subjects

C Nordborg

Publications and source records attributed to C Nordborg.

At least 91 records · Page 5Linked to original sources

PubMed1988

Middle cerebral artery occlusion in the hypertensive and normotensive rat: a study of histopathology and behaviour.

Brain infarct size and behaviour were studied in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) 3 weeks after occlusion of the right middle cerebral artery in order to compare the effects of vascular occlusions on the normotensive and hypertensive cerebral vasculature. The brain tissue reduction, assessed by measuring the cross-sectional area of remaining tissue and weight of the cerebral hemispheres, was greater in SHR than in WKY (P less than 0.01). Deficits in sensorimotor integration were highly correlated to the degree of brain damage (r = 0.91). Amphetamine induced no rotation asymmetry in normal rats, whereas lesioned rats rotated more ipsilaterally to the lesion (P less than 0.05). Rotation asymmetry did not correlate with total infarct size. The more severe outcome after middle cerebral artery occlusion in SHR as opposed to WKY, can probably be explained by reduced collateral capacity secondary to the altered vascular design in hypertension.

Animals↗

PubMed1987

Morphologic changes in nerve cell bodies induced by experimental graded nerve compression.

The effects of experimental nerve fiber compression on the morphology of nerve cell bodies were studied. Rabbit cervical vagus nerves were crushed or subjected to compression at 0 (sham compression), 30, 200, or 400 mm Hg for 2 h. Morphometric measurements and light microscopical evaluation of the nerve cell bodies in the nodose ganglion were carried out 7 days after the injury on the injured and control sides. Crush and compression at 30, 200, or 400 mm Hg induced a slight decrease in total cell profile area compared with the control side, but it was not related to degree of injury. There was a marked decrease in the ratio between nuclear and total cell profile area (nuclear volume density) after compression at 200 and 400 mm Hg, as well as after crush, and to a lesser extent after compression at 30 mm Hg. Compression at 30, 200, or 400 mm Hg as well as crush of the vagus nerve induced migration of the nucleus to the periphery and dispersion of Nissl substance in the cytoplasm of the nerve cell bodies. Sham compression induced no obvious changes in total cell profile area, nuclear volume density, or migration of nucleus. There was a somewhat increased percentage of cells showing dispersion of Nissl substance in sham-compressed animals than in controls. The results show that nerve fiber compression induced pronounced reactive changes in nerve cell bodies, even at low pressures, corresponding to those found in human carpal tunnel syndrome. Such pressures are known to induce reversible inhibition of fast axonal transport as well as inhibition of retrograde axonal transport. The nerve cell body changes in the nodose ganglion may thus be a reaction to disturbances in axonal transport.

Animals↗

PubMed1987

Hepatic arteries in normotensive and spontaneously hypertensive rats. A morphometric study.

The media thickness (m), luminal radius (r) and m/r ratio were determined in the hepatic arterial trunk and in intra-hepatic arterial branches as was the number of arteries per cm2 sectioned liver tissue in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto controls (WKY). The cross-sectional vessel parameters were calculated for a standardized condition, in which the internal elastic membrane is smooth and circular. Both intra-hepatic arterial branches and the hepatic arterial trunk showed significantly higher m/r ratios in SHR than in WKY controls. The luminal radius of the hepatic arterial trunk was larger in SHR than in WKY (P less than 0.05). The number of arteries per cm2 sectioned liver tissue was greater in SHR (P less than 0.05). It is suggested that the consequences of the increased m/r ratio in hepatic arteries of SHR are counteracted to some extent by an increased vascularization, but that during hypovolaemia and compensatory vasoconstriction, a greater decrease in hepatic arterial blood flow occurs in SHR than in WKY.

Animals↗

PubMed1987

Effects of epidural and intrathecal application of collagenase in the lumbar spine: an experimental study in rabbits.

An experimental model is described in which collagenase in different concentrations and volumes were applied epidurally or intrathecally in the rabbit lumbar spine. This made it possible to study the tissue effects in a situation similar to that of collagenase leaking from a disc or accidental epidural or intrathecal injection at chemonucleolysis. Epidurally applied collagenase, in higher concentration, caused a local thinning of the dura. This effect was reduced at lower concentrations and volumes. Intrathecally injected collagenase, even in small amounts, caused intrathecal hemorrhage and acute paraplegia in the hind limbs. Therefore, in the clinical situation, intrathecal injection of collagenase must be avoided.

Animals↗

PubMed1987

The influence of antihypertensive treatment on the renal 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 Ca++-antagonist (felodipine) from 1 to 4 months or 4 to 6 months of age. The renal arterial trunks as well as more distal parts of the renal arterial bed were fixed by immersion and embedded in plastic. The media cross-sectional area and the length of the internal elastic membrane were measured on cross-sectioned arteries. The media thickness, luminal radius and the ratio between media thickness and luminal radius (m/r ratio) were then calculated for a standardized condition, assuming a smooth and circular internal elastic membrane, in which the arteries were compared. The m/r ratio was markedly reduced in the most proximal as well as in more distal arterial segments of the treated animals when compared with untreated rats of corresponding age and category. The quotient was somewhat reduced also when compared with normotensive controls (WKY) although the systolic blood pressure in younger treated rats was not fully normalized. The results may suggest that the present treatment influences the arterial walls not only by reducing the pressure load but also through pressure-independent mechanisms.

Animals↗

PubMed1986

Functional, morphological and metabolic characteristics of isolated hearts from normotensive and spontaneously hypertensive rats before, during and after renal hypertension.

It has been much discussed whether left ventricular hypertrophy (LVH) in hypertension implies improved or impaired cardiac performance, mainly because experiments in various hypertensive models have given controversial results. It has, for example, been suggested that increased collagen content may depress LV function both in renal and spontaneous hypertension (SHR) in rats. For such reasons cardiac performance was studied both in SHR and in normotensive control rats (NCR) before and during superimposed two-kidney, one clip Goldblatt hypertension, and also 1 week after reversal of hypertension by unclipping. The LV function of the isolated hearts was determined in an antegrade working heart perfusion system. Further, myocardial morphology, with regard to fibrous tissue infiltration and energy metabolic status, were evaluated in the renal hypertensive rats before and after unclipping. Compared with NCR, maximal cardiac performance was elevated in the hypertrophied SHR hearts, but depressed when renal hypertension was superimposed, even though this led to further LVH. However, one week after reversal of renal hypertension, when LVH was still considerable, cardiac function was increased well above the control level, even though the stores of high energy compounds and the content of myocardial fibrous tissue was almost the same as during renal hypertension. It is concluded that LVH generally enhances cardiac performance, but that concomitant renal hypertension exerts a cardio-depressive influence which can neither be ascribed to an increased fibrous tissue content nor to a reduced energy charge potential. It is therefore suggested that some negative inotropic agent of renal or extrarenal origin is released during two-kidney, one clip renal hypertension, which offsets the enhanced performance induced by the left ventricular hypertrophy.

Animals↗

PubMed1986

Does sympathectomy or antihypertensive treatment affect the morphometry of basal cerebral arteries in spontaneously hypertensive rats?

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. Cross sections of plastic embedded basal cerebral arteries were measured with a digitizer. The ratio between media thickness and luminal radius (m/r ratio) could then be calculated for a standardized condition assuming a smooth, circular internal elastic membrane. The treatment caused a significant decrease of the m/r ratio in various basal cerebral arteries of young and adult SHR and SHRSP, i.e. the therapy may prevent as well as reverse hypertensive structural changes. Unilateral superior cervical ganglionectomy or preganglionic denervation did not affect the structure of basal cerebral arteries in young SHRSP or normotensive controls. A slight decrease of m/r ratio was indicated in the smallest pial arteries on the sympathectomized side, but the results did not allow any conclusion as to differences in effect between preganglionic denervation and ganglionectomy.

Age Factors↗

PubMed1986

The spread of brain oedema in hypertensive brain injury.

Severe hypertension in humans may lead to fibrinoid necroses of cerebral blood vessels with small hemorrhages and cystic necroses. Similar lesions have also been reported in the experimental model of stroke-prone spontaneously hypertensive rats (SHRSP). We examined the genesis and spreading pattern of the brain oedema in SHRSP. The extravasation of plasma proteins was visualized with the Evans-Blue or the immunoperoxidase method. Most commonly the leakage occurred in the grey matter of the cerebral cortex or basal ganglia. The spreading pattern followed that of vasogenic brain oedema with a local spread in the grey matter and an extensive one in the white matter. In addition, we detected a novel pathway upwards along the perivascular spaces of the penetrating vessels as well as laterally in the subpial zone. This route is likely to serve also as a drainage channel for the oedema into the cerebrospinal fluid in the subarachnoidal space. Transfer of the extravasated proteins from the white matter to the ventricles was also observed, confirming that this previously described pathway for the resolution of oedema fluid exists in the SHRSP model of vasogenic brain oedema.

Animals↗

PubMed1985

Cerebrovascular lesions in stroke-prone spontaneously hypertensive rats.

The cerebrovascular lesions of severe chronic hypertension were studied by light microscopy in perfusion-fixed, subserially sectioned brains from stroke-prone spontaneously hypertensive rats (SHRSP). The leakage and spread of plasma proteins were visualized by immunohistochemical detection of extravasated fibrinogen and by using an exogenous marker (Evans blue injected i.v.) for blood-brain barrier (BBB) dysfunction. In most SHRSP the hypertension did not lead to major BBB lesions in spite of a mean arterial pressure around 200 mm Hg at 6-9 months of age. Multifocal BBB damage occurred in a minor group of SHRSP, particularly within the cortex and the deep gray matter. A close spatial correlation was found between the leakage-spread of plasma constituents and the neuropathologic alterations. Fibrinoid degeneration of penetrating arterioles was found within the leakage sites. The surrounding gray matter showed petechial hemorrhages and abundant proteinaceous exudates rich in antifibrinogen-positive material. The current leakage of Evans blue and wide spread of fibrinoid substances suggested long-lasting damage to the BBB. Most neurons within the edematous gray matter had well preserved nuclei surrounded by a rim of cytoplasm with ill-defined outline as if vacuolation or lysis of the peripheral cytoplasm had occurred. The sponginess of the tissue progressed in severe cases to formation of necrotic cysts. Condensed acidophilic neurons were seen in the border zone between the edematous and more compact gray matter. The appearance and distribution of the gray matter lesions deviated in many respects from those commonly seen in regional ischemic infarcts. The fibrin thrombi found close to the cysts might be regarded as secondary events. The extensive spread of antifibrinogen-positive material within the white matter seemed to originate mainly from the chronic leakage sites in the gray matter. Increased number of large astrocytes were seen within the leakage sites and along the spreading pathways for the edema constituents. The white matter showed a rarefied texture with widely dispersed nerve fiber tracts, volume expansion, and occasional cyst formation. The results indicate a crucial pathophysiologic role for the egress, spread, and accumulation of vasogenic edema in the development of the cerebrovascular lesions in SHRSP.

Animals↗

PubMed1985

Internal carotid and vertebral arteries of spontaneously hypertensive and normotensive rats. A morphometric study on extracranial, intraosseous and intracranial arterial segments.

Arteries from spontaneously hypertensive rats (SHR) and Wistar Kyoto controls (WKY) were investigated. Specified cross-sections were collected from the extra- and intracranial parts of the internal carotid arteries, from the carotid segment situated in the skull bone and from intra- and extracranial segments of the vertebral arteries. The internal radius, media thickness and ratio between media thickness and internal radius (m/r ratio) were calculated for a standardized condition implying a smooth and circular internal elastic membrane. The m/r ratio was significantly increased in all arterial segments of 7-month-old SHR compared to WKY. This was caused mainly by decrease of radius in the vertebral arteries and in the intracranial carotid segment. In the extracranial and intraosseous carotid segments the increase of m/r ratio in SHR was mainly due to an increase of media. Whereas the radius was the same in the intra-osseous and intracranial carotid segments of WKY, the m/r ratio was greater intracranially. The results suggest that the physical properties of supporting tissues may influence the normal arterial development and modify the influence of an increased arterial pressure on the vessel wall.

Age Factors↗

PubMed1984

Hereditary motor and sensory neuropathy of demyelinating and remyelinating type in children. Ultrastructural and morphometric studies on sural nerve biopsy specimens from ten sporadic cases.

Ten autosomal recessive/sporadic cases of hereditary motor and sensory neuropathy type I (HMSN I), nine of which originated from the northern part of Sweden, were included in the study. Parents were free from neurologic symptoms. Motor and sensory conduction velocity was normal when recorded, i.e., in 19 and 17 parents, respectively. Sural nerve biopsies from the ten cases revealed a varying degree of onion bulb formation. In eight of the cases the onion bulbs consisted of abundant basement membranes, whereas the Schwann cells were few and sometimes lacking. There were in some cases considerable differences between separate fascicles as to the loss of myelinated nerve fibers. In the six biopsies in which teasing was performed signs of present and previous demyelination were noticed. Numerous internodal segments were abnormally thin with reference to their length. In many such segments there were marked local thickenings of the nerve fiber. In cross sections the probable counterparts to these thickenings were nerve fibers with unduly thick myelin sheaths and complex folding of the myelin. Ultrastructural axonal changes were seen in the majority of the cases. The pathogenetic and diagnostic implications of the present findings are discussed.

Adolescent↗

PubMed1984

The hemodynamic effect of bilateral carotid artery ligation and the morphometry of the main communicating circuit in normotensive and spontaneously hypertensive rats.

After reducing the number of patent conduit arteries to the brain by bilateral ligation of the carotid artery, the percentage decrease in blood pressure from the aorta to the internal carotid artery distal to the ligation was larger in spontaneously hypertensive rats than in normotensive rats. The pressure drop corresponded to the degree of hypertension as well as to morphometrically determined structural arterial alteration in the main communicating circuit, i.e. larger media to internal radius ratio and smaller internal radius in the posterior communicating arteries, the proximal part of the posterior cerebral arteries, the basilar artery and the vertebral arteries. The discrepancy between the sum of the luminal cross sectional areas of the communicating circuit and the luminal areas of the ligated conduit arteries was larger in the hypertensive than in the normotensive rats. It is to be expected that occlusion of conduit arteries to the brain will have a larger impact on the cerebral arterial perfusion pressure head in the presence of such hypertensive structural alterations known to increase flow resistance.

Animals↗

PubMed1983

Sural nerve biopsies from workers with a history of chronic exposure to organic solvents and from normal control cases. Morphometric and ultrastructural studies.

An ultrastructural and morphometric study was performed on sural nerve biopsies of four industrial spray painters (35-59 years) and 11 controls (6-64 years). No difference could be shown in spray painters and age-matched controls as to the number of myelinated nerve fibres per area, their size distribution, variation of internodal length along single nerve fibres or the ratio between the number of myelin lamellae and the axon circumference. There was marked scattering of the two latter parameters in older exposed and and control individuals. The distribution of NADH2-tetrazolium reductase activity was similar in exposed and control cases. The general ultrastructural appearance of nodal-paranodal regions in controls conformed with that noted in experimental animals. The overall ultrastructural organization and age-related changes of nerves of exposed cases were similar to those of control cases except for a presence of paranodal axonal mitochondria which contained glycogen-like particles in exposed cases. In one exposed case abundant dispersed or clustered glycogen-like particles were seen in the paranodal axoplasm. These findings are suggested to be an effect of chronic exposure to organic solvent vapours. Ageing seems, however, to have a much greater impact on the morphology of the sural nerve fibre than occupational exposure to organic solvent.

Adult↗

PubMed1983

Morphometric study of mesenteric and renal arteries in spontaneously hypertensive rats.

Arteries from spontaneously hypertensive rats (SHR), stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto controls (WKY) were fixed by immersion and plastic embedded. The media cross-sectional area and the length of the internal elastic membrane were measured. The ratio between media thickness and internal radius was then calculated for a standardized condition, implying a perfectly smooth and circular internal elastic membrane. An increase of the media to radius ratio was already demonstrable in visceral arterial branches of SHR and SHRSP by 15 days of age, indicating that changes of arterial structure could be of pathogenetic importance in early hypertension. At seven months of age the ratio was significantly increased in mesenteric arterial branches of SHR and SHRSP and in renal arterial branches of SHRSP. The media to radius ratio was markedly increased in the renal and superior mesenteric arterial trunks of adult SHR (P less than 0.001 in both) and SHRSP (P less than 0.001 and P less than 0.01). This was due to a greater media cross-sectional area in the former vessels and to a combination of greater media and reduced radius in the latter.

Animals↗

PubMed1982

Influence of amygdala lesions on cardiovascular responses to alerting stimuli, on behaviour and on blood pressure development in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR), and often also humans genetically predisposed to hypertension, exhibit cardiovascular hyperreactivity to alerting stimuli, which derives from limbic-hypothalamic levels and seems important for inducing primary hypertension. It is further known that the limbic amygdala complex normally reinforces emotionally induced defence reactions. The amygdala were therefore bilaterally destroyed in 6 week old SHR, and compared with sham-operated SHR concerning development of hypertension, cardiovascular reactivity to environmental stimuli and explorative behaviour. When related to controls, the arterial pressure elevation was significantly attenuated in the amygdalalesioned SHR, though their pressure was nevertheless raised 40% at 6 months of age. Concerning cardiovascular responsiveness to mild environmental stimuli the groups did not differ; neither concerning explorative behaviour nor in general motor activity. However, the amygdala-lesioned SHR responded decidely less than controls to stressful, fear-inducing stimuli. The amygdala complex may therefore play an important role in aggravating SHR hypertension by reinforcing defence reactions to stressful influences, when such stimuli are at hand. However, according to the present study the amygdala nuclei are not the origin of the centrally determined cardiovascular hyperreactivity, which in SHR seems decisive for inducing hypertension.

Amygdala↗

PubMed1981

Cerebral vessels in spontaneously hypertensive rats.

Cerebral arterial vessels of 15- and 200-day-old spontaneously hypertensive rats and normotensive controls were studied concerning the ratio between media thickness and lumen radius. Media/radius ratio among larger vessels was significantly increased already in 15-day-old spontaneously hypertensive rats. Furthermore, the media cross section area and lumen radius was increased in the internal carotid arteries of these animals. The early vascular aberrations could be caused by the slight increase of blood pressure at this age or be due to other genetically determined mechanisms. In 200-day-old hypertensive rats a significantly increased media/radius ratio was seen in arterial vessels with a radius less than 80 microns when compared to local Wistar controls but only in the smallest arterioles (r less than 20 microns) when compared to Kyoto Wistar controls.

Animals↗

PubMed1981

A new type of non-progressive sensory neuropathy in children with atypical dysautonomia.

Three cases of non-progressive, sensory neuropathy with dysautonomia are presented. Light and electron microscopy on whole sural nerve biopsies revealed an almost total lack of myelinated nerve fibres. The total fibre count was also reduced as was the total number of Schwann cell nuclei. No degenerative phenomena were seen within the nerve fibres. The aberrations are probably caused by a maldevelopment of the neural crest implying a stunted proliferation and growth of sensory and autonomous neurones as well as a reduced proliferation of Schwann cells. Since the morphology and clinical features differ from that in other cases of sensory neuropathy with dysautonomia the three present cases are considered to represent a new type of the disease.

Biopsy↗

PubMed1981

A large convexity meningioma followed by liquorrhoea from a nasal encephalocele. A case report.

A 46-year-old woman was readmitted, two years after removal of a large convexity meningioma, because of cerebrospinal fluid rhinorrhoea from a nasal encephalocele eventually visualized by CT-scan. The encephalocele was extirpated via an intracranial approach, and its histological appearance is described. The aetiology of this extracranial brain tissue protrusion is discussed. It is suggested that the mechanisms behind the formation of this encephalocele are a combination of a congenital malformation and the long term increase of the intracranial pressure due to the meningioma.

Brain Neoplasms↗