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Biomedical subjects

H Kalimo

Publications and source records attributed to H Kalimo.

At least 163 records · Page 9Linked to original sources
PubMed1986

Clinical and muscle biopsy findings in malignant hyperthermia susceptibility.

Patients (155) were investigated for malignant hyperthermia susceptibility (MHS), by in vitro testing of muscle taken from the vastus medialis muscle. Histopathological and histochemical investigation of muscle was also performed. Ultrastructural investigation was performed in 13 MHS patients; 90% of the patients replied to a questionnaire concerning present or previous neuromuscular symptoms. The majority of MHS and MH negative (MHN) patients had no or only minor histopathological and histochemical abnormalities. Core-targetoid fibres were the only potentially important abnormalities found in MHS patients. There were no differences in neuromuscular symptoms between MHS, MHN and control patients, and most patients in both the MHS and MHN group were normal on clinical examination.

Adolescent↗
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

The dentate gyrus in hypoglycemia: pathology implicating excitotoxin-mediated neuronal necrosis.

A detailed light- and electron-microscopic study of the damage to the rat dentate gyrus in hypoglycemia was undertaken, in view of the previously advanced hypothesis that hypoglycemic nerve cell injury is mediated by a released neurotoxin. The distribution of neuronal necrosis showed a relationship to the subarachnoid cisterns. Electron microscopy of the dentate granule cells and their apical dendrites revealed dendrosomal, axon-sparing neuronal pathology. Dentate granule cells were affected first in the dendrites in the outer layer of the stratum moleculare, sparing axons of passage and terminal boutons. Subsequently, the neuronal perikarya were affected, and Wallerian degeneration of axons followed. Cell membrane abnormalities preceded the appearance of mitochondrial flocculent densities and degradation of the cytoskeleton, and are suggested to be early lethal changes. The observed early dendrotoxic changes, and the dendrosomal, axon-sparing nature of the lesion implicate an excitotoxin-mediated neuronal necrosis in hypoglycemia.

Animals↗
PubMed1985

The temporal evolution of hypoglycemic brain damage. I. Light- and electron-microscopic findings in the rat cerebral cortex.

In the course of a study on the pathogenesis of neuronal necrosis in severe hypoglycemia, the morphological characteristics reflecting reversible and irreversible neuronal lesions were examined as a function of time following normalization of blood glucose. To that end, closely spaced time intervals were studied in the rat cerebral cortex before, during, and up to 1 year after standardized pure hypoglycemic insults of 30 and 60 min of cerebral isoelectricity. Both the superficial and deep layers of the cerebral cortex showed dark and light neurons during and several hours after the insult. By electron microscopy (EM) the dark neurons were characterized by marked condensation of both karyoplasm and cytoplasm, with discernible, tightly packed cytoplasmic organelles. The light neurons displayed clustering of normal organelles around the nucleus with clearing of the peripheral cytoplasm. Some cells, both dark neurons and neurons of normal electron density, contained swollen mitochondria with fractured cristae. Light neurons disappeared from the cerebral cortex by 4 h of recovery. Some dark neurons in the superficial cortex and almost all in the deep cortex evolved through transitional forms into normal neurons by 6 h recovery. Another portion of the dark neurons in the superficial cortex became acidophilic between 4 and 12 h, and by EM they demonstrated karyorrhexis with stippled electron-dense chromatin. The plasma membrane was disrupted, the cytoplasm was composed of amorphous granular debris, and the mitochondria contained flocculent densities. These definitive indices of irreversible neuronal damage were seen as early as 4-8 h recovery. Subsequently, the acidophilic neurons were removed from the tissue, and gliosis ensued. Thus, even markedly hyperchromatic "dark" neurons are compatible with survival of the cell, as are neurons with conspicuous mitochondrial swelling. Definite nerve cell death is verified as the appearance of acidophilic neurons at which stage extensive damage to mitochondria is already seen in the form of flocculent densities, and cell membranes are ruptured. Our previous results have shown that hypoglycemic neocortical damage affects the superficial laminae, chiefly layer 2. The present results demonstrate that, following the primary insult, this damage evolves relatively rapidly within the first 4-12 h. We have obtained no evidence that additional necrotic neurons are recruited after longer recovery periods.

Animals↗
PubMed1985

The temporal evolution of hypoglycemic brain damage. II. Light- and electron-microscopic findings in the hippocampal gyrus and subiculum of the rat.

Part I of this paper has documented the evolution of dark neurons into acidophilic neurons in the superficial laminae as well as the reversion of dark neurons to normal neurons in the deep laminae of the cerebral cortex in hypoglycemic brain damage. The present study describes the temporal evolution of hypoglycemic brain damage in the hippocampus. The evolution of dark neurons to acidophilic neurons was confirmed in this brain region. Four additional problems were addressed: Firstly, delayed neuronal death was looked for, and was found to occur in areas of CA1 undergoing mild damage. However, it was not preceded by a morphological free interval, had ultrastructural characteristics distinct from delayed neuronal death in ischemia, and hence should be considered a distinct phenomenon. Secondly, the gradient in the density of neuronal necrosis in the rat hippocampal pyramidal cell band was exploited to test the hypothesis that a more severe insult causes a more rapid evolution of neuronal changes. This was found to be the case, with a temporal spectrum in the timing of neuronal death: Necrosis occurred already after 2 h medially in the subiculum, and was delayed by up to several weeks laterally in CA1. Thirdly, the almost universal sparing of CA3 pyramidal neurons after 30 min hypoglycemic isoelectricity was exploited to address the question of whether reactive changes, which could with certainty be deemed reversible, occur in CA3. Mitochondrial injury was seen in these cells, and was found to be recoverable. No reactive changes of the type previously described following ischemic insults were observed. Fourthly, the astrocytic and vascular response of the tissue was studied. A sequence of astrocytic changes representing structural and probably metabolic activation of astrocytes was seen, consisting of morphological indices of increased turnover of cellular components. Capillaries demonstrated endothelial pits, vesicles, and prominent microvilli hours to days after recovery. The results demonstrate that, in the hippocampal gyrus as in other brain regions, hypoglycemic brain damage is distinct from ischemic brain damage and likely has a different pathogenesis.

Animals↗
PubMed1985

The temporal evolution of hypoglycemic brain damage. III. Light and electron microscopic findings in the rat caudoputamen.

The caudate nucleus and putamen belong to the selectively vulnerable brain regions which incur neuronal damage in clinical and experimental settings of both hypoglycemia and ischemia. We have previously documented the density and distribution of the hypoglycemic damage in rat caudoputamen, but the evolution of the injury, i.e., the sequence of structural changes, has not been assessed. Therefore, in the present study we analyze the light and electron microscopic alterations in the caudoputamen of rats exposed to standardized, pure insults of severe hypoglycemia with isoelectric EEG for 10-60 min, or in rats which, following insults of 30 or 60 min, were allowed to recover for periods from 5 min to 6 months. The hypoglycemic insult produced severe nerve cell injury in the dorsolateral caudoputamen. Immediately after the insult abnormal light neurons with clearing of the peripheral cytoplasm were present. These cells disappeared early in the recovery period, as they do in the cerebral cortex. Dark neurons were also present, but unlike those in the cerebral cortex they did not appear until recovery was instituted. Their number increased for a couple of hours and they became acidophilic within 4-6 h. At this stage, electron microscopy revealed severe clumping of the nuclear chromatin and cytoplasm as well as incipient fragmentation of cell membranes, all these changes indicating an irreversible injury. Within 24 h flocculent densities appeared in the mitochondria and by day 2-3 of recovery the great majority of the medium-sized neurons had undergone karyorrhexis and cytorrhexis, their remnants being subsequently removed by macrophages. After some weeks only large and a few medium-sized neurons remained amidst reactive astrocytes and numerous macrophages. The delay in the appearance of dark, lethally injured medium-sized neurons until the recovery was instituted suggests an effect that does not become apparent until the substrate supply and energy production are restored. Furthermore, it points out again the selectivity of the hypoglycemic nerve cell injury with respect to the type (metabolic characteristics?) and topographic location of the neurons.

Animals↗
PubMed1985

Changes in the integrity of the blood-brain barrier in suckling rats with low dose lead encephalopathy.

Previous studies on the toxic effects of lead on the brains of young animals have shown damage to the blood-brain barrier (BBB) which in severe forms appears as hemorrhagic encephalopathy. In those studies the doses of lead have been of such magnitude that lead-induced anorexia resulting in growth retardation has contributed to the extent of the injury (Sundström et al. 1984). The growth retardation can be prevented by using low lead doses (Sundström et al. 1983). Consequently, we have examined to which extent the BBB is injured in suckling rats with low dose lead encephalopathy. This was done by testing the permeability of the BBB to plasma proteins and assessing the possible occurrence of vasogenic edema by measuring the specific gravity of brain tissue. Low dose lead encephalopathy was induced by daily i.p. injections of lead nitrate 10 mg/kg body weight (b.wt.) for the first 15 days. The lead contents of the blood and homogenates of the cerebrum and cerebellum were assayed by atomic absorption spectrophotometry. The brains were examined at 15, 20, or 30 days of age. When Evans blue-albumin (EBA) was injected i.v. 2 h before killing, most 15-day-old rats exposed to lead displayed a bluish discoloration in their cerebellum. Microscopically, red fluorescence of EBA was seen in the blue-stained regions. Immunohistochemically, extravasation of albumin, fibrinogen, and fibronectin was demonstrated as positive staining in the cerebellar cortex, with diffuse spread to the white matter of the corresponding folium.(ABSTRACT TRUNCATED AT 250 WORDS)

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

Characterization of the perivascular reticulin network in a case of primary brain lymphoma. Immunohistochemical demonstration of collagen types I, III, IV, and V; laminin; and fibronectin.

The character of the silver positive reticulin network was analyzed with immunofluorescence and immunoperoxidase methods in an intra vitam diagnosed case of primary brain lymphoma. The network was shown to contain connective tissue proteins rich in hexose-sugars, such as type III collagen (classical "reticulin"), basal lamina constituents type IV collagen and laminin, pericellular type V collagen, as well as fibronectin (protein involved in cell adhesion). On the other hand, very little of the fibrous type I collagen was discernible. Similarly as the silver positive network, the immunohistochemically demonstrable reticulum seemed to hold the cells in the perivascular location, and once it was broken diffuse spread into the tissue occurred. Since malignant cells of B-lymphocyte origin are not known to synthesize so-called reticulin, it is suggested that the network in primary brain lymphomas is produced by cells in the brain parenchyma (possibly pericytes or astrocytes) as a protective attempt to restrict the spread of foreign cells into the brain.

Brain↗
PubMed1985

Amino acid and protein metabolism in dorsal root ganglia of rabbits with experimental allergic neuritis.

Amino acid and protein metabolism has been studied in the dorsal root ganglia of rabbits with experimental allergic neuritis (EAN). The concentrations of a number of nonessential amino acids (glutamine, serine, aspartate, and glutamate) were reduced in the spinal ganglia of EAN animals without any comparable change in the blood plasma. The short-term influx of glycine and GABA was decreased in EAN animals, whereas that of histidine and valine was not altered. The prolonged accumulation of all the four amino acids was unchanged. These results suggest alterations in the cell metabolism of the dorsal root ganglia, rather than unspecific changes in cellular permeability. Furthermore, incorporation of tritiated valine, histidine, and glycine into proteins of EAN-ganglia in vitro was significantly increased. Autoradiography of the protein-bound [3H]-valine indicated alterations in the protein synthesis of the ganglion neurons: A decreased grain density was found in ganglion neurons of EAN animals. The increased grain densities in the affected ganglia were observed in macrophages, and possible in activated Schwann cells, over the demyelinated spots. The results suggest intraneuronal changes in the dorsal root ganglia of amino acid and protein metabolism, possibly in response to peripheral axonal injury and/or to nonspecific cytotoxic effect of active lymphocytes and macrophages.

Amino Acids↗
PubMed1984

Altered muscle saccharide pattern in X-linked muscular dystrophy.

Five lectins were used as fluorescence microscopic markers for sugar residues in skeletal muscle. Biopsy specimens were taken from patients with X-linked muscular dystrophy (Duchenne's and Becker's), patients with other neuromuscular diseases, and normal controls. In both the controls and the pathologic samples, concanavalin A gave a bright fluorescence of the myofiber surface, whereas soybean agglutinin and Dolichos biflorus agglutinin fluorescence was negative. Peanut agglutinin and wheat germ agglutinin were more avidly bound to the sarcolemma and/or endomysial connective tissue in the patients with X-linked muscular dystrophy than in the controls or the patients with other conditions. The altered saccharide pattern may reflect either a myofiber membrane change or a specific mesenchymal reaction in the dystrophic muscle.

Adolescent↗
PubMed1984

Metabolic, circulatory, and structural alterations in the rat brain induced by sustained pentylenetetrazole seizures.

Previous studies have demonstrated that bicuculline-induced seizures of 1-2 h in duration lead to structural, metabolic, and circulatory alterations in the rat brain. Such alterations were observed even though cerebral oxygenation seemed adequate. In the present study, we explored whether pentylenetetrazole, a convulsant which interferes with gamma-aminobutyric acid inhibition by mechanisms other than that of bicuculline, leads to similar structural alterations and to similar cerebral metabolic and circulatory changes. The drug was given to paralyzed and artificially ventilated rats in a dose of 100 mg/kg i.v., and seizures were allowed to continue for 1-120 min. The onset of seizures was accompanied by a small perturbation of cerebral cortical energy state, but sustained changes were confined to decreases in phosphocreatine, glycogen, and glucose and increases in lactate, pyruvate, and cyclic nucleotides. A sustained increase in free fatty acid concentration was observed, with the largest change occurring in arachidonic acid concentration. In the cerebellum, metabolic perturbation was clearly less pronounced, but cyclic nucleotide concentrations rose substantially. Local cerebral blood flow increased in all but two structures (frontal cortex and caudoputamen), but pronounced interstructural changes occurred. Nerve cell changes and astrocytic swelling were observed in the cerebral cortex. There was marked status spongiosus due to edema, which was mainly astrocytic and most prominent in cortical layer 3 and in parts of hippocampus. Nerve cell changes were of two basic types. The type 1 injured neurons, condensed and triangular in shape, were mainly confined to the edematous areas. Many of them had cytoplasmic vacuoles which on electron microscopy proved to be mainly dilated Golgi cisternae or mitochondria. As compared with bicuculline-induced epilepsy such abnormal mitochondria appeared to be more frequent. The type 2 neurons had slit-formed intracytoplasmic and perinuclear vacuoles resulting from dilatation of the endoplasmic reticulum cisternae and the nuclear envelope. The cerebellum looked normal by light microscopy. We conclude that, in the rat, sustained seizure activity induced by pentylenetetrazole is accompanied by alterations in EEG activity, in cerebral metabolism and circulation, and in cell structure similar to those elicited by bicuculline.

Animals↗
PubMed1984

Morphology and function of the parietal cells after proximal selective vagotomy in duodenal ulcer patients.

The effects of proximal selective vagotomy (PSV) on parietal cell morphology and the degree of gastric inflammation were investigated and correlated with changes in gastric acid secretion and serum gastrin concentrations in 17 duodenal ulcer patients. Endoscopy, acid secretion tests, and blood sampling were performed preoperatively and 2 months, 1 year, and 3 years postoperatively. The mucosal biopsy specimens obtained at endoscopy were analyzed both light- and electron-microscopically. Five healthy persons also underwent gastroscopy and biopsy for comparison. Preoperatively, the duodenal ulcer patients differed significantly from this control group, 33% of whose parietal cells appeared 'secretory'; the corresponding figure for the duodenal ulcer patients was 47%. Two months after the operation the number of secretory parietal cells had fallen to 30%, after which the percentage increased slightly again to 35% 3 years after PSV. A similar phenomenon was observed in the acid secretion capacities, which were maximally depressed 2 months postoperatively and recovered slightly but significantly during the 3-year follow-up period. There was a significant increase in the degree of gastric inflammation after the operation.

Adult↗
PubMed1983

Bicuculline-induced epileptic brain injury. Transient and persistent cell changes in rat cerebral cortex in the early recovery period.

It was earlier shown that bicuculline-induced status epilepticus gives rise to profound acute changes in the rat cerebral cortex, i.e. edema and neuronal alterations. In the present study, we explored to what extent interruption of the seizure activity reverses the changes observed. To that end, status epilepticus of 1 and 2h duration was induced by bicuculline before the seizures were arrested by i.v. injection of diazepam. The brain was then fixed by vascular perfusion either 5 min (1 h of seizures) or 2h (1 and 2h of seizures) of recovery and cerebral cortical tissue was studied by light (LM) and electron microscopy (EM). Already 5 min following the arrest of seizure activity most of the astrocytic edema had disappeared, and the 2h of recovery, following 1 h of status epilepticus, the edema was virtually absent, and only few injured cells were found (only about 1% of the neuronal population). When recovery was instituted after 2 h of status epilepticus, numerous dark, triangular neurons were found. In the last group an adequate blood pressure could not be obtained. Therefore, the cellular alterations observed were probably not the result of the seizure activity per se. After 5 min of recovery, Em studies showed condensed, dark-staining injured neurons, similar to those previously observed in non-recovery animals. However, an increased incidence of swollen mitochondria was observed. After 2 h of recovery a few severely injured neurons remained which showed signs of progressive injury with fragmentation of the cell body.

Animals↗