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Biomedical subjects

H Kalimo

Publications and source records attributed to H Kalimo.

At least 199 records · Page 11Linked to original sources
PubMed1983

Cholinesterase activities in the somatic nervous system of rabbits with experimental allergic neuritis.

The allergic inflammatory disorders of the nervous tissue are associated with a complex series of cellular and humoral immune activities and they usually result at least in demyelination, but according to morphologic evidence also in secondary neuronal changes. Using the colorimetric method of Ellman et al. (G. L. Ellman, K. D. Courtney, V. Anders, and R. M. Featherstone, 1961, Biochem. Pharmacol. 7:88-95) the activities of enzymes splitting acetylthiocholine iodide (AThCh) were determined from various parts of the somatic nervous system of rabbits with experimental allergic neuritis (EAN), a primary demyelinating disease of the peripheral nerves. It was found that the total activity of AThCh-splitting enzymes was decreased already in an early phase of the disease in the dorsal root ganglia (DRG). In a well developed phase of the disease the activity of acetylcholinesterase (AChE) seemed to be decreased by 33% in the ventral roots and by a lesser amount in the DRG and the most proximal part of the sciatic nerves. The mechanism of the recorded changes may be related either to specific or to nonspecific immune events or to both. Proteolytic activity released by macrophages in the target tissue may, by inactivating the hydrolytic activity of AChE, at least partly explain these findings. Because the activity of AChE in the structures studied derives from a neuronal origin, our results provide biochemical evidence for the involvement of neurons in the sensory ganglia and of axolemma in the ventral roots in EAN.

Acetylthiocholine↗
PubMed1982

Involvement of autonomic nervous system in experimental allergic neuritis. A light- and electron-microscopic study.

The affection of the sympathetic and parasympathetic structures of the peripheral nervous system in rabbits with experimental allergic neuritis (EAN) was demonstrated light- and electron-microscopically. The general characteristics of the microscopic findings were qualitatively similar to those previously established in the somatic nervous system, but they were less extensive. The neuronal perikarya and the axons in the autonomic nervous system (ANS) were mostly normal. Occasionally, cytoplasmic vacuoles in a few nodose ganglion neurons and some degenerating axons were seen. Other than myelin derived antigens could be operating in whole-nerve induced EAN, since inflammatory cells also infiltrated target tissue areas devoid of myelinated nerve fibers. The presence of numerous plasma cells in the target tissue suggests that local antibody formation may contribute to the destructive process. Our results establish that the ANS is frequently affected in EAN, especially in the more severe forms. Thus EAN was proved to be also in this respect a useful model for the human disease Guillain-Barré syndrome, which likewise is often complicated by autonomic dysfunctions.

Animals↗
PubMed1981

The role of lactic acidosis in the ischemic nerve cell injury.

Severe incomplete cerebral ischemia of 30 min duration with CBF below 5% of normal was induced in rats by clamping both carotids and lowering BP. One group of rats were fasting (f-rats), while the other was infused with glucose before induction of the ischemia (g-rats). In f-rats the lactate accumulating in the cerebral cortex was about 15 mumol . g-1, whereas in g-rats it rose to about 35 mumol . g-1. In f-rats considerable recovery of the energy state and electrical activity occurred during recirculation, whereas in g-rats the energy failure persisted with no electrical activity reappearing. In f-rats the structural alterations were of minor severity, but in g-rats extensive progressive tissue damage was seen. The data indicate that the degree of tissue lactic acidosis has pronounced effects on the development of irreversible ischemic nerve cells injury.

Animals↗
PubMed1981

Pathogenesis of brain lesions caused by experimental epilepsy. Light- and electron-microscopic changes in the rat cerebral cortex following bicuculline-induced status epilepticus.

Status epilepticus was induced in rats by the GABA receptor blocking agent, bicuculline, during artificial ventilation and with closely monitored physiologic parameters. After 1 or 2 h of status epilepticus the brains were fixed by perfusion with glutaraldehyde and processed for light and electron microscopy. In the cerebral cortex two different types of changes were present, i.e., nerve cell injuries and status spongiosus. Type 1 injured neurons, mainly in the areas of most marked sponginess (layer 3), displayed progressive condensation of both karyo-and cytoplasm. In the most advanced stages the nucleus could no longer be distinguished from the cytoplasm in the light microscope, and vacuoles of apparent Golgi cisterna origin appeared in the darkly stained cytoplasm. This type of injured neurons comprised 41 and 56% of the cortical neurons after 1 or 2 h of status epilepticus, respectively. Seven to 9% of the neurons showed another type of injury (type 2). They were mainly located in the deeper cortical layers, and showed slit-formed cytoplasmic vacuoles chiefly due to swelling of the endoplasmic reticulum including the nuclear envelope. Marked sponginess of the cortex developed principally in layer 3 and it spread into deeper layers with longer duration of status epilepticus, but the outermost layers retained a compact structure. As judged by electron microscopy, the sponginess resulted mainly from swelling of astrocytes and their processes causing both perivascular and perineuronal vacuolation. The structural changes observed are considered to be caused by astrocytic and to a lesser extent intraneuronal edema related to the seizure activity. Although the exact pathogenetic mechanisms are not known, our findings indicate that hypoxia-ischemia is not a major determinant of the tissue damage observed.

Animals↗
PubMed1981

Brain lactic acidosis and ischemic cell damage: 2. Histopathology.

The influence of severe tissue lactic acidosis during incomplete brain ischemia (30 min) on cortex morphology was studied in fasted rats. Production of lactate in the ischemic tissue was varied by preischemic infusions (i.v.) of either a saline or a glucose solution. The brains were fixed by perfusion with glutaraldehyde at 0, 5, or 90 min of recirculation. In saline-infused animals (tissue lactate about 15 mumol g-1), changes observed at 0 and 5 min of recirculation were strikingly discrete: slight condensation of nuclear chromatin, mild to moderate mitochondrial swelling, and only slight astrocyte edema. These changes had virtually disappeared after 90 min recirculation and, at this time, only discrete ribosomal changes were observed. In contrast, glucose-infused rats (tissue lactate about 35 mumol g-1) showed severe changes: marked clumping of nuclear chromatin and cell sap in all cells was already evident at 0 and 5 min recirculation, while mitochondrial swelling was mild to moderate. Although tissue fixation was inadequate at 90 min, the ultrastructural appearance indicated extensive damage. It is concluded that excessive tissue lactic acidosis during brain ischemia exaggerates structural alterations and leads to irreversible cellular damage. A tentative explanation is offered for the paucity (less than 0.2%) of condensed neurons with grossly swollen mitochondria, previously considered a hallmark of ischemic cell injury.

Acidosis↗
PubMed1981

Hypoglycemic brain injury: metabolic and structural findings in rat cerebellar cortex during profound insulin-induced hypoglycemia and in the recovery period following glucose administration.

Previous results have shown that severe, prolonged hypoglycemia leads to neuronal cell damage in, among other structures, the cerebral cortex and the hippocampus but not the cerebellum. In order to study whether or not this sparing of cerebellar cells is due to preservation of cerebellar energy stores, hypoglycemia of sufficient severity to abolish spontaneous EEG activity was induced for 30 and 60 min. At the end of these periods of hypoglycemia, as well as after a 30 min recovery period, cerebellar tissue was sampled for biochemical analyses or for histopathological analyses or for histopathological analyses by means of light and electron microscopy. After 30 min of hypoglycemia. the cerebellar energy state, defined in terms of the phosphocreatine, ATP, ADP, and AMP concentrations, was better preserved than in the cerebral cortex. After 60 min, gross deterioration of cerebellar energy state was observed in the majority of animals, and analyses of carbohydrate metabolites and amino acids demonstrated extensive consumption of endogenous substrates. In spite of this metabolic disturbance, histopathologic alterations were surprisingly discrete. After 30 min, no clear structural changes were observed. After 60 min, only small neurons in the molecular layer (basket cells) were affected, while Purkinje cells and granule cells showed few signs of damage. The results support our previous conclusion that the pathogenesis of cell damage in hypoglycemia is different from that in hypoxia-ischemia and indicate that other mechanisms than energy failure must contribute to neuronal cell damage in the brain.

Adenosine Diphosphate↗
PubMed1980

Effects of severe hypoglycemia on the human brain. Neuropathological case reports.

The neuropathological findings in two cases of irreversible hypoglycemic brain injury are described. A 26-year-old diabetic man injected insulin without adequate food intake and died after 2 months in coma. An 84-year-old nondiabetic man accidentally received 10 mg of glibenclamide and died after 3 months in relatively superficial coma. In the first case, an extensive necrotizing injury with gliosis was present in the cerebral cortex with temporal preponderance, as well as in the amygdalae and hippocampus. Lesions were also present in the putamen and caudate nucleus whereas the globus pallidus and thalamus were less severely destroyed. The distribution of the lesions was therefore somewhat different from that commonly seen in hypoxic-ischemic brain injury, which, together with some previously published data, suggests some difference in the pathogenesis of hypoglycemic vs. hypoxic-ischemic brain injury. In the second case only a slight loss of cortical neurons with secondary gliosis could be attributed to the hypoglycemic insult. This case demonstrates the danger of accidental intake of sulfonylurea preparations, which can cause an irreversible brain injury due to their prolonged hypoglycemic effect.

Adult↗