Biomedical subjects

H Kalimo

Publications and source records attributed to H Kalimo.

223 records · Page 13Linked to original sources

PubMedDate not supplied

The early ultrastructural alterations in the rabbit cerebral and cerebellar cortex after compression ischaemia.

The ultrastructural alterations in the rabbit cerebral and cerebellar cortex resulting from 30 minutes complete, permanent cerebral ischaemia were studied. The ischaemia was induced by raising the intracranial pressure (ICP) above the systolic arterial pressure (compression ischaemia). Immediately after releasing the ICP the brain was fixed by intravascular glutaraldehyde perfusion. Samples from the cerebral and cerebellar cortex were processed for electron microscopy. The ultrastructural changes were relatively minor; there was a generalised, slight intracellular oedema, most prominent in the subpial area; the nuclear chromatin was clumped, the endoplasmic reticulum and cisternae of the golgi apparatus became somewhat dilated, the inner matrix of the slightly swollen mitochondria showed increased electron lucency, and microtubules and ribosomes began to loose their compact structure. These changes, unaccompanied by any extensive volumetric change of any cellular compartment, agree well with the recently presented hypothesis of two different types of anoxic-ischaemic nerve cell injury. This cellular reaction to complete, permanent compression ischaemia represents the type of injury that is seen resulting from ischaemic insults during which no flow of fluid irrigates the ischaemically injured cells.

Animals↗

PubMedDate not supplied

Significance of fluid flow for morphology of acute hypoxic-ischaemic brain cell injury.

It has been suggested that the presence or absence of hypoxic fluid flow during ischaemia determines the structural character of the ischaemic nerve cell injury. It is hypothesised that if a flow of fluid irrigates the injured neurons, there will be major shifts of ions and water, with consequent volumetric changes in the tissue and the 'dark' type of neuronal injury will result; otherwise, the structural changes are less striking and are designated as the 'pale' type. To test this hypothesis, rats were subjected to a global cerebral insult by filling the vasculature with a plasma substitute, which was either left stagnant or was flowing, and was either oxygenated (hypoxic flow) or nitrogenated (anoxic flow). Light and electron microscopy of the brain following 10 to 60 min of hypoxic or anoxic ischaemia disclosed that, under all three circumstances, the predominant nerve cell injury was of the pale type. The results indicate that some additional factors present in whole blood (but not in the plasma substitute) are needed during or after the insult to induce in quantity the dark type of ischaemic nerve cell injury.

Acute Disease↗

PubMedDate not supplied

Acetylcholinesterase activity and its fast axonal transport in rabbit sciatic nerves during the recovery phase of experimental allergic neuritis.

Acetylcholinesterase (AChE) activity and its fast axonal transport were studied in rabbit sciatic nerves with a double ligature system during the recovery phase of experimental allergic neuritis (EAN), 6-9 days after the maximal symptoms, in order to obtain biochemical evidence of possible axonal damage in this primary demyelinating disease. The stationary AChE activity was significantly decreased, but the amount of the fast transported enzyme activity remained at the level of the controls. The velocity of the orthograde transport of AChE was slowed by about 15%, but this decrease was not statistically significant. Our results lend further support for the suggested neuronal damage in EAN, which can provide an explanation to the finding that the clinical symptoms in demyelinating diseases of the peripheral nervous system do not always correlate with the state of myelin.

Acetylcholinesterase↗

PubMedDate not supplied

Structural changes in the rat brain after carotid infusions of hyperosmolar solutions: a light microscopic and immunohistochemical study.

A solution of mannitol or urea was infused into the carotid artery of rats to open the blood-brain barrier (BBB) and to find out if such a procedure results in brain injury. Paraformaldehyde-fixed, paraffin-embedded material was available to determine the localization and extent of albumin extravasation by immunochemistry. Other light microscopic and immunocytochemical techniques were applied on consecutive sections to find out if structural damage had occurred. The cerebral cortex, the hippocampus and the basal ganglia of the infused brain hemisphere contained within regions of albumin extravasation scattered, collapsed, acidophilic neurons. In addition, there were multifocal lesions with marked sponginess of the neuropil which contained numerous shrunken, acidophilic neurons and a perifocal astrocytic gliosis. A moderate macrophage infiltration was present in rats with 72 h survival. In conclusion, infusion of hypertonic mannitol or urea into the carotid artery of the rat may result in structural brain damage within regions showing BBB injury. The presence of acidophilic neurons and the macrophage response indicate that some of the brain changes are irreversible.

Albumins↗

PubMedDate not supplied

Parenchymal changes related to plasma protein extravasation in experimental seizures.

To determine whether the transient opening of the blood-brain barrier (BBB) during epileptic seizures may lead to permanent neuronal changes, seizures of a few minutes' duration were induced by intravenous (i.v.) administration of 0.3 mg/kg bicuculline to conscious rats with indwelling catheters for blood pressure (BP) and blood gas monitoring. The rats were killed 5 min to 7 days later, and the distribution of endogenous plasma albumin, fibrinogen, and fibronectin in the brain was studied by immunohistochemistry. Parallel sections were scrutinized for evidence of light-microscopic structural changes in the tissue. Extensive multifocal extravasation of plasma proteins throughout the brain and brainstem was observed. The original clearly focal distribution became more diffuse with prolongation of the recovery time. In addition, the intensity of the immunoreactivity decreased, most likely due to drainage into the cerebrospinal fluid (CSF) in the ventricles and the subarachnoidal space of the extravasated proteins, but some antialbumin-positive material was still visible after 7 days. In areas with extravasation, many nerve cells, especially cerebellar Purkinje cells, became strongly positive for albumin. In some of these areas, neurons appeared to be irreversibly injured. Thus, considerable amounts of plasma proteins are extravasated even during short epileptic seizures, and albumin appear to remain in the tissue for a long time, especially in Purkinje cells. The Purkinje cell loss in chronic epilepsy may be caused partly by cumulative bouts of plasma extravasations.

Animals↗

PubMedDate not supplied

Effects of nonsteroidal antiinflammatory medication on satellite cell proliferation during muscle regeneration.

Previous experimental studies have indicated delayed muscle regeneration after nonsteroidal antiinflammatory drug therapy. Successful regeneration of muscle after injury requires activation of normally dormant satellite cells that share the basal laminae with adjacent muscle cells. In the presence of adequate capillary ingrowth, satellite cells proliferate into myotubes and eventually form new muscle cells. In this study, the onset and extent of satellite cell and fibroblast proliferation as well as the production of myotubes and capillaries were analyzed with immunohistochemical methods after contusion injuries to rats' gastrocnemius muscles. Two groups of animals received daily doses of an intramuscular nonsteroidal antiinflammatory drug (naproxen) starting 6 hours and 3 days after injury, respectively. Treated animals were compared with similarly injured untreated animals. Satellite cell and fibroblast proliferation were unaffected by the treatment, and there were no significant differences in myotube or capillary production between treated and control animals. We conclude that naproxen treatment does not compromise the basic process of myofiber regeneration after injury.

Animals↗

PubMedDate not supplied

Effects of therapeutic ultrasound on the regeneration of skeletal myofibers after experimental muscle injury.

Therapeutic ultrasound is used by many in the treatment of muscle injuries, but no previous attempts to objectively assess its effects on regenerating skeletal myofibers have been published. In this descriptive study, we followed the regeneration of contusion injury to the rat gastrocnemius muscle during treatment with pulsed ultrasound. The speed of myoregeneration in ultrasound-treated animals was compared with that in control animals by immunohistochemical, morphometric, and scintigraphic analyses. Although satellite cell proliferation was enhanced significantly (up to 96%) by the ultrasound treatment during the early stages of regeneration, there was no such effect on myotube production. The period of rapid fibroblast proliferation was extended from 3 to 4 days in the control group to 7 to 10 days in the ultrasound therapy groups, whereas recapillarization was virtually unaffected. We conclude that although treatment with pulsed ultrasound can promote the satellite cell proliferation phase of the myoregeneration, it does not seem to have significant effects on the overall morphological manifestations of muscle regeneration.

Animals↗