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I Klatzo

Publications and source records attributed to I Klatzo.

At least 55 records · Page 3Linked to original sources
PubMed1984

Specific gravity increases and brain water content decreases during short epileptiform seizures in discrete rabbit brain areas.

In rabbits subjected to bicuculline (BC)- or pentylenetetrazole (PTZ)-seizures of 3 or 20 min duration or to adrenaline-induced hypertension, specific gravity (SG) was measured bilaterally in 15 regional brain areas in order to detect possible associations between the regionally limited blood-brain barrier openings due to these insults (see Nitsch and Klatzo 1983) and the presence of brain edema. In controls, a large variation between regional SG levels became evident: between 1.0467 in cerebellum and 1.0417 in preoptic area. A seizure duration of only 3 min was not sufficient to change SG significantly. After 20 min of seizures independent from the inducing agent, SG increased in all brain areas. The degree of increase seemed to be unrelated to presence or absence of a blood-brain barrier opening. In an attempt to avoid the influence of blood impregnation on the SG value, blood was replaced by saline before measurement. In controls, saline perfusion decreased SG only in the two areas with the highest original levels, thus documenting the partial dependency of the regional SG on the hematisation of the tissue. After 20 min of PTZ-induced seizures, SG in saline-perfused rabbits increased, but no longer significantly in all brain areas. This suggests that a part of the seizure-induced SG increase can be attributed to the hyperemia of the brain during the convulsions. On the other hand, an increase in flow volume due to hypertension did not change SG with the exception of the septum, preoptic area and hypothalamus. The direct measurement of water content with the classical wet/dry method in 4 gross brain areas showed that early seizure periods are in fact associated with a dehydration of the brain. This phenomenon could be explained by a glucose- and lactate-induced rise in blood osmolarity which in turn might cause a dehydration of the brain tissue.

Animals↗
PubMed1984

Regional changes in cerebral blood flow and blood-brain barrier permeability during epileptiform seizures and in acute hypertension in rabbits.

Interrelationship between the breakdown of the blood-brain barrier (BBB) to Evans blue and elevations in the regional cerebral blood flow (rCBF) was studied in rabbits subjected to adrenaline- or metaraminol-induced systemic hypertension and also in bicuculline-induced seizures. The rCBF was assessed in small samples from various regions of the brain with the use of [3H]nicotine, and the permeability of the BBB was evaluated with an Evans blue tracer. In acute hypertension, Evans blue extravasations were observed in the occipital cortex and sometimes in the superior colliculus, i.e., the regions which also showed the highest elevations in rCBF. The breakdown of the BBB in acute hypertension was clearly related to the rate of mean arterial blood pressure rise, being much less pronounced in the metaraminol group, which showed a much slower blood pressure elevation rate. In bicuculline-induced seizures, there was no evident correlation between the amplitude of rCBF elevations and Evans blue extravasations. Preservation of BBB integrity was observed in areas showing high elevations in the rCBF.

Acute Disease↗
PubMed1983

Disturbances of the blood-brain barrier in cerebrovascular disorders.

The disturbances of the BBB in cerebrovascular disorders may affect adversely an underlying basic pathological condition. Breakdown of the barrier associated with extravasation of serum proteins leads to development of vasogenic edema in the brain tissue. An abnormal passage of pharmacologically active substances, such as biogenic amines, may significantly affect cerebral blood flow and metabolism and activate neurons equipped with receptors for these substances. Also, a barrier dysfunction related to faulty out-transport of metabolites may contribute to edema and tissue damage. In cerebral ischemia, following release of arterial occlusion there can be two separate openings of the barrier: the first - occurring promptly after recirculation and related to ensuing reactive hyperemia, the second - after some delay and related to pathological changes in the brain tissue. In some circumstances, such as epileptic seizures, both "hemodynamic" and "tissue" factors may be operative at the same time. The selective features of BBB changes are related to multiplicity of barrier systems residing in cerebral endothelium. These selective features are demonstrable during development and during reversibility of postichemic barrier disturbances. Intermittent openings of the barrier observed in chronic hypertension may lead to accumulation of extravasated serum proteins and be responsible for frequently observed edematous changes in this condition.

Animals↗
PubMed1983

The effects of 5-minute ischemia in Mongolian gerbils: I. Blood-brain barrier, cerebral blood flow, and local cerebral glucose utilization changes.

Changes in morphology, behavior of the blood-brain barrier (BBB), regional cerebral blood flow (rCBF), and local cerebral glucose utilization (LCGU) were assessed and correlated in Mongolian gerbils following 5 min cerebral ischemia, produced by bilateral clamping of the common carotid arteries. The morphological changes were confined to the hippocampus and revealed a conspicuously delayed destruction of the CA1 neurons, occurring after 3 days. Following release of carotid occlusions, there were two separate openings of the BBB. One, occurring shortly after recirculation, was associated with focal hyperemia in the cerebral cortex, hippocampus and basal ganglia; the second opening was observed after several days and was associated with severe neuronal destruction in the CA1 sector. Correlation of quantitative and qualitative rCBF assays with 14C-deoxyglucose autoradiographic observations indicated an uncoupling between blood flow and glucose metabolism, observed in the hippocampus at 10 min after recirculation. The described changes provide a further insight into the post-ischemic events which determine the outcome of ischemic injury.

Animals↗
PubMed1983

The effects of 5-minute ischemia in Mongolian gerbils: II. Changes of spontaneous neuronal activity in cerebral cortex and CA1 sector of hippocampus.

Spontaneous neuronal activity was recorded in the cerebral cortex and the CA1 sector of the hippocampus in gerbils during and after 5-min ischemia, produced by bilateral clamping of the common carotid arteries. It was found that spontaneous activity in both cortical and CA1 neurons ceased within 60s after the onset of ischemia and that it began to reappear 10-20 min after the recirculation. During the next 24 h most CA1 neurons which were recorded showed hyperactivity. This was evident primarily by an increase in spike discharges, whereas recordings from the cerebral cortex were within the preocclusion ranges. On the 2nd day after ischemia, functioning CA1 neurons could not be found, as if they were in a state of functional death, although histological sections showed a general preservation of their cellular structure at that time.

Animals↗
PubMed1983

Regional patterns of blood-brain barrier breakdown during epileptiform seizures induced by various convulsive agents.

In unrestrained rabbits with generalized epileptic seizures induced by systemic application of convulsant drugs, regional changes in blood-brain barrier (BBB) permeability to macromolecules were investigated using Evans Blue (EB) as indicator. BBB leakage due to seizures was present only in animals in which the mean arterial blood pressure rose about 50 mm Hg with the onset of convulsive motor activity. However, a blood pressure increase was not necessarily associated with the occurrence of BBB opening. Pentylenetetrazole-induced seizures resulted in bilateral EB leakage mainly in the hypothalamus, with exception of the mammillary bodies, and the preoptic area, and they were associated, in most cases, with an intensive staining of the cerebellum and also of the midbrain tegmentum. In contrast, seizures due to the GABA receptor blocker bicuculline brought about a penetration of the dye in the region of the pallidum, whereas the GABA synthesis inhibitor methoxypyridoxine produced BBB breakdown in the hippocampus. Methionine-sulfoximine convulsions resulted in a selective stain of the corpora mammillaria, and kainic acid induced a diffuse leakage in neocortical brain areas. As a rule, BBB breakdown was bilateral and confined to anatomically limited brain areas, suggesting that BBB integrity was not only disturbed by abrupt increases in the intraluminal pressure, but was also influenced from the brain tissue. The fluorescence microscopic observations revealed that the tracer penetrated into the neuropil through larger vessels. It had the tendency to accumulate in neurons. In case of the hippocampus, CA2 pyramidal cells revealed more intense uptake of EB than those of the adjacent fields.

Animals↗
PubMed1981

Evaluation of the dye-protein tracers in pathophysiology of the blood-brain barrier.

1. Sodium fluorescein and Evans Blue, commonly used tracers in the study of blood-brain barrier disturbances, revealed considerable differences in their respective protein binding capacity in the plasma, passage through the barrier and in the rate of their elimination from the brain parenchyma. 2. In the plasma a considerable portion of the sodium fluorescein remains free and behaves like a micromolecular barrier tracer. On the other hand, almost complete binding of the Evans Blue to albumin confers to it properties of a protein tracer. 3. Following the extravasation of the tracers, the sodium fluorescein is relatively soon eliminated, whereas Evans Blue remains in the cellular elements of the brain parenchyma for a considerable time, although the protein moiety of the tracer is removed much sooner from the cytoplasm of glial cells, presumably by the lysosomal digestion.

Animals↗
PubMed1981

Factors in the reproducibility of the gravimetric method for evaluation of edematous changes in the brain.

In the gravimetric method for estimation of water content in brain tissue, four factors that may affect specific gravity (SG) measurements are described and evaluated. These factors are: (1) the purity of kerosene (K) and monobromobenzene (MBB), (2) duration of interaction of MBB with tissue and/or standard solutions, (3) the size of tissue samples, and (4) the temperature. A water-soluble contaminant in K, which can be effectively extracted by water treatment, may significantly decrease SG values. Conversely, in MBB, the SG of tissue samples tends to increase in proportion with time. The SG of the tissue samples appears to be influenced by their size, the smaller pieces registering higher SG values. Also, the temperature of the column affects the SG, with higher temperatures resulting in higher SG values; a difference of 5 degrees C produces a significant difference in SG (p less than 0.05). A standardized procedure providing highly reproducible SG values is presented in which the size of the tissue samples, the recording time, and the temperature of the column consisting of water-treated K and MBB are kept strictly constant.

Animals↗
PubMed1980

Serial measurements of CT attenuation and specific gravity in experimental cerebral edema.

Vasogenic cerebral edema was induced cryogenically in rhesus monkeys. Serial scans in both axial and coronal planes were used to study the onset, peak, and regression of edema. Progression of edema, predominantly involving the white matter, was analyzed from the postmortem distribution of a blood/brain barrier indicator (Evans blue) injected at surgery. Specific gravity was measured in fresh, unfixed specimens from both the edematous and normal hemispheres and correlated with corresponding CT attenuation values obtained before death. The drop in specific gravity closely corresponded to the decrease in CT attenuation.

Animals↗
PubMed1979

Histochemical investigation of the Mongolian gerbil's brain during unilateral ischemia.

The ischemic effect on cerebral enzymes and glycogen content was histochemically evaluated in mongolian gerbils subjected to unilateral common carotid artery occlusion for various periods of time from 1/2 to 9 h. In early stages (up to 2 h), the only enzyme affected was the phosphorylase which revealed a decreased activity. Thereafter, the observed changes inclusive of glycogen and other enzymes such as the dehydrogenase, nonspecific acid and alkaline phosphatases, leucine aminopeptidase and thiamine pyrophosphatase progressed proportionally to the duration of ischemia. There was an overall inverse appearance of histochemically demonstrated enzymatic disturbances between the severely damaged ischemic regions and its marginal zones; the former revealing a conspicuous decrease and/or loss of enzymatic activities while the latter showing an increase of the same enzymes. Correlating the various ischemic responses of the intracellular organelles it appears that the changes in the lysosomes and Golgi apparatus occurred slower than those of mitochondria.

Acid Phosphatase↗
PubMed1978

Transient ischemic alteration of synaptosomal neutral amino acid uptake.

The effect of cerebral ischemia and postischemia on the synaptosomal uptake of some neutral amino acids was determined in mongolian gerbils at various periods of time. A transiently increased uptake of 3H isoleucine, 14C cycloleucine and 3H phenylalanine in the synaptosomes was found after 3 min of bilateral common carotid occlusion which returned to normal at 30 min of reestablished cerebral blood circulation.

Amino Acids↗