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Biomedical subjects

M Spatz

Publications and source records attributed to M Spatz.

At least 145 records · Page 8Linked to original sources
PubMed1977

Role of pressure gradients and bulk flow in dynamics of vasogenic brain edema.

The authors present the results of an investigation of the vasogenic type of brain edema using cold injury in cats as a model. Their findings indicate that bulk flow and not diffusion should be considered the main mechanism for the spread of edema through the white matter. This conclusion is based on: 1) comparison of the distances actually traveled by various substances during edema spread with those calculated theoretically for migration of the substances by diffusion; 2) coincidence in the speed of movement by two substances (sucrose and albumin) with widely different diffusion coefficients; 3) measurement of interstitial fluid pressure (IFP) at various distances from the lesion showing the presence of increased IFP in the lesion area and decreasing pressures along the edema pathway toward the normal tissue; and 4) the fact that spreading of edema can be significantly impeded by inducing before the cold lesion an intracellular type of brain edema that reduces the size of the extracellular space (ECS) and increases the resistance to flow of edema fluid. The pressure-volume curve of the brain ECS, as derived from determinations of IFP and tissue water content, indicates that initial steep slope in IFP probably represents the high resistance to fluid mobility through the small diameter extracellular channels and the counteracting resistance of the intermingled structures of brain parenchyma to be separated. Once the IFP exceeds these opposing forces, the ECS dilates, fluid mobility increases, and the edema front advances.

Animals↗
PubMed1976

Experimental cerebral ischemia in Mongolian gerbils. v. Ultrastructural changes in H3 sector of the hippocampus.

Mongolian gerbils exposed to relatively short (7 or 15 min) unilateral or bilateral occlusions of the common carotid artery develop, 20 h after release of the clipping, characteristic morphologic changes in the H3 sector of the hippocampus. Ultrastructural study of these changes revealed an eccentric shift of the nuclei associated with chromatolytic perikarya which showed a dense accumulation of lysosomes and mitochondria in their central parts. The Golgi apparatus was recognizable only by clusters of vesicles, and this change was associated with a negative thiamine pyrophosphatase reaction.

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PubMed1976

Experimental cerebral ischemia in Mongolian gerbils. IV. Behaviour of biogenic amines.

Behaviour of biogenic amines was studied in the brains of Mongolian gerbils subjected to unilateral occlusion of the common carotid artery. Assays on the hemispheres ipsilateral to occlusion revealed in symptom-positive animals a progressive decrease in norepinephrine and dopamine, and an increase in serotonin throughout the duration of an ischemic insult. In post-ischemic periods following the release of the clip, changes in biogenic amine levels generally conformed to the principles of a previously described "maturation" phenomenon, with delayed reactions occurring after the shorter ischemic insults.

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PubMed1976

Increased permeability of cerebral vessels to horseradish peroxidase induced by ischemia in Mongolian Gerbils.

Cerebral ischemia was induced by occlusion of the left common carotic artery in adult Mongolian gerbils. The period of occlusion was 3, 6, or 18 h. Horseradish peroxidase (HRP) was intravenously injected in animals with clear neurological signs 1 h release of the clip. The HRP was allowed to circulate for 5 min. Fixation was carried out by perfusion with aldehydes. Tissue, incubated for peroxidatic activity, from the left side of the brain was treated for electron microscopy. During the postischemic period enhanced permeability was demonstrated in the brains of all animals. The amount of HRP transferred into the neuropil depended on the duration of ischemia. Thus the gerbils with 18 h occlusion showed the greatest content. The cells comprising the neuropil adjacent to vessels were studied and the degree of the pathological changes described below was increased proportionally to the time period of occlusion. The intercellular spaces, often filled with peroxidase, were expanded and the astrocytes swollen, especially the endfeet. Sometimes the astrocytes were pervious to HRP. The neurons were also swollen, but to a lesser degree than the astrocytes. No endothelial cell damage was observed. Even 18 h of occlusion did not change the plasma membranes. The intercellular spaces were free of HRP from the first luminal to the first abluminal tight junction. The cytoplasm exhibited HRP-containing vesicles of various types and shapes. Some were freely situated; others were connected to the plasma membrane and then open to the vessel lumen or to the basement membrane. Since no cell damage was demonstrated, and since no HRP was diffusely dispersed in the cytoplasm it is assumed that vesicles are responsible for the enhancement of the vesicular transport that normally occurs after intravenous injection of HRP.

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PubMed1976

Experimental cerebral ischemia in Mongolian gerbils III. Behaviour of the blood-brain barrier.

The behavior of the BBB in cerebral ischemia was studied in symptom-positive Mongolian gerbils subjected to left common carotid artery occlusion using Evans Blue dye as indicator of BBB injury. The BBB damage was demonstrable grossly by the presence of areas of blue discoloration, and microscopically by the presence of a bright red fluorescent tracer, localized mostly in the neurons. The survey of various groups of animals revealed a direct relationship between the incidence and time of appearance of the BBB lesions and the duration of the ischemic occlusion. This relationship can be interpreted as another example of the previously described "maturation" phenomenon. A relatively late occurrence of the BBB injury in cerebral ischemia, at the time when the affected brain tissue shows severe, edematous histopathologic changes indicates that the brain edema, as the main complication of ischemia, could be regarded as being primarily of the cytotoxic type.

Animals↗
PubMed1976

Pathological aspects of brain transport phenomena.

The aim of this paper has been to review and discuss the past and the recent investigations concerned with the study of cerebral transport phenomena in pathological conditions which have been divided into two main parts: (1) the effects of experimentally induced blood brain barrier (BBB) injury by (a) HgCl2 or (b) hyper-osmolar intracarotic perfusate; and (2) the effects of ischemia or of an altered oxygen saturation and pCO2 tension on glucose and/or amino acids and/or protein transport across the BBB, in the syanptosomes and cerebral capillaries. The most important observations were as follows: (1) HgCl2 or hyperosmolar perfusates produced an increased BBB permeability to protein tracers but the brain uptake of glucose analogues was found decreased following the former, and increased (except for lactamide) after the latter treatment. (2) (a) In ischemia, the noted increased vesicular transport of peroxidase, as well as the increased saturable and non-saturable passage of glucose analogues across the BBB depended on the duration of cerebral deprivation of blood supply which never resulted in degeneration of endothelial cells of the brain vessels. (b) The progressively decreased specific 2-deoxy-D-glucose uptake in the synaptosomes seen during cerebral ischemia of 30-180 minutes returned to the level of controls 1 hour after reestablishment of cerebral circulation. (c) A decrease in brain uptake of glucose analogues and amino acids (with few exceptions) was observed in severe hypoxia and hypercapnia while an increase or no change in the brain uptakes was seen in hypocapnia. (d) Preliminary investigations of the 2-DG uptake by the cerebral capillaries obtained by fractionation of the brain from animals subjected to normal or altered oxygen saturation and pCO2 tension suggested that cerebral glucose uptake may be directly related to its capillary function.

Amino Acids↗
PubMed1976

Brain serotonin after experimental vascular occlusion.

Unilateral ligation of a common carotid artery in gerbils causes a decreased rate of serotonin synthesis and degradation but an increased release of this monoamine. In the brain, reduction of cerebral serotonin content during ischemia is followed by accumulation of its main metabolite, 5-hydroxyindolacetic acid. These data support the contention that serotonin plays an important role in the progression of cerebral infarction.

Animals↗
PubMed1975

Experimental cerebral ischemia in Mongolian gerbils. II. Changes in carbohydrates.

A cerebral ischemia was produced by unilateral ligation of the common carotid artery in the neck of Mongolian gerbils (Meriones unguiculatus), which are frequently characterized by deficiencies in the circulus of Willis. Concentrations of glucose, lactate, pyruvate and glycogen were measured in the hemisphere on the side of occlusion and in the contralateral control hemisphere of animals sacrificed after 5, 15 and 30 min, as well as after 1,3,5 and 9 hrs of carotid clamping. Significant decrease of glucose, and increase in lactate and pyruvate concentration were found in the hemisphere ipsilateral to occlusion; the extent of the changes was proportional to the duration of the ischemia. After an initial fall, an increase in the glycogen content occurred in the later stages of ischemia. Glycogen, glucose, lactate and pyruvate were determined also at 1, 5, 20 hrs and 1 week intervals following release of an occlusion lasting for 1 hr. Return to normal values of glucose and pyruvate was seen at 1 hr after release. The lactate and glycogen levels were significantly raised on the occluded side after 20 hrs release. An increased level of glycogen was observed as long as 1 week after a 1-hr carotid occlusion.

Animals↗
PubMed1975

Experimental cerebral ischemia in mongolian gerbils. I. Light microscopic observations.

Light microscopic observations were carried out on Mongolian gerbils (Meriones unguiculatus) subjected to a partial cerebral ischemia by occlusion of the left common carotid artery at the neck. About 30% of gerbils developed an ischemic injury in the ipsilateral hemisphere and their brains revealed the following histopathologic features: 1. the changes were related to the intensity (duration) of the ischemic insult and to the time elapsed following release of the occlusion. The ischemic lesions appear to progress after re-establishment of the circulation and this presents one facet of a "maturation" phenomenon which seems to be a general principle applicable to various parameters of ischemic injury. The rate of "maturation" of the lesions is related to the intensity of the ischemic insult, a lesser intensity resulting in longer development of lesions. 2. The changes were either focal or diffuse in character. The former were assumed to be directly related to a vascular involvement; among the latter the topistic distribution of the hippocampal changes suggested a feature of selective vulnerability. 3. An indirect indication of neuronal recovery was surmised from observations on animals sacrificed after different periods following occlusions of the same duration. Also capable of recovery was a "reactive change" observed in the H3 neurons of the hippocampus. This change was characterized by central chromatolysis and resembled the "rimäre Reizung" of Nissl.

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