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Biomedical subjects

F Matakas

Publications and source records attributed to F Matakas.

At least 19 recordsLinked to original sources
PubMed1978

The effect of prolonged experimental hypercapnia on the brain.

Thirteen adult rabbits were exposed to a breathing air mixture containing an increasing amount of CO2 for eight weeks. When the CO2 content reached 9 Vol% the animals became apathic and lost body weight. The EEG showed a reduction of the amplitudes of 1o Hz frequences. Blood gases revealed an increase of bicarbonate but no change of pH. The blood brain barrier which was tested when the animals were killed was not disturbed. Enzyme histochemistry, light and electron microscopy revealed that moderate brain edema had occurred. From these results it is concluded that chronic hypercapnia has a hypnotic effect which in combination with chronic edema may depress vital activities considerably. However, there seem to be no irreversible morphological alterations of the brain.

Animals↗
PubMed1977

Spastic constriction of cerebral vessels after electric convulsive treatment.

The brains of nine cats were subjected to bitemporal electric convulsive treatment. The current (AC, 220 V, 50 Hz, ca. 500 mA, 500 ms) was applied two to five times. Pial vessels were observed through a skull window. Immediately after current application, some pial arteries exhibited segmental spastic constriction which usually did not disappear until the animals were killed. Before sacrificing the animals, 20 min after convulsive treatment they were perfused with a carbon suspension. In some cortical areas blackening was impaired indicating that perfusion was not complete. Electron-microscopic investigation revealed that spasm also occurred in arterioles of the brain parenchyma. Many arterial vessels, some of them possessing only one muscular cell sheat, had collapsed so that the lumen was merely a small cleft. The spasms were irregularly distributed and confined to small segments of the vessel. Small arteriolar vessels were more affected than large pial arteries. Arterial spasms continued for 20 min. In a total of 39 control animals spastic constriction was observed only once; this animal had been subjected to prolonged hypocapnia.

Animals↗
PubMed1976

Effect of central venous pressure on brain tissue pressure and brain volume.

In cats, brain tissue pressure (BTP) was measured by the wick-catheter method. The BTP was positive, but lower than cerebrospinal fluid pressure. Elevation on central venous pressure led only to a transient proportional increase of BTP. When the calvaria and dura of one hemisphere were removed, the rise of BTP was even less. Water content of the brain was normal in either case, even after prolonged venous hypertension. Venous hypertension led in all cases to a marked increase of the brain volume which was caused by vessel dilatation. In brain edema, produced by rinsing the brain surface with ouabain and concentrated saline, BTP was increased permanently by venous hypertension. The water content of the brain was much greater than normal. From these results it was concluded that congestive edema does not occur in the brain unless the tissue is damaged. However, venous hypertension does cause brain swelling.

Animals↗
PubMed1975

Effect of systemic arterial blood pressure on cerebral blood flow in intracranial hypertension.

In five baboons and 11 cats cerebral ischaemia was produced either by inflating an epidural balloon and or by ligating major arteries supplying the brain. Fifteen of the animals developed intracranial hypertension after cerebral ischaemia. If ICP were high, but still significantly lower than MABP, elevation of MABP by noradrenaline infusions was accompanied by a proportional increase of ICP. However, the increase of ICP was lower than that of MABP so that CPP was raised. CBF measured by the 133Xenon clearance technique was significantly increased by arterial hypertension in eight cases. The proportional increase of CPP and CBF by elevation of arterial blood pressure was substantially greater, the lower ICP was immediately after ischaemia. There was no effect of MABP in cases in which ICP equalled MABP.

Animals↗
PubMed1975

Increase in cerebral perfusion pressure by arterial hypertension in brain swelling. A mathematical model of the volume-pressure relationship.

Brain swelling was produced in monkeys and cats by the inflation af an epidural balloon against the parietal lobe. Resulting changes in intracranial pressure (ICP) were correlated to variation in systemic arterial pressure (SAP). Intracranial perfusion pressure (ICPP) defined as the difference between SAP and ICP, was found to vary with the degree of arterial hyper-and hypotension. The relationship between SAP and ICP can be explained by an existing equilibrium between extramural pressure and vessel wall circumferential tension. A positive perfusion pressure can exist in brain swelling as long as vessel wall tension is preserved and the degree of expanding brain tissue volume is held below certain limits.

Animals↗
PubMed1975

The ulstratructure of reticulin.

The electron microscopic examination of various organs and tumours of different species proved that the ultrastructural equivalent of reticulin fibres is not a uniform substance. Reticulin fibres are either basement membranes or an amorphous mass which appears as argyrophil fibres under the light microscope. Microfibrils may in some cases produce an argyrophilic reticulum. The claimed identity of reticulin and collagen can partly be explained by the chemical similarity of collagen and basement membranes. It seems possible, moreover, that the amorphous mass and microfibrils, which may be an ultrastructural substrate of reticulin, are composed of a material essentially similar to that of collagen.

Animals↗
PubMed1973

Experimental brain death. I. Morphology and fine structure of the brain.

The morphological characteristics of brain death were examined in baboons and cats after artificial cerebral ischaemia. All animals showed autolytic changes in the brain, ischaemic neuronal changes, midbrain haemorrhages, focal necrosis of the brain-stem, demarcation at C 1/C 2 cord segment, and displacement of cerebellar tissue. Ultrastructural examination revealed extreme brain oedema, autolytic changes, and complete obstruction of capillaries by astrocytic and endothelial swelling and intravascular blebs. These data indicate that brain death develops in several stages. If the process starts in the supratentorial space it first leads to a breakdown of the cerebral circulation and to transtentorial herniation. As a result, midbrain haemorrhages develop and the infratentorial pressure begins to rise. The second stage is terminated by demarcation of the brain. The circulatory arrest is initially caused by venous compression but becomes irreversible when vascular obstruction develops.

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