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A Eke

Publications and source records attributed to A Eke.

15 recordsLinked to original sources
PubMed1990

Histologic assessment of neurons in rat models of cerebral ischemia.

We describe a method for typing neurons into four progressive stages of ischemic deterioration based on visual characterization of the nucleus in terms of its optical contrast, delineation along the nuclear-cytoplasmic interface, and its shape. Difficulty in assessing nuclear shape required the introduction of an angularity comparator chart to improve the investigator's accuracy. Three investigators typed neurons obtained from normal, ischemic, and ischemic-reperfused rat brains. Accuracy and reproducibility of the investigators' typing decisions with and without the angularity comparator charts were evaluated. The accuracy of subjective shape assessment was compared with objective digitizer measurements of the same. The angularity comparator charts reduced subjective shape classification error by two thirds, and group error (overall performance expressed by the coefficient of variance) decreased from 15.9% to 4.7% for Type I (normal cells), from 33.9% to 17.3% for Type II (cells with angular nuclei), from 15.5% to 14.1% for Type III (cells with smeared nuclei), and from 3.2% to 5.5% for Type IV (dead cells). Thus, Type I and IV neurons can be assessed at a higher reproducibility than the intermediate Types II and III. Our typing method can also be used to evaluate the effect of treatment regimes on ischemic neuronal damage.

Animals↗
PubMed1989

Hematocrit changes in the extra- and intraparenchymal circulation of the feline brain cortex in the course of global cerebral ischemia.

Based on distinctly different hemodynamic behavior of erythrocytes and plasma affecting properties of the circulating blood in vivo, such as apparent viscosity, flow resistance, axial streaming of erythrocytes, plasma skimming, etc., hematocrit (Htc) can have an apparent impact on tissue perfusion. Hematocrit also shows a diameter dependent decrease along the extraparenchymal arterial vascular routes that levels off being markedly lower in the microcirculation than in the central arterial blood. It was postulated that the impact of Hct may become a critical aspect of the macro- and microcirculatory compensatory mechanisms under ischemic conditions, when excessive fluid shifts between the extra- and intravascular compartments can in fact alter both systemic and local Htc, and when a decreased perfusion pressure sets the stage for sluggish flow velocities at which orientation of erythrocytes in the plasma stream can abruptly change and impair the macro- and microcirculation alike. To test this hypothesis, systemic (Htcs), feed (Htcf) and local hematocrit (Htcl) were simultaneously monitored in anesthetized and mechanically ventilated cats from the abdominal aorta, a pial artery of 100 micra in diameter and 500-600 cerebrocortical microareas of 0.01 cubic mm each respectively, by a television densitometric method while global cerebral ischemia was induced and maintained by adjusting the systemic mean arterial blood pressure to 40-50 mmHg by controlled arterial hemorrhage. Global cerebral ischemia was terminated when cerebrocortical microcirculation collapsed or shed blood completely got reinfused to the animal. The data show that under control conditions Htcf is 44% of Htcs, while hemoconcentration in the tissue brings Htcl up to 67% of Htcs. Under ischemic conditions, in cases of short survival time, the extraparenchymal arterial hemoconcentration can not be sufficiently compensated by intraparenchymal hemodilution and the microcirculation collapses under the conditions of lowering or moderately rising local tissue hematocrit. In case of longer survival , the rate of extraparenchymal hemoconcentration is increasingly lower and therefore the intraparenchymal hemodilution becomes more effective and prolonged. Due to factors most likely pertinent to the tissue proper, microcirculation collapses under abruptly developing secondary tissue hemoconcentration. Since terminal Htcl was only slightly higher than that at the beginning of the ischemic episode, attention to other hemodynamic and rheological factors in the microcirculation--not directly influenced by Htc--have been turned to.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Classifying cells from light microscopic bit features by binary logic. Application to grade neuronal injury in cerebral ischemia.

Degradative cellular processes within neurons were analyzed and graded by a conceptually new approach that decoupled the process of subcellular feature analysis and grading, the latter being based on the severity of observed deterioration in subcellular features. Rather than evaluate the cell's histologic image in a panoramic manner, investigators were required to give simple yes-no decisions about the presence or absence of a specific pathologic feature (bit feature as opposed to panoramic analysis). Multiple elementary decisions create a binary representation of the cell image that can be easily handled and analyzed using computer techniques to generate all possible unique phenotypes of the scanned neuronal population. In the first application of this method, however, the number of possible phenotypes were reduced by imposed a priori logic on the separation scheme focusing on a single cellular structure (the nucleus) that was followed through the stages of structural decay. We experimentally validated four neuronal types of five theoretical possibilities when three nuclear bit features were used in typing. Grading of neuronal injury for groups of normal, ischemic, and ischemic and reperfused rats into two, three, and four categories are reported. The consistency at which the method can be implemented was assessed by calculating the mean and standard deviation of the reconciled typing decisions given by the four investigators. The group of the four investigators showed less than 2, 3, and 5% error when grading cells from control, ischemic, and ischemic-reperfused animals, respectively.

Animals↗
PubMed1977

[The protecting action of a combination of vasoactivating substances (CRP) on disturbances of the cerebral blood flow and metabolism and the cortical electrical activity (author's transl)].

The effect of anoxia and direct cortical stimulation was investigated in control, hypotensive and post reinfusional periods, before and after treatment with a combination of coumarin/rutin sulphate sodium salts/proxyphylline (CRP, Theokal). Theokal lowered the mean arterial pressure and a slight NADH oxidation appeared. Blood flow did not change after Theokal in spite of the 30 mm Hg blood pressure drop. This suggests an improved oxygen supply to the cortical cells. The increase in anoxic NADH reaction and the faster reoxidation kinetics of NADH following anoxia provided further evidence for the beneficial effect of Theokal on brain circulation and metabolism. It is to be emphasized that the described action of the drug can be observed only in hemorrhagic shock but not in normal animals.

Animals↗
PubMed1976

In vitro investigation of biological specimens by electron microscopy.

A microchamber was developed for the examination of biological specimens in nearly natural environments, in an electron microscope, at 70kV accelerating voltage.. The chamber can be supplied continually with the sample and with the reagents, which makes it suitable for the study of biochemical reactions, too. Temperature and vapour pressure in the chamber can be controlled and the thickness of the specimen can be varied. Transmission electron micrographs of biological specimens, such as human blood cells, bull gametes and Bacillus subtilis have been obtained. Mobility of microorganisms, which is regarded as a criterion of the wet state, has been observed.

Animals↗
PubMedDate not supplied

Transient metabolic and vascular volume changes following rapid blood pressure alterations which precede the autoregulatory vasodilation of cerebrocortical vessels.

It has been shown by surface fluoro-reflectometry that stepwise decrease of arterial blood pressure causes a biphasic cerebrocortical vascular volume response. After the arterial blood pressure decrease the vascular volume first decreased and later increased. In both parts of the biphasic reflectance change, the cerebrocortical NAD-NADH redox state shifted considerably towards reduction and there was no reoxidation after the onset of cortical vasodilatation. Since a very rapid NADH reduction occurred during the first 30 secs. of the arterial hypotension in parallel with the vascular volume decrease, it is suggested that in the transient phase of arterial hypotension cerebral hypoxia may occur. Furthermore it is suggested that anaerobic tissue metabolites or some unknown NAD-NADH dependent process might dilate the cerebrocortical arterial network during the autoregulatory adjustment of CBF. The participation of the sympathetico-adrenal system in transient brain hypoxia caused by bleeding is a possibility since both the early vasoconstriction and the steep NADH reduction were prevented by the administration of phenoxybenzamine (1 mg/kg) before bleeding.

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