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Biomedical subjects

M Le Poncin-Lafitte

Publications and source records attributed to M Le Poncin-Lafitte.

29 records · Page 2Linked to original sources
PubMed1981

Deoxyglucose uptake in pathological conditions.

In case of quick physiological variations or in pathological conditions, it is impossible to measure the deoxyglucose consumption by means of the deoxyglucose technique and we propose a method for the study of the deoxyglucose uptake by the cerebral tissue. It is simultaneously measured with the blood flow, 3 min following the intravenous administration of deoxyglucose (2-deoxyglucose-14C). Hypercapnia induces an increase in the flow but does not modify the deoxyglucose uptake and moderate hypoxia results in a decrease in the deoxyglucose uptake without modifying the flow. In pathological conditions such as ischemia or stricture, the blood flow and deoxyglucose uptake variations are not parallel. These results show that the 2-deoxyglucose uptake does not follow the blood flow and that it depends on the cell activity. It is therefore possible to use this method when the consumption studies cannot be implemented.

Animals↗
PubMed1981

Short-term memory and cerebral ischemia: pharmacological application.

Transient ischemia results in changes in the cerebral blood flow at the level of microinfarcts, enzymatic and metabolic changes and the development of a cerebral edema; all these disorders regress in the week following ischemia. Besides, the observed functional disorders disappear as the cerebral edema regresses. The brain functional activity is protected by the use of treatments which reduce the development of the cerebral edema and/or a quicker regression of the edema.

Animals↗
PubMed1981

[Cerebral blood flow, metabolism and learning after a cerebral infarction in the rat (author's transl)].

Experimental microembolization of the rat brain has been used as a model for the production of cerebral microinfarction which resulted in a decrease in blood flow and secondary brain edema with changes in the oxidative metabolic pathways. The use of radioactive microspheres as embolizing agents allowed to determine the number of microinfarctions and their localization. In every microinfarct, oedema developed and it could be quantified by measuring the water percentage as soon as the fourth hour following the microembolization. The activity of oxygen-dependent enzymes was severely reduced in the ischemic area around which hyperemia was present. A quick decrease in the ATP and glucose levels and an increase in the lactate levels were observed, showing that the energetic metabolism was deviated towards the anaerobic pathway. On the fifth day following the microembolization, the oedema disappeared. The cellular metabolic activity and the cerebral blood flow almost returned to normal values within the same time. The simultaneously study of an avoidance response in a conditioned learning test showed a correlation between the reappearance of this response and the regression of the oedema.

Animals↗
PubMed1980

Age-associated changes in deoxyglucose uptake in whole brain.

Cerebral blood flow, studied by means of a diffusible indicator, remains unchanged in the aging process (developmental changes). On the contrary, brain activity, evaluated by deoxyglucose uptake, is significantly reduced. Papaverine, which increases cerebral blood flow, and vincamine, slightly but significantly, act on this parameter in the older animals.

Aging↗
PubMed1980

Blockade of the different enzymatic steps in the synthesis of brain amines and memory (CAR) in hypobaric hypoxic rats treated and untreated with L. dopa.

L. Dopa associated with an extracerebral inhibitor of dopadecarboxylase is able to protect the rat against the deleterious effects of hypobaric hypoxia on a conditioned avoidance response. L. Dopa loses its protective effect against hypoxia if tyrosine hydroxylase, dopadecarboxylase, or dopamine beta hydroxylase is previously blocked. L. Dopa's protective effect must therefore be due to an indirect action on the endogenous catecholamine metabolism.

Acoustic Stimulation↗
PubMed1978

[Effect of citidoline on hemodynamics in the normobaric hypoxic dog].

In dogs submitted to a normobaric hypoxia, we found an elevation of the arterial blood pressure, of the heart rate, of the cardiac output and of the regional blood flows, the total peripheral resistance remaining unchanged. Treatment with citidoline abolishes these hemodynamic responses and the authors hypothetize that this effect is correlated with the agonist dopaminergic effect of the drug.

Animals↗
PubMedDate not supplied

[Experimental model of cerebral ischemia preventive activity of Ginkgo biloba extract (author's transl)].

Unilateral embolization of the brain was performed in rats by intracarotid injection of 4 000 radioactive microspheres (50 mu). Local blood flow in hippocampus, striatum, hypothalamus and remainder of the brain were determined using the iodoantipyrine technique. Embolization resulted in a decreases in blood flow and modificationof the distribution of microflow. Furthermore, embolization produces changes in energy metabolism : particularly a fall in ATP and glucose levels and an increase in lactate level. Subsequently, severe vasogenic edema developed. There was a correlation between the number of microspheres injected and the amount of edema. Pretreatment using an extracted of Ginkgo biloba leaves partially suppressed the effect of embolization. An improvement of the flow in the ischemic areas associated with an improvement of the energy metabolism explain the decreases of the edema.

Animals↗
PubMedDate not supplied

[Hypobaric hypoxia effects on a conditioned avoidance response and on ADP, AMP dopamine and noradrenaline cerebral levels in rats treated or not with naftidrofuryl (author's transl)].

Hypobaric hypoxia (300 mm Hg = 7180 m) was performed during 30 min. for a day during five consecutive days in rats treated or not with naftidrofuryl (15 mg/kg- i.p. daily). A conditioned avoidance response studied on five days shows a reduction of the performances in control rats but not ir treated ones. AMP and ADP cerebral levels were unchanged in the two groups. Hypoxia induced in control rats a reduction of the catecholamine cerebral levels which was not observed in treated rats. In conclusion the protection afforded by naftidrofuryl seems to be due mainly to a reduction of the catecholamine utilization during hypoxia.

Adenosine Diphosphate↗