Biomedical subjects

R Charbonne

Publications and source records attributed to R Charbonne.

4 recordsLinked to original sources

PubMed1996

Absence seizures induce a decrease in cerebral blood flow: human and animal data.

Our previous studies on cerebral metabolic activity in genetic absence epilepsy rats from Strasbourg (GAERS) were in favor of decreased functional activity during absences and normal or increased interictal activity. To ascertain that hypothesis, in the present study we performed continuous measurements of CBF in both children with typical absence epilepsy and GAERS, using Doppler ultrasonography and laser-Doppler flowmetry, respectively. CBF fluctuations during absences were recorded in four children between 5 and 6 years of age and 16 adult GAERS. In both children and animals, CBF measured in the middle cerebral artery and cortical capillaries, respectively, significantly decreased by a median value of 20-24% under basal levels during spontaneous absences. In GAERS, CBF levels were continuously decreased during haloperidol-induced absence status epilepticus, while they were not affected by ethosuximide. Conversely, convulsive seizures induced in rats either by kainate or picrotoxin led to a 175-664% increase in CBF levels. In conclusion, the present data show that during spontaneous absences, CBF decreases under basal levels in both cortical capillaries (GAERS) and the middle cerebral artery (children). Moreover, these fluctuations occur in vessels with normal vascular reactivity, are not mediated by changes in PO2, PCO2, or arterial blood pressure, and represent rather a response to reduced metabolic demand.

Animals↗

PubMed1994

Spreading depression reversibly impairs autoregulation of cortical blood flow.

The experiment examines whether the mechanisms responsible for the autoregulation of cerebral blood flow (CBF) in response to hypotension were affected during the initial phase of cortical spreading depression (CSD). CSD was induced by a cortical pinprick in anesthetized rabbits, and CBF was measured by laser-Doppler flowmetry through a chronically implanted Plexiglas window. The reactivity to CO2 and papaverine was also studied before and after CSD. Fifteen minutes after CSD, autoregulatory vasodilation was reduced (P < 0.01). This impairment was reversible, since the autoregulatory response was restored 35 min after CSD. The time course of the reactivity to papaverine after CSD paralleled the autoregulatory response, with a significant correlation between the two reactivities (r = 0.47; P < 0.01). Conversely, the reactivity to CO2 was significantly reduced after CSD (P < 0.001) and remained affected for at least 95 min. We conclude that the mechanisms underlying autoregulation are transiently disturbed by CSD and that these mechanisms are not mediated by an accumulation of CO2 but seem instead to be related to an increase in adenosine 3',5'-cyclic monophosphate concentration.

Animals↗

PubMed1994

Cortical blood flow and +Gz acceleration in conscious rabbits.

We examined whether superficial cortical blood flow (CBF) of nonanesthetized rabbits (n = 11) is affected by gravitational (G) stress. Blood flow was measured by laser-Doppler flowmetry through a chronic Plexiglas window implanted over the parietal cortex. Mean arterial blood pressure (MABP) was recorded via an aortic catheter with the pressure transducer situated at the level of the head. The electrocorticogram (ECoG) was also studied in seven rabbits. The animals were exposed to tail-to-head acceleration [6, 10, 15, and 20 G acceleration (Gz) for 1 min]. MABP fell with increasing acceleration (regression line equation: MABP = -7.0 Gz + 129.1; P < 0.001, r = 0.85), whereas CBF was statistically either not different from or greater than control. In one rabbit exposed to 20 Gz, high voltage and slow waves were observed on the ECoG and these changes were preceded by a decrease in CBF to 66% of control. We conclude that the stress and the siphon effect may account for the maintenance of elevated CBF despite low or negative MABP until the occurrence of vascular collapse that induces loss of consciousness.

Acceleration↗

PubMed1993

Effect of nimodipine on the autoregulation of cerebral blood flow studied by laser-Doppler flowmetry.

The present work examines whether nimodipine impairs autoregulation of CBF during hypotension. The CBF of 16 anesthetized rabbits was measured with a laser-Doppler flowmetry probe placed on the external surface of a plexiglas window, chronically inserted in the skull. Autoregulation was triggered by aortic bleeding. First, the effects of three doses of nimodipine (1, 3 and 10 micrograms/kg) and the solvent were studied in 10 rabbits in which MABP was maintained at 50 mmHg for one minute. Second, 10 micrograms/kg i.v. nimodipine was administered to 6 rabbits in which MABP was kept at 30 mmHg for one minute. Before bleeding, the 10 micrograms/kg dose significantly decreased MABP (from 96 +/- 11 mmHg to 81 +/- 11 mmHg, P < 0.01) and increased CBF (from 104 +/- 20% to 147 +/- 25%, P < 0.01) as compared to the solvent. In the first set of experiments, only the 10 micrograms/kg dose suppressed the autoregulatory vasodilation, but CBF was not different from control (84 +/- 17% versus 87 +/- 12%), probably because of the previous induced vasodilation. In the second set of experiments, active vasodilation occurred and the CBF during hypotension was not different from control (72 +/- 26% versus 65 +/- 11%). We conclude that under nimodipine the triggering of the active autoregulatory vasodilation is dependent on both the severity of hypotension and the previous nimodipine-induced vasodilation.

Animals↗