Search PubMed⌕ Search

Biomedical subjects

J Seylaz

Publications and source records attributed to J Seylaz.

At least 145 records · Page 8Linked to original sources
PubMed1985

Intrinsic and extrinsic mechanisms involved in the cerebrovascular reaction elicited by immobilization stress in rabbits.

Variations in cerebral blood flow and partial pressures of oxygen and carbon dioxide (pO2, pCO2) were studied in rabbits during short-duration (1 min) immobilization stress. The techniques used enabled us to determine these variables locally in the caudate nucleus in a continuous, simultaneous and quantitative fashion. It could be shown that cerebral blood flow and arterial blood pressure increased in parallel immediately after inducing the stress reaction, and that pO2 increased further, indicating that cerebral oxygen supply is maintained by the hyperaemia. Previous administration of a beta-receptor blocker or of a cholinergic receptor blocker significantly diminished the cerebrovascular reaction to stress, inducing a decrease in pO2 during the reaction. Administration of both blockers nearly abolished the cerebral vasodilation studied. Previous administration of an alpha-receptor blocker enhanced the reactive hyperaemia. No disturbance of the blood-brain barrier could be observed in rabbits subjected to stress. Intravenous injection of adrenaline, as well as angiotensin II inducing similar increases in blood pressure, had no comparable effect on the blood flow. The conclusion is that in this model of anxiety, neurogenic mechanisms are involved in the provision of a sufficient oxygen supply to the brain.

Animals↗
PubMed1985

Adrenergic receptors on cerebral microvessels in control and parkinsonian subjects.

The binding of adrenergic ligands (3H-prazosin, 3H-clonidine, 3H-dihydroalprenolol) was studied on a preparation of cerebral microvessels in the prefrontal cortex and putamen of control and Parkinsonian subjects. The adrenergic receptor density in microvessels of control patients was less than 0.5% and 3.3% respectively of the total binding. A significant decrease in the number of alpha-1 binding sites was observed on microvessels in the putamen of patients with Parkinson's disease.

Aged↗
PubMed1985

Long-term effects of superior cervical ganglionectomy on cortical blood flow of non-anesthetized rabbits in resting and hypertensive conditions.

The long-term effects of sympathectomy on cerebral cortical blood flow (CBF) were studied in the conscious rabbit. The quantitative, repeated measurements of blood flow were made by determination of helium clearance by mass spectrometry and were obtained simultaneously with measurements of local tissue pO2 and pCO2. Eight to 10 weeks after unilateral sympathectomy, resting blood flow in the homolateral cortex was decreased by a mean of 17% compared to the heterolateral cortex. In two animals in which blood flow was recorded both before and after the sympathectomy, the same phenomenon was observed from 8 to 30 days after the operation. The response to i.v. infusion of noradrenaline was identical in both hemispheres: doses inducing a 40% rise in blood pressure did not significantly modify CBF. The responses to angiotensin II-induced hypertension were also identical. Histochemical verifications demonstrated the effectiveness of the denervation in the pial arteries and the intraparenchymal arteries in the region studied. Thus the decrease in CBF induced by chronic sympathectomy cannot be attributed to the development of hypersensitivity to catecholamines. This decrease remained stable whatever the value of resting flow and was maintained under anesthesia. It is concluded that, as in the peripheral circulation, chronic sympathectomy affects the equilibrium of the vascular smooth muscle fibers, but that circulating amines play no compensatory role in the cerebral circulation because of the blood-brain barrier.

Adrenergic Fibers↗
PubMed1985

Vascular monoamine oxidase activity in the rat brain: variation with the substrate and the vascular segment.

Brain vascular monoamine oxidase (MAO) was assayed in order to determine (a) whether microvessel MAO is more or less specific for certain substrates and (b) if the extraparenchymal, pial arteries possess an MAO activity as high as that in the microvessels. Rat brain microvessels were prepared by gentle homogenisation of grey matter, followed by filtration and differential centrifugation of the matter retained. Pial arteries were carefully freed of the meninges and cut into small segments. For comparison, rat mesenteric arteries were also dissected out and cut up. MAO was assayed by measuring the rate of oxygen consumption in a small cell with a Clark electrode. Although a high microvessel MAO activity (2.2 +/- 0.3 nmol min-1 mg prot.-1) was found using noradrenaline as substrate, significantly higher rates were found with tyramine, serotonin and beta-phenyl-ethylamine. By contrast, both pial and mesenteric arteries showed a 6-7 fold lower activity (substrate tyramine). These results indicate first, that a certain specialisation of the microvessel MAO activity exists which is apparently independent of the classical A or B-form category of the substrates, and second, that the extraparenchymal vessels (pial arteries) appear to possess significantly lower MAO activity, in accordance with the concept that blood-brain properties are induced by the cerebral parenchyma.

Animals↗
PubMed1985

Fluorocarbons: a potential treatment of cerebral air embolism in open-heart surgery.

This study was designed to assess whether an oxygenated fluorocarbon solution could reduce ischemic brain damage related to arterial air embolism. Air embolism was produced by injecting air bubbles into the carotid artery of barbiturate-anesthetized rats breathing 100% oxygen. Results were assessed on electrocorticogram. In an additional set of experiments, mass spectrometry was used to provide continuous monitoring of intracerebral tissue oxygen (PO2) and carbon dioxide (PCO2) tensions and intermittent measurement of cerebral blood flow (CBF). Fluorocarbon or saline solution (containing the emulsifying agent of fluorocarbons) was given intravenously after the initial air embolism (0.2 ml), and injections of air (0.1 ml) were repeated thereafter every five minutes. The maximal amount of air required to achieve complete and irreversible flattening of the electrocorticogram was 1.60 +/- 0.06 ml (mean +/- standard error of the mean) in the saline-treated rats and 5.20 +/- 0.44 ml in the fluorocarbon-treated group (p less than 10(-7)). In the second experiment, air embolism caused CBF to rise in both groups, the average percent of increase being higher in treated (41.6%) than in control animals (38.3%) (p less than 0.02). However, in the control group, the increase in CBF did not prevent intracerebral tissue PO2 from decreasing by 7.4 +/- 7.0% over the same period; conversely, in the fluorocarbon group, PO2 levels fell by only 2.5 +/- 3.7% (p less than 0.001 versus controls), but this time-averaged percentage was calculated over a longer period of cumulative ischemia because of the greater number of air emboli tolerated by treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Pial artery responses to norepinephrine potentiated by endothelium removal.

The effect of endothelium removal on pial artery constriction in response to norepinephrine (NE) was studied in vitro using a perfused vessel setup in which pressure increases indicate vasoconstriction. In deenodothelialized rabbit arteries, the reaction to extraluminal NE was found to be characterized by a much higher Emax (2.0 times) and a slight (but significant) leftward shift of the concentration-response curve (lower EC50) compared with control vessels. In cat arteries subjected to either extra- or intraluminal NE, the Emax was also substantially higher in deendothelialized preparations (4.4 and 5.1 times, respectively), but there was no significant difference in the EC50 values. Anatomical verification and functional tests (acetylcholine-induced dilatation) confirmed the presence and the absence of the endothelium in control and lesioned arteries, respectively. This modulatory influence of the endothelium may be of importance in cerebrovascular pathology.

Animals↗
PubMed1985

Sympathetic regulation of cerebral blood flow during reflex hypertension.

The cerebral circulatory effects of physiological stimulation of the sympathetic nervous system have been examined in the present study. In lightly anesthetized rabbits, reflex sympathetic activation was provoked by bilateral sinus deafferentation and vagotomy. Regional cerebral blood flow (CBF) was measured by the [14C]-ethanol technique and compared in paired brain structures following unilateral superior cervical ganglionectomy. Two subgroups of hypertensive rabbits were statistically distinguished. In the first (19 of 28 rabbits), CBF in the innervated hemisphere was little modified by hypertension but there was a significant side-to-side difference in CBF between the hemispheres. In the second group (9 rabbits) CBF was markedly increased by the systemic hypertension, and little difference was noted between innervated and denervated hemispheres. We demonstrate that, during acute hypertension, the superior cervical system contributes to cerebrovascular autoregulation; this contribution varies according to the brain region studied. In a subgroup of animals, little sympathetic activity could be evidenced, and it is hypothesized that in these rabbits a vasodilatory system was activated that counteracted the myogenic, autoregulatory responses.

Animals↗
PubMed1984

Blood flow compensates oxygen demand in the vulnerable CA3 region of the hippocampus during kainate-induced seizures.

Local blood flow, and partial pressures of oxygen and carbon dioxide were directly monitored in the vulnerable region of Ammon's horn (e.g. CA3) of unanaesthetized, freely breathing rats in which epileptic seizures of 120 min duration were induced by parenteral kainic acid. Blood flow was periodically determined by helium clearance. Partial pressures of oxygen and carbon dioxide were simultaneously and continuously measured by means of mass spectrometry, in order to determine if the neuronal damage occurring during the seizures were due to local hypoxia or if blood flow compensated the metabolic demand. During the wet shakes period, a decrease of 35% in the partial pressure of oxygen occurred, concomitant with an increase of 33% in the partial pressure of carbon dioxide and of 330% in local blood flow in Ammon's horn. During the limbic motor seizures, the partial pressure of oxygen increased progressively to twice its baseline value, while the partial pressure of carbon dioxide returned to its baseline value and blood flow underwent a six-fold increase. Thus the seizures produced by kainate do not lead to a mismatch between oxygen supply and blood flow. Our results provide direct evidence that hypoxia cannot be considered responsible for the damage produced by the seizures in CA3. It is concluded that brain damage in CA3 is due to an enhanced neuronal activity associated with the release of a toxic endogenous substance and an excessive rise of intracellular concentration of calcium.

Animals↗
PubMed1984

Significance of the cerebrovascular effects of immobilization stress in the rabbit.

The question of the significance of the cerebrovascular effects of stressful situations in animals is still controversial. In the present article, an experimental model of immobilization stress in the rabbit is described, and its specificity in relation to arterial blood pressure and PaCO2 is investigated. CBF was measured with the multiregional tissue sampling technique using [14C]-ethanol as tracer. After dissipation of althesin anesthesia, the stress reaction was elicited by tactile abdominal stimuli. The response was evidenced by an instantaneous acute hypertension (+33.8% during the CBF measurement period). Within the first minute of the reaction, the CBF was significantly increased in all nine structures studied by 39% (caudate nucleus) to 82% (parieto-temporal cortex). The study of the influence of arterial blood pressure and the PaCO2 on CBF showed that cerebrovascular autoregulation and CO2 sensitivity were differently affected in the various structures during the stress reaction. However, the stress response of the brain circulation could not be entirely ascribed to one or both of these two systemic factors, thus suggesting the contribution of a local intrinsic activation. The model presented here could be useful for long-term studies of cerebrovascular repercussions of repeated acute hypertensions of a stressful nature.

Animals↗
PubMed1984

Monoamine oxidase activity in the cerebral vasculature: comparison between fresh microvessels from different structures and cell cultures derived from microvessels.

Monoamine oxidase (MAO) activity was studied in various preparations of porcine brain microvessels to explore further the role of this enzyme in the blood-brain barrier to catecholamines. No difference was noted (Vm and Km) between microvessels isolated from three structures (caudate nucleus, thalamus, and cerebral cortex) in which the responses to circulating catecholamines in vivo are markedly different. Large and small microvessels from the caudate nucleus and the thalamus presented the same specific activity. Cell cultures obtained from small microvessels were rich in endothelial cells as identified by the presence of Factor VIII-related antigen. These preparations displayed an MAO activity about ninefold less than freshly isolated microvessels, although their prostaglandin synthetase activity appeared normal. These results suggest that MAO activity is not the main factor determining the regional differences in the cerebrovascular reactions to catecholamines, that MAO is not specifically localized in the endothelium but must be also present in the smooth muscle, and that the MAO activity is greatly decreased during cell culture.

Animals↗
PubMed1983

Generalized cerebral vasoconstriction induced by intracarotid infusion of angiotensin II in the rabbit.

This study investigated the influence of angiotensin II, perfused into one common carotid artery at a dose of 0.065 micrograms/kg/min, on the cerebrovascular resistance of the anesthetized rabbit by means of complementary in vivo methods. Heat clearance and mass spectrometry measurements indicated that in the homolateral caudate nucleus angiotensin induced a significant decrease in local blood flow (18.2 +/- 9%), a fall in pO2 (14.2 +/- 5.3%) and no significant change in pCO2. The [14C]ethanol tissue sampling technique revealed a significant decrease in flow in all 10 structures sampled in the brain. This decrease was similar in magnitude in both the ipsilateral and the contralateral hemisphere with regard to the site of injection. When expressed in terms of cerebrovascular resistance (CVR) and allowing for a slight increase in blood pressure (less than 10%), these results show that angiotensin II infusion induced an increase in CVR of 18-32%. We conclude that: A unilateral intracarotid infusion of a low dose of angiotensin II induces an increased vascular tone in all cerebral structures. This action, being bilateral, cannot readily be explained by a direct action of angiotensin II on the cerebral vessels in view of the very low recirculating concentration of angiotensin II (less than 10(-9) M). The hypothesis of a cerebral vasomotor influence of angiotensin II by action on a central structure is discussed.

Angiotensin II↗
PubMed1983

Hyperfrontal pattern of human cerebral circulation. Variations with age and atherosclerotic state.

The phenomenon of relative hyperperfusion of the frontal areas of the cerebral cortex (hyperfrontal flow distribution) was analyzed in 84 patients between 13 and 78 years of age. Fifty-two patients (group 1) had histories of vascular disease or vascular risk factors, and 32 (group 2) did not. Regional cerebral blood flow was measured by an atraumatic xenon Xe 133 method. The mean hemispheric gray-matter flow was found to decrease similarly with age in the two groups. Other findings were as follows: (1) the level of flow within the frontal region was not homogeneous in young adults; (2) in group 1, the frontal hyperperfusion decreased progressively with age, disappearing during the fifth and sixth decades according to a specific topographic pattern; (3) in group 2, hyperperfusion persisted into old age; and (4) hyperperfusion appeared more persistent with age in women than in men.

Adolescent↗
PubMed1983

Monoamine oxidase activity in brain microvessels determined using natural and artificial substrates: relevance to the blood-brain barrier.

The possible contribution of cerebrovascular monoamine oxidase (MAO) to the blood-brain barrier to catecholamines was studied in isolated porcine and rat microvessels by determining its activity with various substrates. Michaelis-Menten kinetic constants, Km and Vmax, were determined using noradrenaline (NA) as substrate in a Tris medium. Km values were 0.25 +/- 0.05 mM in control and 0.16 +/- 0.09 mM in ultrasonically disintegrated (USD) preparations (difference not significant); Vmax in USD preparations (1.83 +/- 0.20 n.atoms O2 min-1 mg protein-1) was slightly higher (p less than 0.05) than in control preparations (1.35 +/- 0.11 n.atoms O2 min-1 mg protein-1), suggesting a certain restriction by the plasma membrane of substrate access to the enzyme. This phenomenon was confirmed in a more physiological, ionic medium; the activity was then approximately doubled for 1 mM NA, whereas that for 1 mM beta-phenylethylamine (beta-PEA), a lipid-soluble substrate, tended to decrease with USD treatment. These results show that this highly active form of MAO is unlikely to be saturated by physiological concentrations of catecholamine. It can be estimated that, for a plasma concentration of NA of 1 microM, a facilitated diffusion accelerating the entry of the catecholamine into the cells by at least 15-fold would be necessary in order to exceed the catabolic capacity of MAO. It is concluded that circulating catecholamines are not likely to cross the endothelial barrier of cerebral microvessels intact, and that the small quantities of radioactivity detected in the parenchyma in measurements of the brain uptake index essentially represent metabolites due to MAO activity.

Animals↗
PubMed1983

Local cerebral PO2, PCO2, and blood flow measurements by mass spectrometry.

Partial pressures of intracerebral tissue gases (PO2, PCO2) and local cerebral blood flow (local CBF) were determined simultaneously by means of a single cannula implanted stereotaxically in a given structure. Minute quantities of the gases (O2, CO2, and tracer gas) were withdrawn continuously. After a short period of tracer (He) inhalation, CBF was measured by determination of the clearance rate (T1/2). The measurements of PO2 and PCO2 were continuous and quantitative, whereas the measurements of local CBF were sequential and quantitative. The results obtained for local CBF were compared with those found with two other methods (H2 clearance by polarography, thermoclearance) in the same structure of the same animal.

Animals↗
PubMed1983

Relaxation of rabbit cerebral arteries in vitro by clonidine. Evidence of H2-receptor mediation.

The action of the antihypertensive agent, clonidine, was studied in a perfused preparation of rabbit middle cerebral arteries (MCA) in vitro. The MCA segments (8 mm long) were perfused at constant flow, the perfusion pressure upstream being monitored as an index of smooth muscle tone. In both normal (K+ = 2.7 mM) and high potassium (K+ = 30 mM) solutions, clonidine (3.10(-10) - 10(-4) mol.l-1) relaxed the arteries in a concentration-dependent manner. Expressed as a percentage of the maximum relaxation obtained in normal and high K+ solution with 10(-4) mol.l-1 papaverine, the Em was 79 +/- 3.9% (mean +/- SEM) and 63.7 +/- 2.4% respectively, and the EC 50 (4.3 +/- 2.0) 10(-8) mol.l-1 and (1.3 +/- 1.0) 10(-8) mol.l-1 respectively. The action of 6 specific antagonists at 3.10(-6) mol.l-1 was tested on the relaxation obtained in high potassium solution. The concentration-response curve was shifted to the right in a parallel manner, compatible with competitive inhibition, only by the H2-antagonist, cimetidine. Phentolamine and especially propranolol depressed the Em, suggesting antagonism by non-specific mechanisms. Methysergide and sulpiride induced no significant change in Em, but slightly displaced the curve in a nonparallel manner. Yohimbine had no effect on the relaxation. These results are interpreted as indicating that clonidine relaxes rabbit cerebral arteries in vitro, even at low, therapeutic concentrations, possibly by acting on H2-histaminergic receptors.

Adrenergic alpha-Antagonists↗
PubMed1981

Continuous estimation of cerebral metabolic changes.

The purpose of the present research has been to estimate rapid metabolic changes. By means of mass spectrometry, the partial pressure of physiological gases are continuously analyzed in a local area of the brain tissue. The method we have developed allows quantitative measurement of the variables with a response time of less than 1 min. When coupled with continuous measurement of(1) PaO2 and PaCO2 by means of mass spectrometry, and (2) cerebral blood flow by thermoclearance, this method is able to indicate rapid metabolic changes when quantitative methods of determining metabolism are not usable.

Animals↗