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Biomedical subjects

E Pinard

Publications and source records attributed to E Pinard.

At least 55 records · Page 3Linked 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

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↗
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↗
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

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↗
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↗
PubMed1979

Is there an active mechanism limiting the influence of the sympathetic system on the cerebral vascular bed? Evidence for vasomotor escape from sympathetic stimulation in the rabbit.

The influence of the cervical sympathetic chain on cerebral circulation in the rabbit was studied by means of 3 complementary techniques. Two dynamic techniques involving chronically implanted probes were used: blood flow in the caudate nucleus (CN) was measured by thermal clearance; tissue PO2 and PCO2 in the same structure were measured by mass spectrometry. Other variables measured continuously and simultaneously included arterial blood pressure (BP), PaO2 and PaCO2. The third technique was a tissue sampling method based on the Fick principle and using 14C1 ethanol as tracer. Blood flow in 7 regions was measured at stable BP, PaO2 and PaCO2. Stimulation of the sympathetic chain at 15 Hz induced mean maximal decreases in CN blood flow of 23.9% (thermal clearance) and 24.4% (ethanol technique). Mean decrease of PO2 in the CN at 15 Hz was 16.6%. Significant falls in blood flow were observed with the ethanol technique in all 7 structures measured. During prolonged stimulation (greater than 1 min) CN blood flow and PO2 were found to escape towards the baseline level, which was sometimes even exceeded during the stimulation (blood flow). Stimulation frequency had only a very moderate influence on the rate of escape, and no evidence of a metabolic mechanism was found, although injection of barbiturate decreased the escape. These results are discussed with respect to the conflicting evidence on the effects of sympathetic stimulation in the brain, and to possible mechanisms for the escape phenomenon.

Anesthesia, General↗
PubMed1979

The cholinergic pathway to cerebral blood vessels. II. Physiological studies.

The effect of stimulating the greater superficial petrosal nerve (g.s.p.n.) upon retroglenoid venous blood flow has been tested in anaesthetized, paralysed and artificially ventilated rats. In 11 out of 15 tests, blood flow increased by an average of 25% with a time to peak response of 28 s. This response was abolished with the injection of atropine 0.1 mg kg-1 injected intra-arterially. With both petrosal nerves intact, the administration of 6-7% CO2 in air or 15% O2 in N2 caused average increases in blood flow of 105% and 45% respectively. These responses were not affected by bilateral section of the g.s.p.n. Similar experiments were carried out in 5 anaesthetized, spontaneously breathing rabbits in which, in addition to PaCO2 and PaO2, PO2, PCO2 and blood flow in the caudate nucleus were measured continuously using chronically implanted mass spectrometer catheters and heated thermistors. Caudate nucleus blood flow increased in response to hypoxia and hypercapnia and this response was not significantly affected by section of one or both g.s.p.n., sinus or vagus nerves. With section of sinus and vagus nerves, blood flow changed passively with arterial pressure.

Animals↗
PubMed1978

Intracerebral gas partial pressure changes under vasoactive drugs. A mass spectrometry study.

An original technique based on mass spectrometry has been used to measure simultaneously in undrugged, freely-breathing animals local PO2 and PCO2 in the brain (caudate nucleus) and arterial PO2 and PCO2 in the aorta. Injection of vasoactive drugs brought about significant modifications of the partial pressures of the physiological gases in the brain. The origin of these variations was discussed, based on the combination of 3 possible factors: cerebral vascular changes, systemic metabolic changes (PaO2 and PaCO2) and local metabolic changes. It was demonstrated that local variations of PCO2 cannot be held to be responsible for the modifications of cerebral blood flow induced by papaverine or the sympathomimetic drugs.

Animals↗
PubMed1978

Continuous measurement of gas partial pressures in intracerebral tissue.

A mass spectrograph technique has been developed for measurement of physiological gas partial pressures locally in the brain. The sampling cannula is implanted stereotaxically and remains in situ for several weeks. It is a thin cylinder in shape, and is covered with a thin polyethylene membrane across which gas molecules can be sampled continuously. The conductance of this membrane is well adapted to the limited rate of replacement of gas molecules afforded by the cerebral tissue, hence there is no depletion around the cannula; this depletion has until now been the major problem of this technology. The present technique provides a continuous measurement with fast response time, which is directly proportional to the partial pressures of the gases. The variations can be expressed as a percentage of the base-line value.

Animals↗
PubMed1978

[Action of vaso-active drugs on gasz of cerebral tissue. Experimental study by mass spectrometry (author's transl)].

The authors describe a method for measuring cerebral tissue respiration by mass spectrometry. The first applications concern the action of vaso-active drugs on intracerebral PCO2 and PO2. The information gained with this method may prove of value in elucidating the mechanisms of drug action and the regulatory mechanisms of cerebral blood flow. Further prospects of experimentation offered by the method are mentioned.

Animals↗
PubMed1975

Neurogenic influence on local cerebral blood flow. Effect of catecholamines or sympathetic stimulation as correlated with the sympathetic innervation.

Local cerebral flow was measured continuously in conscious rabbits (thermoclearance technique), and PaO2 and PaCO2 were recorded by mass spectrometry. Though inhalation of CO2 increased flow in caudate nucleus and lateral geniculate body, catecholamines only had effect on caudate nucleus where isoproterenol enhanced and epinephrine and norepinephrine reduced flow. Reduction by electrical stimulation of the neck sympathetic trunk was particularly evident in the caudate. Blood flow increased markedly in both regions after preganglionic conduction blockade. The effects were correlated with a significantly lower degree of sympathetic arteriolar innervation (fluorescence histochemistry) in the lateral geniculate body compared with the caudate nucleus.

Animals↗