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Biomedical subjects

N Moore

Publications and source records attributed to N Moore.

At least 163 records · Page 9Linked to original sources
PubMed1985

Hemodynamic, behavioral and biochemical disturbances induced by an experimental cranio-cervical injury (whiplash) in rats.

Two days after an experimental whiplash performed on anesthetized Long-Evans female rats, without any direct blow to the head, we observed: (1) a hypotension (in supine position) (P less than 0.01), (2) a disturbance of the postural regulation of cerebral blood flow (P less than 0.01), (3) a disturbance of learning behavior characterized by decreased acquisition and retention (conditioned avoidance response and labyrinth tests), (4) an increase of the dopamine level (whole brain, cerebellum, thalamus + hypothalamus, corpus striatum and rest), (5) a decrease of the noradrenaline level in whole brain (P less than 0.05) and in the medulla oblongata but an increase in thalamus plus hypothalamus, hippocampus and corpus striatum, (6) an increased reactivity of the peripheral alpha and beta receptors, determined by analyzing the hemodynamic consequences of i.v. injection of norepinephrine or isoproterenol, (7) there was no modification of the brain content of water or of serotonin and (8) finally, the injured rats displayed a remarkably aggressive behavior, though this was not quantified. These results are in agreement with the hypothesis that a change in brain amines metabolism could explain the different functional effects of whiplash. We therefore believe that the postconcussion syndrome is not subjective and that the neck injury is primary in the determination of the syndrome.

Animals↗
PubMed1985

Oxotremorine-induced cholinergic syndrome: modifications by levodopa and/or oral cytidine diphosphocholine.

A peripheral and cerebral cholinergic syndrome was induced in mice by oxotremorine administration; pretreatment orally with cytidine diphosphocholine (CDP-choline) does not potentiate this syndrome and even antagonizes oxotremorine-induced salivation. Levodopa antagonizes the oxotremorine-induced cerebral symptoms (akinesia + tremor); however this antagonism disappears when mice are chronically pretreated orally with CDP-choline, confirming the action of CDP-choline on dopaminergic pathways. The proven efficacy of CDP-choline in Parkinsonism could then be mediated by a hypersensitivity of some cerebral dopamine receptors, and not by a direct stimulating effect of the striatal dopaminergic receptors.

Administration, Oral↗
PubMed1985

Use of RU 25960, a new calcium antagonist, in normobaric and hypobaric hypoxia.

RU 25960--3-[Bis(3,3-diphenylpropyl)-amino]-propan-1-ol hydrochloride--a vasodilator with calcium antagonist properties, was tested on learning in hypobaric hypoxic rats and survival time in normobaric hypoxic mice. It decreased learning in hypobaric hypoxia, but did not change survival time in mice. This suggests that the mechanisms underlying learning and survival are not the same, and that like other calcium antagonists, RU 25960 has no protective effect against the deleterious effects of hypoxia on the brain.

Aerospace Medicine↗
PubMed1984

A homotaurine derivative reduces the voluntary intake of ethanol by rats: are cerebral GABA receptors involved?

The effects of some derivatives of homotaurine (3 APS), the well known GABA agonist, were tested on the voluntary intake of ethanol by rats. Spontaneously ethanol drinking rats (DR) were selected and had a constant voluntary intake of ethanol by rats. Spontaneously ethanol drinking rats (DR) were selected and had a constant voluntary intake of a 12% ethanol solution (VIE) during 14 days (about 5 g/kg body weight daily). Calcium acetylhomotaurine (0.26 and 0.52 mmol/kg daily IP) significantly reduced VIE and this was inhibited by the GABA antagonist bicuculline (2 mg/kg IP). The conditioned aversion test to saccharin was negative. Bicuculline alone did not affect VIE. Other homotaurine (3-APS) derivatives: sodium acetyl homotaurine (Na AOTA), homotaurine (OTA), sodium acetyltaurine (Na A TA) and calcium chloride (CaCl2) did not affect VIE. These data suggest that the gabaergic system could be implicated in VIE. MERAM Lab. patent.

Acamprosate↗
PubMed1984

The effects of chronic treatment with captopril in spontaneously hypertensive rats (SHR) and their offspring.

Ten consanguine monogamous SHR couples (G1) were treated from their 5th to their 37th week of age with captopril, 50 mg/kg/day i.p. Male rats were treated without interruption. Treatment was withheld in female rats from delivery to weaning. They were compared to ten similar SHR couples which were only daily i.p. injected with the same volume of solvent. Second (G2) generation rats (untreated) were studied. In G1 rats, systolic blood pressure (SBP) and heart weight/body weight (HW/BW) ratio were decreased, while heart rate (HR) was not changed. Plasma renin activity remained unchanged at 37 weeks of age though the treatment was effective. Parental treatment did not reduce SBP and HW/BW ratio in G2 rats. This indicates that reduction of hypertension in SHR is not enough to prevent hypertension development in the offspring of the treated rats.

Animals↗
PubMed1984

HLA antigens and toxic reactions to sodium aurothiomalate in patients with rheumatoid arthritis.

HLA typing studies were performed on 60 consecutive patients with seropositive definite or classical rheumatoid arthritis (RA). Patients were treated with gold and were followed for a minimum of 18 months for identification of adverse reactions to gold therapy. HLA-DR3 was increased significantly in patients who developed gold induced rash, proteinuria or thrombocytopenia. On the other hand, the incidence of HLA-DR4 was lower in patients with these adverse reactions. Our results demonstrate that patients with RA carrying DR3 are at a higher risk of developing adverse reactions to gold. The most interesting finding was the low incidence of DR4 in patients who developed adverse reactions to gold, suggesting that DR4 positive patients may have some degree of protection against gold toxicity.

Adult↗
PubMed1984

[Captopril in cardiac insufficiency. Immediate and long-term effects].

Captopril was administered to 23 patients in cardiac failure refractory to digitalo-diuretic therapy. Four patients had a large fall in systolic blood pressure (less than 70 mmHg) with a single dose of 25 mg of captopril. In the other 19 patients a significant fall in mean pulmonary capillary pressure (16,8 +/- 6,1 mmHg vs 27,2 +/- 8,5 mmHg, p less than 0,001), mean pulmonary artery pressure (26,3 +/- 11,3 mmHg vs 38,3 +/- 12,4 mmHg, p less than 0,001), mean right atrial pressure (5 +/- 5 mmHg vs 8 +/- 6 mmHg, p less than 0,01) was observed: there was a moderate fall in mean systemic arterial pressure (13%, p less than 0,001). There was a significant fall in pulmonary resistance (27%, p less than 0,001). The cardiac index increased (2,8 +/- 0,5 l/min/m2, p less than 0,001) and systemic resistance fell by 25% (p less than 0,001). The heart rate decreased by an average of 7 beats/min (p less than 0,02). The treatment was stopped in one patient because of the inefficacy of captopril at 100 mg per dose. The average daily dose in the 18 patients on long-term treatment was 212,5 +/- 106,8 mg. At the second month, the haemodynamic parameters were remeasured before the morning dose of captopril. The effects observed after the single dose were maintained apart from the systemic blood pressure, heart rate and systemic resistances which had returned to the value observed before administration of captopril. The mean pulmonary capillary pressure was significantly lower than before treatment but was higher than after the single dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Intracoronary thrombolysis in evolving myocardial infarction. Sequential angiographic analysis of left ventricular performance.

Since November 1979 left ventricular angiography and coronary arteriography have been performed in 80 patients with evolving acute myocardial infarction in order to attempt coronary recanalisation by local streptokinase infusion. The average delay between the onset of symptoms and streptokinase infusion was 3.6 hours. Thrombolysis was successful in 64% of cases. No serious complications related to the procedure were noted. Of the 12 patients in cardiogenic shock, recanalisation was achieved in only four, of whom two survived. To evaluate the left ventricular salvage resulting from early recanalisation the last 58 patients had a second left ventricular angiogram and further coronary arteriograms 21 +/- 10 days later and 16 patients had a third study three months later. From the left ventricular angiogram in the right anterior oblique projection the ejection fraction and two graphic variables of regional wall motion were computed quantifying the hypokinetic zone. Patients were divided into two groups, according to the patency of the infarct related artery at the second control: group 1 consisted of 28 patients with successful recanalisation confirmed, and group 2 of 30 patients in whom no recanalisation was achieved or secondary reocclusion had occurred. At the second study the ejection fraction was unchanged in group 1 but had significantly decreased in group 2. Regional wall motion improved in group 1 and worsened in group 2, more so in patients without recanalisation than in those in whom secondary reocclusion had occurred. The third study showed a further decrease in ejection fraction in group 2. A progressive decrease in percentage residual stenosis was observed in group 1. This sequential angiographic study confirms the partial myocardial salvage resulting from early coronary recanalisation during acute myocardial infarction.

Adult↗
PubMed1983

The effects of nicergoline on spontaneously hypertensive rats and their offspring.

Six consanguine monogamous SHR couples (G1) were treated from 5 weeks of age on with an alpha blocker, nicergoline, 0.1 mg/kg/day i.p.. Male rats were treated without interruption; treatment was withheld in female rats from delivery to weaning. They were compare to six similar SHR couples who were only daily i.p. injected with the same volume of solvent in the same conditions as controls, as well as with naive (untreated) rats. Second (G2) and third (G3) generation rats (untreated) were studied. In G1 rats, systolic blood pressure (SBP), heart rate, heart weight/body weight ratio and bulbar noradrenaline content were decreased (compared to control or naive rats), while plasma renin activity (PRA) and hypothalamic noradrenaline content were not changed. In G2 rats, SBP and PRA were decreased, all other parameters being unchanged. No parameter was changed in G3 rats. This appears to be the first report of a preventive effect of antenatal treatment on the development of hypertension in SHR.

Animals↗
PubMed1983

Effects of parenteral treatment by nicergoline on the development of hypertension of S.H.R.

Six consanguine monogamous SHR couples (G 1) were treated from 5 weeks of age on with an alpha blocker, nicergoline, 100 mcg. kg-1 day-1 i.p. Male rats were treated without interruption; treatment was withheld in female rats from delivery to weaning. They were compared with six similar SHR couples who were only daily i.p. injected with the same volume of solvent in the same conditions, as controls. Second (G 2) and third (G 3) generation rats (untreated) were studied. In G 1 rats, systolic blood pressure (SBP) was decreased, and no change was found in heart rate (H R), heart weight to body weight ratio (HW/BW), hypothalamic and bulbar noradrenaline content (HNA,BNA). In G 2 rats, SBP, BNA and plasma renin activity were significantly decreased, all other parameters being unchanged. No parameter change was observed in G 3 rats. We think that such long acting effects after antenatal treatment could only be due to an action on the origin of the SHR hypertension.

Animals↗
PubMed1983

Modification by sulpiride, pimozide, or domperidone of apomorphine's effects on learning in hypoxic rats.

The study of apomorphine's interaction with three dopaminergic antagonists (domperidone, sulpiride and pimozide) is an attempt to characterize the dopaminergic receptors involved in the dopaminergic agonist-induced protection against hypobaric hypoxia. Apomorphine (1 mg X kg-1 but not 0.01 mg X kg-1) reduced total performance (avoidance + escape responses); this effect was antagonised by domperidone and pimozide--not by sulpiride--and appeared to have a peripheral origin. Apomorphine (0.01 and 1 mg X kg-1) increased the avoidance performance during hypoxia. This antihypoxic protection was not suppressed by domperidone, confirming its central origin, but was antagonised both by sulpiride and pimozide. The receptors involved in the anti-hypoxic protective effect appear therefore to be cerebral D4 receptors, according to the classification of Seeman.

Animals↗
PubMed1983

Potentiation by an alpha-adrenolytic agent, nicergoline, of the cardiac effects of propranolol.

Ten young healthy volunteers were given placebo, propranolol (20 or 40 mg), nicergoline, an alpha blocking agent (30 mg) or the association of nicergoline (15 mg) and propranolol (20 mg) in a randomized double blind study. The results show that nicergoline potentiates the cardiodepressant action of propranolol, whereby the effects of 20 mg become the same as those of 40 mg given alone on cardiac output and myocardial oxygen demand, though the plasma propranolol levels are not changed. We, therefore, propose that nicergoline blocks alpha 1 agonist effects of propranolol, which are usually masked by the greater beta 1 blocking effects but could have clinical and therapeutic relevance.

Adult↗
PubMed1982

Piribedil-induced anti-hypoxic protection in rats.

The action of the dopaminergic agonist, piribedil, on a conditioned avoidance response was studied in normoxic or hypobaric hypoxic rats. This agonist has no effects in normoxia, but induced an anti-hypoxic protection (improvement of learning in hypoxia), antagonised by low doses of pimozide. The mechanism of the anti-hypoxic property seems to be mediated by the stimulation of the postsynaptic dopaminergic receptors, but does not exclude the role of noradrenergic pathways, as shown by the stabilisation of norepinephrine levels during hypoxia after treatment with piribedil.

Air Pressure↗
PubMed1981

Dopaminergic agonists and conditioned avoidance response in normoxic or hypoxic rats.

The actions of four dopaminergic agonists (apomorphine, bromocriptine, amantadine, piribedil) on a conditioned avoidance response were studied in normoxic or hypobaric hypoxic rats. Low doses of agonists have no effects on normoxia, but induce an antihypoxic protection (improvement of learning both in normoxia and hypobaric hypoxia. The possibility of an antihypoxic property induced by dopaminergic post-synaptic receptors stimulation is discussed and seems to be the main receptors stimulation is discussed and seems to be the main phenomenon while action or other non-specific sites seems to be responsible for the high dose-induced impairment of learning and of resistance to hypoxia.

Amantadine↗
PubMed1981

hypobaric hypoxia: central catecholamine levels and cortical PO2 and avoidance response in rats treated with apomorphine.

The learning of a conditioned avoidance response, the catecholamine levels in some cerebral structures, and the evolution of the cortical PO2, were studied under hypobaric hypoxia (300 torr) and under normoxia, in rats treated or not with apomorphine, at the dose of 1 or 10 mg/kg i.p. Apomorphine at 1 mg/kg improves the learning capacity and stabilises the cerebral catecholamine levels under hypoxia; no modification of the evolution of the cortical PO2 during hypoxia was observed between control rats and rats treated with this dose of apomorphine. Apomorphine at 10 mg/kg totally inhibits learning under normoxia or hypoxia. It is therefore possible to suppose that the antihypoxic protective mechanism of low-dose apomorphine is due to a stabilization of the levels of both dopamine and noradrenaline during hypoxia, but not to an increase in the cerebral oxygen availability. These data suggest the clinical possibility of using other dopaminergic stimulating agents for their eventual antihypoxic properties.

Air Pressure↗
PubMed1981

Avoidance learning and mechanism of the protective effect of apomorphine against hypoxia.

We have analyzed a conditioned avoidance response (CAR) in rats, under both normoxia and hypobaric hypoxia (300 torr), to try to elucidate the mechanism of apomorphine's protective effect against hypoxia. The resistance to hypoxia is markedly increased by apomorphine (1 mg/kg i.p.) and, to a lesser degree, by an alpha-adrenergic pre-synaptic (yohimbine 1 mg/kg i.p.) or post-synaptic (phenoxybenzamine 1 mg/kg i.p.) blocker. The anti-hypoxic property of apomorphine is not altered when associated with domperidone (0.5 mg/kg i.p.), a peripheral blocker of the dopaminergic receptors. Resistance to hypoxia is decreased by propranolol (1 mg/kg i.p.) and pimozide (1 mg/kg i.p.). It is not modified by tylciprine (2 mg/kg i.p.) or by metergoline (2.5 mg/kg i.p.), a blocker of the 5-hydroxytryptamine (5 H T) receptors. However, the association of any of the above pharmacological agents with apomorphine destroys apomorphine's anti-hypoxic effect. There has even been shown a positive potentialisation ( i.e. an increase of the inhibitory effect) between apomorphine, hypoxia, and the added drug. This potentialisation is already noticeable under normoxia for the association of each of the drugs with apomorphine. Free alpha, beta adrenergic, cerebral dopaminergic, and serotoninergic receptors and an intact amine metabolic pathway therefore seem required for apomorphine to develop its anti-hypoxic activity.

Animals↗