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Biomedical subjects

J R Boissier

Publications and source records attributed to J R Boissier.

At least 19 recordsLinked to original sources
PubMed1979

The role of beta-adrenoceptors in coronary blood flow distribution in normal and ischemic canine myocardium.

beta-Adrenoceptor agonists increase myocardial ischemic injury, mainly by elevating myocardial oxygen consumption. Moreover, it has been shown that isoprenaline may "steal" regional myocardial blood flow (RMBF) from ischemic to non ischemic areas and from epicardium to endocardium. The mechanisms of these two isoprenaline-induced redistributions of RMBF have been investigated by the use of radioactive microspheres in an experimental model of canine myocardial ischemia with simultaneous measurement of ST-segment elevation. Isoprenaline increased RMBF in both epi- and endocardial non ischemic areas and in epicardial ischemic areas, leading to a significant decrease in the endo/epi ratio. After atenolol, isoprenaline still increased RMBF but to a lesser extent and the endo/epi ratio was still decreased. Salbutamol, in doses inducing no significant changes in cardiac parameters or myocardial oxygen consumption, produced effects similar to those of isoprenaline. These results indicate a non-homogeneous beta2-stimulation-induced vasodilation in endo- and epicardium, which might be due either to the higher epicardial coronary vasocilatory reserve or to a heterogeneous distribution of transmural beta2-adrenoceptors. Isoprenaline also decreased the ischemic/non ischemic total blood flow ratio (I/NI) and caused further increases in ST-segment elevation. These effects were abolished by atenolol pretreatment, indicating the deleterious effects of isoprenaline-induced tachycardia in this I/NI decrease and in the ischemic injury.

Albuterol↗
PubMed1979

Is dopamine-sensitive adenylate cyclase involved in regulating the activity of striatal cholinergic neurons?

The dopamine (DA)-receptor mediated changes in striatal acetylcholine (ACh) levels have been studied to determine if this effect involves a D1-(adenylate cyclase dependent) or D2-(not linked to an adenylate cyclase) type of DA-receptor, Various DA-agonists (apomorphine, N-diphenethylamine derivatives) increased striatal ACh levels in both intact and 6-OHDA lesioned rats whereas only apomorphine stimulated the adenylate cyclase activity of striatal homogenates. The N-diphenethylamine compounds (RU 24213, RU 24926 and RU 26933) were without effect either on basal or DA-stimulated activities of this enzyme. In contrast, D-LSD (which acts as a partial agonist of the striatal DA-sensitive adenylate cyclase) did not modify the striatal ACh content. More interestingly, an intrastriatal injection of cholera toxin greatly stimulated striatal adenylate cyclase without altering ACh concentrations. Both haloperidol and methergoline antagonized the DA stimulation of adenylate cyclase, but only haloperidol decreased striatal ACh levels. These results indicate that the DA receptor involved in regulating the activity of striatal cholinergic neurons is of the D2-type.

Acetylcholine↗
PubMed1979

Amoxapine in experimental psychopharmacology: a neuroleptic or an antidepressant?

2-Chloro-11-(piperazinyl)dibenz[b,f][1,4]-oxazepine (amoxapine) gives an unusual spectrum in psychopharmacological tests. Many of its effects are similar to those of neuroleptics: sedation, decrease in motor activity, catalepsy (which is, however, qualitatively different from that induced by classical neuroleptics), transitory suppression of avoidance reaction, antagonism of amphetamine induced toxicity in crowded mice and inhibition of stereotyped behavior induced by amphetamine in rats, and antagonism to various effects of apomorphine (stereotyped behaviour in rats, climbing behaviour, stereotyped behaviour and hypothermia in mice). At similar doses which produce the above mentioned effects, amoxapine also shows effects atypical for a neuroleptic, but which are relatively characteristic of antidepressants: antagonism of prochlorperazine-induced catalepsy in rats, inhibition of reserpine induced hypothermia in mice and enhancement of yohimbine toxicity in mice. The profile of this substance does not facilitate the anticipation of therapeutic effects in humans.

Amoxapine↗
PubMed1978

Benzodiazepines and behavioral effects of reward (water) omission in the rat.

Two behaviors related to nonreward (omission of water in an enclosure where the rats were habituated to drink) were studied. The time spent licking the bottles during water omission and the time spent drinking during a subsequent 5-min drinking session (water available) were recorded. The drinking session was performed 30 min after the water-omission session. Rats subjected to water omission showed an enhanced drinking time that varied with the length of the water omission session, with the motivational state of the animals, and with the previous number of water-omission sessions. Diazepam, chlordiazepoxide, lorazepam, and meprobamate (i.p., 30 min before water omission), increased the time spent licking the empty bottles, but failed to abolish subsequently enhanced drinking. However, some of our data suggested that minor tranquilizers weakly reduced the increased drinking induced by nonreward, despite their direct stimulation on water drinking. It is proposed that either minor tranquilizers are devoid of general antifrustration activity or nonreward-induced frustration and nonreward-induced drive enhancement may not be correlated.

Amobarbital↗
PubMed1978

Benzamides and classical neuroleptics: comparison of their actions using 6 apomorphine-induced effects.

The effects of 6 benzamides and 8 classical neuroleptics were studied on 6 different apomorphine-induced effects. These drugs did not antagonize all the effects in the same way. The differences are discussed according to the two types of dopaminergic receptor hypothesis. Some apomorphine-induced effects (stereotyped behavior, circling behavior, climbing behavior, and increased motor activity) could be related to stimulation of one type of dopaminergic receptor, other effects (hypothermia and decreased activity) to the other type. Pimozide, sulpiride, thioproperazine, GRI 1665 and TER 1546, could block selectively one type of dopaminergic receptor, at least in a given range of doses. Clozapine, chlorpromazine, levomepromazine, and thioridazine, could block selectively the other type of dopaminergic receptor. Haloperidol, metoclopramide, prochlorperazine, sultopride, and tiapride, could block both types of dopaminergic receptors with equal intensity whatever the dose.

Animals↗
PubMed1978

Chronic atenolol treatment and hypertension development in spontaneously hypertensive rats.

Changes in systolic blood pressure (SBP), heart rate (HR), heart rate and plasma renin concentration (PRC) have been compared in three different groups of rats between the ages of 5 and 20 weeks. The groups were: spontaneously hypertensive rats (SHRs), atenolol-treated SHRs (200 mg/kg/day orally throughout the 15 weeks) and normotensive rats of the same strain (WKYs). Treatment with atenolol markedly inhibited the onset of genetic hypertension, reduced HR and PRC from the outset and diminished the heart weight/body weight ratio. Comparison of changes in these parameters in atenolol-treated SHRs, control SHRs and WKYs strongly suggests that the mechanism of atenolol's preventive action against hypertension development in SHRs primarily involves its effects on heart and on the renin--angiotensin system.

Animals↗
PubMed1978

The effects of pentobarbitone and urethane on pulmonary airway resistance in guinea-pigs and their interactions with drugs.

1 Propranolol increased pulmonary airway resistance (PAR) in the conscious guinea-pig, whereas atropine had no effect, suggesting the existence of a continual sympathetic bronchodilator tone. 2 The direct bronchoconstrictor effects of histamine, acetylcholine and 5-hydroxytryptamine were modified by autonomic reflexes: a bronchodilator one, abolished by propranolol, and a cholinergic bronchoconstrictor one, seen with histamine. 3 Pentobarbitone increased PAR, an effect which was reduced by propranolol but which was unaffected by atropine. The bronchoconstrictor effects of histamine, acetylcholine and 5-hydroxytryptamine were potentiated by pentobarbitone. 4 Pentobarbitone therefore appears to inhibit the adrenergic bronchodilator tone and to depress adrenergic reflexes, these being the preponderant autonomic influences in these experiments. 5 Like pentobarbitone, urethane increased PAR in the conscious guinea-pig and potentiated the bronchoconstrictor effects of the three amines. These actions are similarly attributed to a reduction in adrenergic influences.

Airway Resistance↗
PubMed1978

General pharmacology of ergot alkaloids.

Ergot alkaloids possess a wide and divergent spectrum of central and peripheral pharmacodynamic actions. They interfere with different receptor sites to stimulate and/or inhibit effector structures. The concept of partial agonism on alpha-adrenoreceptors has replaced the ancient hypothesis of direct stimulation of vascular and uterine smooth muscle. The mechanisms which are considered to be relevant for the therapeutic use of dihydroergotamine, a potent drug increasing venous tone, and of bromocriptine, a specific inhibitor of prolactin secretion, are discussed in more detail.

Animals↗
PubMed1978

Beta adrenergic blockade, regional left ventricular blood flow and ST-segment elevation in canine experimental myocardial ischemia.

The effects of dl-propranolol, d-propranolol, dl-pindolol and dl-practolol on regional myocardial blood flow (assessed by means of tracer microspheres) and on ST-segment elevation in ischemic and nonischemic areas of the canine left ventricle have been investigated. dl-Propranolol and dl-pindolol, but not dl-practolol and d-propranolol, induced blood flow redistribution from the epicardium to the endocardium both in ischemic and nonischemic areas. dl-Propranolol-induced redistribution was abolished by atrial pacing at the control heart rate value. These results indicate that the redistribution phenomenon only occurs if both a bradycardia-inducing beta1 adrenoreceptor blockade and a coronary vessels beta2 adrenoceptor blockade are simultaneously achieved. All four drugs significantly decreased ST-segment elevation in ischemic areas. Under atrial pacing, this effect was abolished with dl-practolol but only reduced with dl- and d-propranol, suggesting that, besides bradycardia, membrane stabilization might be involved in protection against ST-segment elevation in ischemic areas.

Adrenergic beta-Antagonists↗
PubMed1978

Pharmacological findings on cetiedil.

The molecule of cetiedil (Stratène) has strong papaverine-like and weak atropine-like properties. It brings about peripheral vasodilation at doses which do not affect arterial blood pressure, heart beat and cardiac efficacy; this new drug increases the activity of beta-adrenergic stimulants. There may be different hypotheses to explain the therapeutic effect of cetiedil; beside its papaverinic and synergistic beta-stimulant properties, it increases the haemodynamic coefficient, plays a role in the process of membrane Ca++ exchange and inhibits phosphodiesterase and platelet aggregation.

Animals↗