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Biomedical subjects

J van den Driessche

Publications and source records attributed to J van den Driessche.

At least 19 recordsLinked to original sources

[Pharmacology of the venous system].

The presence of alpha 1-receptors has been demonstrated in numerous venous fragments for various animal models. On the other hand, the presence of alpha 2-receptors in the saphenous of the dog is a matter of debate. Beta 2-receptors are activated by isoproterenol, noradrenaline and adrenaline in precontracted veins (part of the facial vein of the rabbit may be an exception). Preferential blocking by atenolol of beta 1-receptors in the jugular veins of the rat suggests that these receptors may mediate vasodilation. The saphenous veins of the dog provide the only example where specific dopaminergic receptors have been noted following partial antagonism with haloperidol. The vasoconstrictive action of acetylcholine has been seen in venous segments of numerous species and indicates the presence of muscarinic receptors. The existence of angiotensin receptors can be postulated despite the weak and inconstant in vitro and in vivo (the dorsal cerebral sinus in the dog excepted) reactions observed and the use of a non-specific antagonist. The same is true for bradykinin and vasopressin. The marked vasoconstrictive action of serotonin on all veins studied is evidence for the presence of receptors. The nature of the antagonists is subject to some divergence of opinion. Nevertheless, D tryptamine muscular receptors (or 5 HT2) can be identified due to the lack of morphine-mediated response and the efficacy of methysergide. The presence of a third type of serotoninergic receptor has only been reported once, following observations of vasodilation in the sheep. H1 receptors are involved in histamine-mediated vasoconstriction. The presence of H2 receptors which mediate vasodilation in precontracted veins remains hypothetical. Prostaglandins exhibit different efficacies in producing contraction in isolated veins; PGF2 alpha is more efficacious than PGE1 and PGE2. Prostacyclin induces contraction of human saphenous veins in a dose-dependent manner. PGE2 and particularly PGE1 can induce relaxation in precontracted veins, as is also true for prostacyclin. Receptors for these prostaglandins must exist at the post-junctional level. P2-receptors mediate transmission of the vasoconstrictive action of various purine derivatives.

Animals↗

[Epidural anesthesia using the bupivacaine-fentanyl combination for cesarean section].

This prospective study was designed to evaluate the benefit of a bupivacaine-fentanyl mixture vs bupivacaine alone in epidural anaesthesia for caesarean section. In 10 women, 0.5% bupivacaine (1.18 ml per metamer) was injected in the epidural space. In 20 women, 0.5% bupivacaine (1.06 ml per metamer) was injected by the same route together with fentanyl (1.70 +/- 0.09 micrograms X kg-1). The bupivacaine-fentanyl group showed a significantly shortened onset of analgesia (p less than 0.001), as well as a significant reinforcement of this analgesia graduated from 0 to 4 (p less than 0.01 at 25 min, p less than 0.001 at 75 min and at the maximum of pain, for the two sets of scores). All the Apgar scores were maximal at 5 min. No clinical respiratory depression was observed in either the mothers or the neonates. Fetal and maternal blood concentrations were in favour of respiratory innocuousness of the method (peak fentanyl concentrations: in mothers 1.5 ng X ml-1, in neonates 0.8 ng X ml-1). Fentanyl never induced any significant haemodynamic variations. Pruritus and nausea respectively occurred in six and two patients respectively in the bupivacaine-fentanyl group. In conclusion, in caesarean section, the adjunction of fentanyl to bupivacaine significantly improved analgesia without any clinical respiratory depression both in the mother and the neonate.

Adult↗

[Hemodynamic and biological effects of bromocriptine in essential hypertension].

Central dopaminergic dysfunction has been suggested as the cause of essential hypertension. Agonist dopaminergic substances (AD) possess documented anti-hypertensive properties. We studied the cardiovascular effects of a single oral dose of 10 mg of Bromocriptine (Br) in untreated subjects with essential hypertension. A number of hemodynamic and biological parameters (direct blood pressure, pulmonary arterial and capillary pressures, cardiac index, heart rate, right ventricular and left ventricular work indices, systemic arterial and pulmonary vascular resistance, plasma renin activity, prolactin, and circulating Br levels) were measured before and after ingestion of the drug (at I, 1,5, 2, 3, 4, 5, 6, 8, 10 and 12 hours). Despite great individual variability, under the experimental conditions, Br displayed a strong anti-hypertensive action. The fall in blood pressure was early (Ist our) progressive, stabilising between the 3rd and 6th hour and prolonged (12 hour). This response was independent of the basal blood pressure with basal plasma renin activity (R = 0.64; p less than 0.05) but not with the prolactin level. The left ventricular work index underwent a similar change. Systemic arterial resistance fell, but this occurred after the fall in blood pressure. There was an independent and significant fall in pulmonary arterial pressure and pulmonary vascular resistance. The prolactin level fell very quickly and remained low throughout the 12 hours. There was an excellent correlation between the direct blood pressure and prolactin level (r = 0.97; p less than 0.01). Plasma renin activity rose after the third hour to reach a maximum at the 8th hour. There was a weak correlation between the blood pressure and plasma renin activity (r = 0.65, p less than 0.05). The serum Br level varied from patient to patient but reached a maximum at 1 hour, remaining stable until the 6th hour before decreasing. There was a correlation between the plasma renin activity and prolactin levels at each dosage (r = 0.66; p less than 0.005). The hemodynamic effects of Br are similar to those of central anti-hypertensive agents. The changes in plasma renin activity are comparable to those observed in central dopaminergic dysfunction. The excellent chronological correlation between the change in blood pressure and prolactin level is compatible with the hypothesis of this type of dysfunction in essential hypertension, if the inhibition of prolactin is accepted as a central dopaminergic effect of bromocriptine.

Adult↗

The use of bromocriptine for testing central dopaminergic reactivity.

A single oral intake of 10 mg of Bromocriptine can modify both plasma renin activity (PRA) and arterial blood pressure (BP). The changes in both variables depend on the integrity of the central dopaminergic systems. The parkinsonians whose extrapyramidal symptoms are markedly improved by L-Dopa in association with a decarboxylase inhibitor (IDC) and the untreated parkinsonians are the only patients whose PRA and BP are lowered 1 h after Bromocriptine ingestion. The results obtained in the L-dopa-induced dyskinetic parkinsonians are similar to those obtained in the group of L-Dopa-resistant patients. This points to the paradoxical hypothesis of dopaminergic hyposensitivity in the dyskinetic patients. In spite of the absence of correlation between PRA and BP, it is possible that lowering of BP by Bromocriptine is linked to the parallel decrease of PRA. An increase of the BP may be obtained in the dyskinetic and L-Dopa-resistant groups. These data point to a possible involvement of central dopaminergic systems in some aspects of hypertension.

Blood Pressure↗

[Contribution to the pharmacology of a novel neuroleptic drug: flupenthixol (author's transl)].

Flupenthixol, which is chemically closely related to clopenthixol and fluphenamine, has the following properties: it reduces spontaneous motor activity, disturbs the behaviour, potentiates hexobarbital and chloral sleep, lowers central temperature and protects from death due to amphetamine; it is cataleptigenous and antagonizes apomorphic vomiting; it has marked adrenolytic and antihistaminic properties; its analgesic action is noteworthy. Flupenthixol presents the pharmacological profile of a neuroleptic drug.

Amines↗

[Toxicologic and pharmacologic study of tributyltin oxide (TBTO)].

Toxicological study on bis-(tributyl-tin) oxyde shows a delayed toxicity of this compound in acute experiments. The same result is obtained in sub-chronic study. Most of the animals die after a great loss of weight. In pharmacological study, T. B. T. O. depresses central nervous system, but his action on ortho and parasympathetic system is slight and non specific. In rat, rabbit and dog, the effect is a fall in blood pressure that result from a depression of the vascular smooth muscle. The death of the animal is due to respiratory arrest by a central mechanism.

Animals↗

[Anti-cerebral edema properties of PEG 300 in triethyltin poisoning].

The polyethylene glycols (PEG) frequently used as solvents of non hydrosoluble molecules present toxic and pharmacodynamic properties. The effect of PEG 300 (10 ml/kg) on the modifications of the central nervous system (CNS) previously induced by a subchronic intoxication with triethyltin salt (TEE) (2 mg/kg p.o. for 5 days) has been studied in rat. The following parameters are recorded: measure of brain edema, concentration of the aminergic neurotransmitters in four different brain areas, neurological status, behaviour, mortality. The PEG 300 antagonizes or reduces some of the effects of the TEE: edema, behavioral disturbances, mortality. On the opposite, no change in the amines and their metabolites induced modifications is observed. This selective antagonism towards some of the components of TEE brain toxicity brings more information on pharmacological properties of this solvent and opens a discussion on the role of neurotransmitters on brain edema.

Animals↗