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Biomedical subjects

R G Boulu

Publications and source records attributed to R G Boulu.

66 records · Page 4Linked to original sources

[Urinary N-acetyl-beta-glucosaminidase as index of renal toxicity (author's transl)].

Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) has been studied in rats submitted to potentially nephrotoxic drugs (acetylsalicylic acid, gentamicin). Both drugs induced increase in NAG excretion which was reversible and dose-dependent. The date presented in this paper suggest that urinary NAG determination may have value as screening device for the study of nephrotoxic effects in experimental toxicology.

Acetylglucosaminidase↗

Relaxation by dopaminergic agonists in cerebral and peripheral arteries (in vitro).

The receptors involved in dopamine-induced relaxation were investigated in whole segments of rabbit middle cerebral (M.C.A.) and central ear arteries (C.E.A.) by measuring pressure changes in a constant-flow in vitro set-up. Drug administrations were made in the perfusate. During treatment with high-K+ solution to induce active contraction, and in the presence of 3 x 10(-5) M phenoxybenzamine to prevent alpha-adrenergic contractions, cumulative concentration-response curves were obtained for dopamine, apomorphine, bromocriptine and piribedil. The effects of the dopamine receptor antagonists, sulpiride, haloperidol and droperidol, and a beta-adrenergic antagonist, propranolol, were tested on the concentration-response curves obtained with dopamine. The results can be summarized as follows: the dopaminergic agonists had a relaxant effect in 50% of C.E.A. and in 70% of M.C.A. after alpha-adrenergic receptor blockade. This effect was blocked by the 3 antagonists in the M.C.A., and this antagonism appeared to be competitive in the case of sulpiride. In the C.E.A., haloperidol and droperidol exerted complex effects on the dopamine relaxation, and sulpiride had inconsistent effects. Propranolol reduced the concentration-dependent relaxation in the C.E.A., but did not modify the relaxant effect of dopamine in the M.C.A. The present results are consistent with the hypothesis that dopaminergic agonists relax cerebral arteries by acting on specific receptors. The relaxant action on the C.E.A. seems more complex and may occur partly via beta-adrenergic receptors.

Animals↗

Model of global forebrain ischemia in the unanesthetized rat.

Global forebrain ischemia was induced in unanesthetized rats by electrocauterization of the vertebral arteries and transient occlusion of the common carotid arteries for 30 minutes. Local cerebral blood flow (l-CBF), cortical tissular pO2 (tpO2), electrocorticogram (ECoG), mean arterial pressure, pH and blood gas determinations and neurologic deficit were evaluated during and after ischemia. Cerebral ischemia induced a substantial decrease in l-CBF and tpO2 and the ECoG was flattened. One hour after ischemia, the neurologic deficit was at its maximum, l-CBF was still decreased and ECoG depressed. Twenty-four hours later, the neurologic deficit was still present but ECoG, l-CBF and tpO2 had returned to their preischemic values. Treatments with naloxone were performed during, after or during and after ischemia. When naloxone was administered during or after ischemia, postischemic neurologic deficit was not influenced by the treatment. A slight but significant improvement of the neurologic score was observed when naloxone was injected during ischemia and infused thereafter. Our results show that this experimental model of cerebral ischemia is suitable for quantification of neurologic alterations during the postischemic period. The slight improvement observed with naloxone suggests that endogenous opioids may have a minor role in the neurologic consequences of ischemia.

Animals↗

Effect of indomethacin on the coupling of cerebral blood flow to brain metabolism.

The effect of indomethacin (10 mg.kg-1 i.p.) on frontal cerebral blood flow has been investigated in male Sprague Dawley rats using the hydrogen clearance technique. Indomethacin elicited a marked reduction in cerebral blood flow in awake free-moving animals. The response to indomethacin was prevented by pretreatment with pentobarbital (50 mg X kg-1, i.p.). On the other hand, indomethacin was able to antagonize the cerebral vasodilation due to apomorphine chlorhydrate (2 mg X kg-1, i.p.), dexamphetamine tartrate (3 mg X kg-1, i.p.) or immobilization stress. Taken together, the above results lead to the suggestion that indomethacin can suppress the coupling of cerebral blood flow to brain metabolism. Further investigations are needed to ascertain whether this uncoupling influence is related to brain cyclooxygenase inhibition.

Anesthesia↗