Taurine and myocardial noradrenaline.

Taurine (CAS 107-35-17) is an anticonvulsant used also as an adjunct in the treatment of cardiovascular disorders. Therefore, we studied its effects noradrenergic transmission in the isolated rabbit heart prelabelled with 3H-noradrenaline. At the concentrations of 1 and 10 mmol/l taurine treatment was without effect on the neuronal and extraneuronal uptake of noradrenaline by the myocardial tissue. At the highest concentration, it decreased the spontaneous release of the transmitter and enhanced its catabolism. Without any significant effect on tyramine-induced noradrenaline release, taurine decreased the release of the amine induced by dimethylphenylpiperazinium and nerve stimulation. These results suggested that taurine may reduce the peripheral sympathetic activity by accelerating noradrenaline catabolism and decreasing its release probably via its ability to prevent a rise of intracellular calcium ion.

[Alveolar hemorrhage after cocaine inhalation]. / Hémorragie alvéolaire après inhalation de cocaïne.

Following inhalation of cocaine two young men developed haemoptysis associated with dyspnoea. One of these patients had severe clinical symptoms. There was blood eosinophilia, and haemosiderin was found in the macrophages that were present in the fibroscopic alveolar lavage fluid. X-ray films of the chest showed bilateral micronodular opacities. The outcome was favourable after treatment with parenteral dexamethasone, oxygen therapy and mask-administered continuous positive pressure ventilation. The frequency of cocaine-induced alveolar haemorrhage is probably underestimated; the condition must be suspected in subjects who inhale cocaine and have haemoptysis, no matter how small.

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.

Possible non-involvement of lipoxygenase pathway in the cerebral blood flow decrease due to indomethacin.

Indomethacin (10n mg/kg i.p.) induced a marked decrease in local cerebral blood flow (l.CBF), which was measured in the frontal cortex of unanesthetized rats by the hydrogen clearance technique. Brain prostaglandins (PGD2, PGE2, PGF2 alpha,) and 6kPGF1 alpha the stable metabolite of prostacyclin, were significantly decreased. Treatments with inhibitors of lipoxygenase (BW 755C and nordihydroguaiaretic acid) and with FPL 55712, a leukotriene receptor antagonist, did not influence the effect of indomethacin on 1.CBF. The results suggest that the release of vasoconstrictory leukotrienes does not play a major role in the lowering of 1.CBF by indomethacin.