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Notes: Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opicid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses (“empty neuron” condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in inbalance of synaptic neurotransmission.

Notes: The venoconstrictive activity of sumatriptan and its interaction with noradrenaline (NA)- and 5-hydroxy-tryptamine (5HT) venoconstriction was studied in vivo in the hand vein of migraineurs. Sumatriptan, injected at increasing doses into the vein, caused local venoconstriction after a 500 mg dose, comparable to that induced by 0.5–1 mg of 5HT. This venoconstriction was completely inhibited by low doses of ketanserin (5 mg). Subcutaneous sumatriptan (6 mg) provoked a minor increase in vein tone, lasting less than 30 min. Non-venoconstrictive doses of sumatriptan (10–100 mg), injected in the hand vein, produced an amplification of NA-venoconstriction but not of 5HT-induced venoconstriction. A similar increased effect was displayed by subcutaneous sumatriptan (6 mg) for at least 1 h. Sumatriptan appears to cause peripheral venoconstriction only at high doses locally applied (in the hand vein), by acting on 5HT2 receptors. Clinical subcutaneous doses (6 mg) do not show significant venoconstrictive effects. The amplifying effect on NA venoconstriction, also caused by 5HT, ergotamine and dihydroergotamine in human cranial arteries, may be important in explaining the therapeutic action of sumatriptan in migraine attacks.

Notes: The action of ergotamine on the 5-hydroxytryptamine (5-HT) venous sensitivity was studied in ergotamine abuser and non-abuser migraine patients. Ergotamine abusers showed reduced 5-HT hand vein contraction during abuse, compared to seven days after ergotamine withdrawal. In non-ergotamine users, the 5-HT venoconstriction was not significantly modified 12 h after a single intramuscular ergotamine (0.25 mg) administration. Even the administration of ergotamine locally into the vein did not change the venospasm of 5-HT given acutely in the same vein. Therefore, it seems that the 5-HT antagonism does not contribute to the therapeutic effect of ergotamine during the migraine attack. Moreover, the reduced 5-HT responsiveness during ergotamine abuse may possibly be compatible with the chronic headache present in some abusers, the withdrawal headache attacks and the abuse itself.

Notes: Abstract Sea urchin embryos and sperm were utilized for evaluating the toxicity of water and sediment from two rivers, the Sarno (S) River and the Volturno (V) River, in the Campania region, Italy. The effects on developing embryos were evaluated by scoring developmental defects, whereas sperm exposure was tested for the effects on fertilization and offspring quality. Ten sampling sites from the rivers (S.1–S.4 and V.1–V.6) were monitored for water and sediment quality. Water sampling was carried out biweekly for a year (1988–1989); the samples were tested at dilutions 10−4 to 10−2 in natural seawater. Sediment tests were carried out on solid phase samples (collected in 1989 to 1992), at concentrations ranging from 2 to 10 mg/ml (dry wt) in seawater. The tests conducted on water samples mostly led to nonsignificant results in either embryo-or spermiotoxicity, possibly due to sharp changes in pollutant levels in the water column. Unlike water, sediment samples displayed clear-cut results both on embryogenesis and on fertilization success. The grain size of sediment failed to reveal any relationship with toxicity, which could only be referred to the presence of toxic contaminants (Melluso et al., 1993). The most polluted sediment samples displayed a dramatic embryo-toxicity, up to approximately 87% developmental arrest in embryos reared in 2 mg/ml of sediment from site S.1 (affected by leather tanning effluent). These results were independent of storage conditions of sediment samples (i.e., at +4°C or −20°C). A decrease in fertilization success was also induced by sediment samples from polluted sites (not by a relatively unpolluted reference sample). Interestingly, sediment spermiotoxicity appeared to be related to storage temperature in samples from two agricultural sites (S.3 and V.6), in that freezing caused a drop in sample spermiotoxicity compared to refrigeration; e.g., a sample from site V.6 stored at +4°C decreased fertilization rate (FR) to 9% versus a control value of 86%, whereas the same sample induced but a minor change following storage at −20°C (FR=68%). In general, a better reliability was observed for sediment bioassays than for water bioassays, thus suggesting that future biomonitoring studies should mainly focus on sediment quality. The use of solid phase sediment in toxicity testing by sea urchin embryos and sperm is warranted by the present results.