C. Curradi

Hyperresponsiveness of migraine patients to the hypotensive action of bromocriptine.

SYNOPSIS

Prekallikrein and Kallikrein Inhibitor in Plasma of Patients Affected by Recent Myocardial Infarction

Different causes may carry to the shock. The shock credibly has a pathological substrate, that is a damage of the microvessels, particularly capillaries and venules, vasa vasorum included; the sufference of the microvessels concerns mainly the endothelial and basal membrane. Pathogenetically the basic mechanism of the shock is the capillary damage by hypoxia. Hypoxia, in order to establish a capillary damage, must be calibrated in intensity and duration; differently hypoxia, if too important and acute, provokes death following an acute brain damage; if instead too slight, hypoxia does not damage sufficiently the microvessels.

Substance P in the Human Iris: Possible Involvement in Echothiophate-Induced Miosis in Cluster Headache:

Substance P-like immunoreactivity (SP-LI) was measured by radioimmunoassay in iris, choroid, and retina obtained from men after death. Although present in different amounts, SP-LI, eluting as authentic SP or SP sulfoxide in the high-performance liquid chromatography system, was found in the three ocular structures. The retina contained higher concentrations of SP-LI than the iris and choroid. The possible functional involvement of iris SP was studied in 22 episodic cluster headache (CH) patients by using the anticholinesterase agent echothiophate iodide (EI), which also induces an atropine-resistant miosis, putatively due to release of SP from trigeminal sensory neurons. In CH patients EI eye drops instilled into both eyes provoked a prolonged miosis with a more marked response in the pupil of the symptomatic eye. It is proposed that the hyperfunction of SP-containing neurons may coexist with the previously documented sympathetic hypofunction in the innervation of the symptomatic pupil of CH.

Comparison Between Venoconstrictor Effects of Sumatriptan and Ergotamine in Migraine Patients

SYNOPSIS

Painful vein overdistension in migraine patients: no relationship with serotoninergic parameters

Overdistension of the hand-forearm veins after a period of ischaemia-induced stasis causes local pain in a high percentage of migraineurs, but never in healthy subjects. To investigate the mechanism of such pain, we compared 5-hydroxytryptamine (5HT) whole blood levels and hand vein 5HT reactivity of migraine subjects who did experience pain during venous overdistension to those who did not. No differences were found in whole blood 5HT levels or in the venoconstrictor activity of 5HT between subjects experiencing pain and those who did not. No correlation was found between whole blood 5HT levels and the degree of 5HT-induced venoconstriction. Our results suggest that, if platelets are considered as a model of central antinociceptive 5HT neurons, pain appearance is not due to reduced 5HT at a central level and, therefore, to increased perception of peripheral nociceptive stimuli. Moreover, the similar 5HT venoconstrictive effect (indirect marker of venous tone and, therefore, of venous distensibility) seems to indicate that a mechanical factor is not involved in pain appearance during the HAVD test.

Pentazocine in Migraine: Subjective and Pupillary Abnormal Effects

SYNOPSIS

Amplifying Effect of Sumatriptan on Noradrenaline Venoconstriction in Migraine Patients

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.

Monoamine Oxidase Defect in Essential Arterial Hypertension

: A defect in the level of monoamine oxidase activity of platelets was observed in essential arterial hypertension. This defect seems dependent upon a lower rate of synthesis of the enzyme and not to the presence of an isoenzyme, as the net rate of return of the enzymatic activity after pargyline inhibition does not significantly differ between hypertensive and normotensive subjects.

Kallikreinogen-kallikrein system during muscular work in patients with intermittent claudication: Influence of taurine treatment

Studies with indomethacin now show that raised plasma kininogen levels of rheumatoid patients are suppressed within 30 minutes of ingestion of the drug and occur as soon as indomethacin can be detected in the blood. Aspirin is also shown to lower raised plasma kininogen in rheumatoid patients. The significance of these findings will be discussed.