Migraine attacks can be provoked by administration of nitroglycerin, suggesting a role for nitric oxide (NO). The fact that release of the neuropeptide CGRP from trigeminal sensory nerves occurs during the pain phase of migraine and that NO can augment transmitter release prompted us to study CGRP release from the in situ dura mater in guinea pig skulls. Release of CGRP by capsaicin or by high potassium concentration was concentration-dependent and counteracted in calcium-free medium. The anti-migraine compound, sumatriptan, inhibited CGRP release via the 5-HT1-receptor. The NO donors, nitroglycerin, sodium nitroprusside and S-nitroso-N-acetylpenicillamine did not influence CGRP release, alone or together with the stimulants. We concluded that the skull preparation is well suited for scrutinizing CGRP release from dura mater. The fact that sumatriptan inhibits CGRP release as in migraine patients suggests a use for the present preparation in headache research.

The balance of net base in groups of male weanling Wistar rats exposed to sustained oral loads of net base were studied. In response to dietary loads of sodium bicarbonate (approx. 50 mmol·kg^––1·day^––1) an average increment in the mean rate of retention of net base of 21.8 mmol·kg^––1·day^––1 was observed in the absence of significant changes in the blood ‘base excess’. Following withdrawal of sodium bicarbonate, mean rates of gastrointestinal absorption, renal excretion, and retention of net base promptly returned to control values, accumulated net base being retained in the body, presumably as skeletal sodium carbonate. In response to equimolar loads of net base in the form of trisodium citrate, a similar, albeit less pronounced, rise in the rate of retention of net base occurred.

No abstract

Net base and mineral balances were evaluated in a group of male 350 g Wistar rats exposed to 10% carbon dioxide in air for 10 days with a view to identifying the source of net base subject to retention during renal compensation of sustained respiratory acidosis. In response to hypercapnia, the rate of renal net acid excretion rose but insignificantly. However, a rise in whole body net base concentration from about 215 mmol/kg to about 250 mmol/kg came about by ongoing gastrointestinal absorption in the weight-losing animal, absorbed net base being distributed to extracellular and non-extracellular compartments of the body, presumably including bone. During an 8-day recovery period, a small decrement in whole body net base concentration was observed.

Anoxia profundly affects brain function. If the blood flow is interrupted for a few minutes, the interstitial fluid shows a dramatic increase of potassium and lowering of sodium, chloride, and calcium concentrations, which lead to arrest of nerve conduction and synaptic transmission. These changes, however, cannot explain that consciousness is lost within seconds. This may be caused by activation of potassium conductance in nerve cell membranes.