Subarachnoid hemorrhage (SAH) was induced in 13 adult mongrel cats by a slow injection of fresh autogenous blood into the cisterna magna. Serial determinations of regional cerebral blood flow (rCBF) in the cortex and deep-seated areas (internal capsule, thalamus, and caudate nucleus) were made during the following 2 hours, while intracranial pressure (ICP) was maintained at normal values. A decrease in rCBF was observed in all the areas examined. This reduction followed a characteristic triphasic pattern with an initial steep decline immediately after the SAH. The clinical implications of these findings are discussed.

Nerve injury sometimes triggers neuropathic pain states that are exacerbated by sympathetic efferent activity. A classic example is causalgia. The mechanism of coupling between sympathetic efferent activity and the afferent discharge responsible for pain sensation is a subject of controversy. Some authors hold to the 'direct coupling hypothesis' which proposes that noradrenaline (NA), released from sympathetic varicosities, acts directly on alpha-adrenoreceptors located in the membrane of injured primary afferents. Others believe that coupling is indirect; that the effects of NA are mediated by additional, non-adrenergic, chemical substances and their receptors (the 'indirect coupling hypothesis'). For example, it has been proposed that in inflamed skin NA acts back on the sympathetic endings which, secondarily, release a prostanoid mediator which sensitizes afferent endings. We report that the responsiveness of injured afferent axons to systemically applied NA persists, and in fact increases in prevalence, in rats that underwent prior chemical or surgical sympathectomy. The observation of adrenosensitivity in injured afferents in the absence of sympathetic postganglionic endings is consistent with the direct coupling hypothesis, which associates adrenosensitivity with the injured afferent axon. It is not consistent with the indirect coupling hypothesis which requires the presence of sympathetic endings as a source for NA-evoked prostanoid release.

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This study examined the effect of Oriental hornet venom sac extract (VSE) on the rate of local blood flow in the cerebral cortex of rats. Sublethal doses of VSE in isotonic saline solution were injected into the femoral vein of anaesthetised rats and the rate of blood flow was assessed by the hydrogen clearance technique both before the envenomation as well as during the following 150 min. The injection of VSE was found to induce a prolonged elevation of blood flow in the cerebral cortex. The time of occurrence of this elevation varied in different rats and so also the intensity of the elevation, ranging between 47-212% of the basal values. No exceptional or toxic phenomena were recorded in the course of this investigation. It would seem that the factor(s) responsible for boosting the blood flow is probably one or more of the water soluble components of the hornet venom.

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