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Summary: Recently, the origins and pathways of cere brovascular acetylcholine-and vasoactive intestinal poly peptide-containing nerves have been elucidated in detail in the rat: The sphenopalatine ganglion is the major source for postganglionic parasympathetic fibers to the vascular beds of the cerebral hemispheres. To clarify the functional role of the nerves on cerebral blood vessels in vivo, brain cortical microvascular blood flow was mea sured in rats during electrical stimulation of these partic ular postganglionic fibers. Animals were subjected to transection of the right nasociliary nerve 2 weeks before the flow measurements to eliminate activation of pepti dergic sensory fibers. Relative change in microvascular blood flow was continuously recorded by a laser-Doppler flowmeter system under a-chloralose anesthesia. The postganglionic fibers were electrically stimulated just proximal to the ethmoidal foramen by a bipolar platinum electrode (5 V; 0.5 ms; 3, 10, 30, 60 Hz; as a continuous stimulation for 90 s). Stimulation at 10 Hz induced a Cerebral blood vessels are well supplied with sympathetic, parasympathetic, and sensory nerve fibers (for refs. see Owman et aI., 1986Owman et aI., , 1988. The origin and distribution for the sympathetic nerves are well defined, whereas corresponding informa tion for parasympathetic nerves has been sparse un-

It has recently been demonstrated in the rat that the majority of cerebrovascular pain fibres containing immunoreactive substance P and calcitonin gene-related peptide reach the vessels via the nasociliary nerve, a branch of the ophthalmic trigeminal division. In order to elucidate the effect of these nerves on blood flow in vivo, the relative changes in cortical microvascular flow were continuously monitored by a laser-Doppler flowmeter system during electrical nerve stimulation, with the central nerve connection cut and after removal of neighbouring dilatory parasympathetic nerves. The nasociliary nerve on one side was stimulated proximal to the ethmoidal foramen by a bipolar platinum electrode. Activation at different frequencies, continuously or as bursts with a constant voltage, impulse duration and total stimulus length, revealed that a maximum increase in blood flow amounting to 16.7% after 36 s was obtained with continuous stimulation at 10 Hz. Flow markedly declined during the following 1-min stimulation period. No changes in contralateral cortical blood flow, mean arterial blood pressure or blood gases were observed during or after stimulation. The present study demonstrates for the first time that direct and selective electrical activation of trigeminal cerebrovascular nerves induces an increase, albeit small and transient, in blood flow within the brain.

Recent evidence points to the negative surface charge of the luminal endothelial membrane of brain vessels as one determinant for morphologic blood-brain barrier function. The present study evaluates, in awake rats, how barrier function is affected by the polycation protamine to neutralize the negatively charged groups. High local doses of protamine, as infused intracarotideally, are able to substantially impair barrier capacity against albumin and inulin, which normally do not pass the blood-brain barrier. Evidence is presented that it is the positive charge of protamine that is a major factor underlying the barrier opening. However, when comparing the barrier opening obtained by corresponding concentration of the polycation lysine, it was obvious that another property of protamine contributed. This property was not linked to hyperosmolar, hypertensive or vasodilatory barrier opening, but may be a direct, cytotoxic effect of protamine. It is discussed whether barrier opening through transendothelial vesicular or channel transport occurs only at locations on the cell membrane deprived of negative surface charge areas.

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