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The rete, a vascular system between the extra- and intracerebral arteries of certain animals, may have a variety of functions in different species. The calibres of the vessels of the rete and its arteries of supply have been measured under different conditions of blood pressure and PaCO2. It has been shown that the rete and its afferent arteries behave in an autoregulatory fashion down to a blood pressure of 60 mmHg. They also dilate with a rise in PaCO2. It has also been found that some parts of the system dilate even when the blood pressure drops lower than 60 mmHg. It is suggested that this autoregulatory capacity of extradural vessels limits the requirement for CSF spaces to change with blood pressure changes. A general rule has been sought which would link the known facts about cerebral autoregulation and the possession of extra- to intracranial anastomoses with the bodily shape and posture of the particular animal.

Rupture of human cerebral arterial aneurysms is followed by prolonged cerebral arterial constriction; there is evidence that cerebrospinal fluid (CSF) from such patients contains vasoconstrictor substances which may cause the arterial constriction. The aim of this study was to develop a small animal model for investigating the effects of such CSF on the calibre of cerebral vessels in situ. Carotid angiography of the cerebral arteries of the rat visualizes the internal carotid, middle cerebral, anterior cerebral and stapedial arteries plus the vertebrobasilar system. Prostacyclin was injected during carotid catheterisation to prevent spontaneous and random occlusion of these cerebral arteries; in the presence of prostacyclin there was no arterial occlusion for up to 5 h. The resolution achieved by the angiographic technique, which magnified the cerebral circulations 2.9 times, was sufficient to measure the diameter of the internal carotid and stapedial arteries of the rat. Intracarotid infusion of 1.0 ml CSF collected from patients with ruptured cerebral arterial aneurysms caused a rapidly developing contraction of cerebral arteries lasting up to 5 h. Thus, we consider that the rat may also be used as a model for investigating the aetiology of human cerebral arterial constriction after aneurysmal rupture.

Angiography under experimental conditions shows that Urografin has a vasodilator action of the order of 8% upon the basal cerebral arteries of the baboon. This action is not seen within the first 4 sec of the angiogram and the dilator effect of a single injection has passed off completely 15 min later. Three successive injections within 7 min show little evidence of cumulative vasodilatation. The vasodilator action of three successive angiograms has disappeared 22 to 29 min later. Because of wide variations in the degree of vasodilatation shown by individual baboons it may be necessary to use each baboon as its own control in subsequent work.

By grouping patients who had carotid angiograms under unusually carefully monitored conditions it has been shown that hypocapnia is associated with vasodilation at low blood pressure but not at high blood pressure. The mechanism is discussed in general terms and it is suggested that the hypocapnic vasodilation may be a response to cerebral hypoxia and may be transmitted via an intracerebral autonomic pathway. Clinical and angiographical diagnoses are given for 50 patients.

The effects of leukotriene D4 (LTD4), a component of the slow reacting substance of anaphylaxis (SRS-A), and the putative SRS-A antagonist FPL 55712 were studied on cerebral arteries in vivo and in vitro. Intracarotid injection of LTD4 (1-15 nmols/kg) into the cerebral vasculature of the anaesthetised rat constricted internal and external carotid, facio-lingual and stapedial arteries for up to 40 minutes. LTD4 at 3 nmol/kg caused a slight fall in heart rate, and at 6 and 12 nmol/kg, an increase in diastolic (but not systolic) blood pressure was observed. In some experiments, constriction was followed by dilatation (possibly due to enhanced prostacyclin synthesis). FPL 55712 (0.3 to 30 nmols/kg) injected in the same manner caused both constriction and dilatation of rat cerebral arteries. In vitro experiments were performed on isolated human intracranial arteries (basilar, vertebral and Circle of Willis) obtained at autopsy, and on the isolated rat stomach fundus. LTD4 (2 x 10(-9) to 2 x 10(-7) M) caused sustained contractions of isolated human intracranial arteries. FPL 55712 (up to 4 x 10(-7) M) failed to antagonise the vasoconstrictor effects of LTD4, and higher concentrations (8 x 10(-6) to 8 x 10(-5) M) directly relaxed cerebral arteries. In contrast, FPL 55712 (2 x 10(-8) M) was a competitive antagonist of the contractile effects of LTD4 on the isolated rat fundus. This data suggests that the cerebral arterial leukotriene receptor differs from the peripheral smooth muscle receptor typified by the guinea-pig ileum and rat fundus preparations. Furthermore, leukotrienes may be involved in pathological vasoconstriction of various vascular beds after immunological reaction and trauma.

The responses of baboon cerebral and extracerebral arteries to prostaglandin endoperoxide (PGH2) and prostacyclin (PGI2) were investigated on isolated arteries and in vivo by serial angiography. Both PGH2 and PGI2 could produce dose-dependent contraction or relaxation of isolated arteries. PGH2 induced relaxation was indicative of prostacyclin synthetase activity, the enzyme which converts PGH2 to PGI2. In isolated arteries tested one to four hours post mortem only the vertebral artery showed prostacyclin synthetase activity. Thus PGH2 induced contraction of cerebral arteries may be indicative of a physiological function. Vasomotor tone may in part be the result of a balance between PGH2 constriction and PGI2 dilatation. In vivo PGI2 infusion caused pronounced and prolonged dilatation of cerebral arteries, which lasted longer than the cardiovascular changes. As PGI2 is the most potent cerebral vasodilator drug tested, it may be of clinical use in the treatment of cerebral vasospasm.

Angiography, either with Iohexol or Hexabrix, was carried out on a series of baboons, each of which had both contrast media, but on separate occasions. A double blind trial showed that in the carotid and middle cerebral arteries: Hexabrix generally caused vasoconstriction by 1.5 min, but in spite of a subsequent injection at 6 min constriction had largely disappeared by 20 minutes. Iohexol was generally followed by less severe constriction, but it may persist for longer and even show an increase at 20 min.