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Pial veins, choroid plexus veins, and the cerebri magna vein were investigated with regard to their ultrastructural organization, adrenergic nerve supply, and in vitro reactivity. The vessel walls consisted of a continuous layer of endothelial cells, large amounts of collagenous material, and occasional pericytes. Smooth muscle cells were observed only in a few specimens from the cerebri magna vein. All veins were surrounded by adrenergic nerve fibres. Potassium (124 mM) and noradrenaline (10(-5) - 10(-4) M) induced small contractions (0.2-0.5 mN) of isolated veins during in vitro conditions. The magnitude of these responses was less than one-tenth of that obtained in small pial arteries.

Pial arterial and venous calibre were continuously recorded through a closed cranial window preparation during cervical sympathetic nerve stimulation in 10 cats before and after alpha- and beta-adrenoceptor blockade. In addition, the intracranial pressure (ICP) was simultaneously recorded in 4 of the cats. Under resting conditions 33 arteries (mean diameter 130 micron) constricted by 11.7 +/- 0.8% and 80 venous portions (mean diameter 152 micron) constricted by 13.7 +/- 0.7% during sympathetic nerve stimulation. ICP decreased simultaneously by 16.5 +/- 6.2%. Administration of the alpha-adrenoceptor antagonist phenoxybenzamine i.v. (1.5 mg X kg-1) abolished the reduction of ICP and markedly reduced, but did not completely abolish, the constrictor response of arteries and veins. The beta-adrenoceptor antagonist propranolol (1.5 mg X kg-1) did not significantly alter the reduction of ICP or the response of pial veins and small arteries, whereas the response of arteries with a diameter greater than 150 micron was attenuated. It is concluded that the constriction of pial veins and arteries during sympathetic stimulation is mediated predominantly via alpha-adrenoceptors. The sympathetic nerves of cerebral blood vessels may have stronger influence on the cerebral capacitance than on resistance vessels under normotensive and normocapnic conditions.

Reactions of pial arteries and veins as well as intracranial pressure (ICP) and mean arterial pressure during intravenous administration of methohexital were observed in two groups of cats totaling 24 animals in order to investigate hypothesized direct barbiturate effects on cerebral vascular volume. Group 1 had bolus injection of 1 mg/kg followed by infusion of 0.1 mg/kg/min over 60 minutes. This induced a 6 to 7% arterial dilatation at 50 to 60 minutes (not significant); a 20% reduction of pial vein calibers was observed (P less than 0.01). In Group 2, the same treatment protocol administered under conditions of ICP elevation to 20 mm Hg by the cisternal infusion of mock cerebrospinal fluid resulted again in consistent, although less extensive, venous caliber reduction (5 to 7%, P less than 0.01). In Group 2 controls, pial arteries dilated by 15 to 20%; this reaction was suppressed in the methohexital-treated animals. After stopping methohexital, however, arteries in the methohexital group dilated to almost the same extent as in controls. Mean arterial pressure remained stable in both groups. ICP was not reduced by methohexital. EEG-activity was slightly increased during treatment. We conclude that methohexital has a direct effect on vessel caliber and thus cerebral blood volume via absolute diminution of venous vessels and suppression of ICP-induced autoregulative arterial dilatation. This direct vascular effect, however, seems to be counterbalanced by unknown intracranial mass effects that prevent a reduction in ICP.

Twelve patients with small burr hole skull defects after extra-intracranial arterial bypass surgery were studied. The amplitude and frequency of the sensorimotor rhythm were measured 7 days and 1, 2, 4, and 6 months after surgery in follow-up EEGs from the central region. Seven patients showed a frequency decrease (compared with preoperative measurement) on the operated side 7 days and/or 1 month after surgery. There was no case of frequency decrease 6 months after surgery; four patients displayed a late frequency increase. Ipsilateral amplitude enhancement was never found 7 days postoperatively, but after 6 months in nine patients. Such physical factors as burr holes and bone replacement can only partially explain the amplitude enhancement, and cannot explain the frequency decrease. It may be assumed that temporary clamping of the middle cerebral artery and/or reperfusion of an ischaemic area result in a brief deterioration of brain function, as indicated by frequency slowing and delayed amplitude enhancement; related observations were made in patients with cerebrovascular disorders and mild to moderate neurological deficit about 20 days after the onset and correlated with clinical recovery.

In a series in 8 cats, cerebral perfusion pressure (CPP) was evaluated over a period of 5 min after production of an acute arterial hypertension. The mean percentual increase of blood pressure, CPP and ICP equalled 100%. the fact, that ICP does not play any role in acute hypertension, indicates that an abrupt elevation of filtration pressure within the capillaries must be the decisive factor leading to edema.

In experiments during stepwise increases in intracranial pressure, B-waves could be provoked synchronously with pial vascular diameter oscillations. The vascular oscillations are known to be a sign of myogenic cerebrovascular regulation. An increase in their amplitude indicates vessel wall relaxation and impending failure of myogenic autoregulation. Therefore, vascular oscillations provoked during intracranial hypertension can be ascribed to a fall in transmural pressure and vessel wall tension. The resulting oscillations in the cerebral blood volume are reflected by ICP oscillations and lead to synchronous variation in ICP, the so-called "B-waves" with a frequency of 0.5 to 2 per minute.

Recently blood flow velocity in large cerebral arteries became measurable non-invasively by transcranial Doppler sonography (TCD). The present study tries to quantify the relation between flow velocity and the more important volume flow in the middle cerebral artery (MCA) by means of computersimulation. A mathematical model of the MCA territory was developed. The model is able to take into account the non-Newtonian behaviour of blood viscosity and is also able to handle turbulant and laminar flow. Autoregulation is simulated by increasing or decreasing diameter of arteries as an answer to intraluminal pressure changes. Two processes are simulated: Vasospasm in the stem of the MCA, and vasospasm in the entire MCA territory. Results show that the relation between flow velocity and volume flow is rather complicated. Vasospasm in the MCA stem first leads to an increase of flow velocity at a constant level of volume flow. At higher grades of vessel constriction volume flow and flow velocity start to fall.

In 6 cats, cerebral infarction was produced by transorbital occlusion of the left middle cerebral artery (MCA). Five animals developed typical cortical infarcts. Eight weeks later, cerebral blood flow (CBF) was determined by 14C-iodoantipyrine autoradiography and the number of intact neurons was counted histologically. Two non-operated cats served as controls. Cortical blood flow in the infarcted hemisphere was reduced by 24.6-74.4% when compared to the flow in the contralateral cortex and in controls. Averaged white matter flow was decreased by 39.1%. Regional cortical flow was gradually reduced from parasagittal regions towards the infarct. In the surrounding of the infarct, cortical perfusion was decreased to 24.8 +/- 9.7 ml/100 g/min, i.e. 19.7% of contralateral flow. Although the infarcts were sharply demarcated macroscopically, the number of cortical neurons decreased gradually from the midline to the peri-infarct zone. A significant linear correlation was found between absolute CBF-values and the number of neurons in areas of the infarcted hemisphere. The homolateral gyrus lateralis had normal neuronal density but flow was reduced by 20%. These findings suggest that the blood flow reduction in tissue surrounding chronic infarcts is due to neuronal cell loss and to functional inactivation caused by damage of afferent fibers.

In a series of 13 patients with cerebrovascular occlusive disease regional cerebral blood flow (rCBF) measurements (two-dimensional intravenous 133Xe clearance method) and quantitative EEG analysis (sensorimotor rhythms) as well as electronic measurement of handforce were performed before and during intravenous infusion of 1 microgram kg/min of one of the lipophilic dihydropyridine calcium channel blocker nimodipine (Nimotop). The aim of the study was to test the hypothesis of the existence of hypoperfusion (ischaemic penumbra) in the surroundings of chronic cerebral infarcts. All 3 parameters improved in one patient. Sensorimotor rhythms increased in 5 patients, rCBF in 3. EEG and rCBF improved in 2 patients. In 3 instances, a redistribution of rCBF in favour of the peri-infarct zone was noted (significant increase of rCBF from 35 +/- 2 SEM to 53 +/- 4 ml/100 g/min (p less than 0.01), whereas rCBF fell from 61 +/- 5 to 46 +/- 2 ml/100 g/min on a collimator remote from the infarct but in the infarcted hemisphere. The parallel improvement of rCBF and EEG in brain regions surrounding chronic infarcts in 3 patients was interpreted as functional improvement as a consequence of nimodipine-induced normalization of peri-infarct hypoperfusion, i.e. reversal of flow-dependent neuronal silence and/or dysfunction.

Pial arterial and venous calibre changes during intracranial hypertension were studied in 11 cats under barbiturate- and nitrous oxide-anaesthesia by using a closed cranial window technique and multichannel videoangiometry. Intracranial pressure was elevated from a normal mean level of 6.4 mm Hg by cisternal infusion of mock CSF in steps to 20, 30, 40, 50 mm Hg and finally to the level of systolic pressure. Pial arteries dilated significantly, small ones more than large ones, by 42 +/- 5.6% and 33 +/- 3%, respectively at ICP 50. With a further elevation of ICP up to systolic pressure, dilatation diminished to 28 +/- 10% in small, and to near resting calibres in large arteries. Pial veins remained unreactive on the average. Grouping into veins smaller and larger than 100 microns of resting size revealed, however, minor though statistically significant 5-10% dilatation of small, and a 5-10% diminution of large veins. Blood flow stopped, when cerebral perfusion pressure was zero, however, neither arteries nor veins collapsed. The present data support the hypothesis that CBF during acute elevation of CSF pressure depends on perfusion pressure rather than local vascular compression.

The effect of serotonin (5-HT) and its antagonist ketanserin on the cerebral circulation was investigated in two series totaling 24 cats using the cranial window technique. 5-HT elicited a marked dilatation of small pial arteries, whereas large arteries tended to constrict. Intravenous administration of ketanserin reversed the constriction of large arteries, causing dilatation, and reduced the extent of small arteries' dilatation. In a randomized study, i.v. administration of ketanserin in its solvent versus the solvent alone revealed a strong dilatatory effect of the solvent on pial arteries (17 +/- 1.8%), which partly jeopardized a possible constrictory effect of ketanserin, as ketanserin plus solvent induced less dilatation of small pial arteries than the solvent alone. The present data support the view that serotonin exerts a dual effect on cerebral arteries, namely, dilatation of small and constriction of large vessels. The antagonist ketanserin reverses this effect, but the strong dilatatory effect of the solvent alone masks the antiserotoninergic effect.

Flow property measurements were performed in a plexiglass model of six various types of end-to-side anastomosis (as clinically shown in extracranial to intracranial arterial bypass surgery). Three anastomoses were made without, another three anastomoses with a ringshaped stenosis restricting the lumen to between 25 and 46% of the cross-section as it occurs clinically by formation of thrombi out of the striching canals. A rectangular type and two of 45 degree oblique types--one directed centrally and one directed peripherally--were tested. Pressure head losses at the site of anastomosis were measured under various circumstances of different anastomoses and different flow speeds along the proximal portion of the middle cerebral artery and the superficial temporal artery. Flow resistance values originated by the different types of anastomoses were expressed in terms of additional recipient vessel length. Differences between different types of anastomoses with and without stenosis were very small and under no circumstances exceeded the equivalent of lengthening the recipient vessel by 2 cm. Theoretically, the optimal type of anastomosis is the oblique and centrally directed version; the worst type is the rectangular form. Practically, however, such differences are not relevant. The explanation for such unexpectedly small differences can rheologically be given by considering the dominating role of blood viscosity under the given circumstances, other variables such as short stenosis and angling of flow playing a secondary role.

The behaviour of Pial vessels to levels of CSF-pressure between 10 and 100 mmHg induced by vetricular infusion of mock CSF, was observed in 6 cats under barbiturate and N2O anaesthesia, using the cranial window technique and videoangiometry. Supratentorial pressure (STP) equaled infratentorial pressure in the cisterna magna (CMP) throughou. No changes in pial arterial calibres were noted up to a CMP of 13 mmHg (i.e. a cerebral perfusion pressure (CPP) of 100 mmHg). Further increase of CMP to 45 mmHg induced significant arterial dilatation of 40 +/- 3.4%. With a further rise of ventricular fluid pressure (VFP) no marked further arterial dilatation occurred. Dilatation of arteries up to 100 um resting diameter and arteries between 100 and 250 um resting diameter and arteries between 100 and 250 um was not significantly different. When CPP approached 40 mmHg, arteries were still 47 +/- 3.6% dilated. Pial venous calibre did not vary by more than 20% during elevation of VFP. At CPP 47 mmHg, small and large veins were dilated by 14%. Single venous segments were compressed by crossing pial arteries and caused upstream venous congestion and distension.

This study in cats investigates the action of sodium nitroprusside on the pial vessels by systemic and local administration, with an intravital microscopic window technique and a photometric technique for graphic documentation of vessel diameter changes. Intravenous infusion caused vasodilatation parallel with decreasing blood pressure. Pial arterioles dilated more than venules, smaller vessels more than larger ones. Local administration caused maximal dilatation within 5--10 seconds. With blood pressure returning to normal after i.v. therapy, pial vessels remained wider than they were before hypotension at the same pressure level. From these data it is concluded that the substance acts longer on the brain vessels than on vessels elsewhere in the body, and that cerebrovascular autoregulation to blood pressure changes is disturbed during this period.