Alterations of mechanical properties in canine basilar arteries after subarachnoid hemorrhage

The purpose of this study was to examine the hypotheses that structural stiffening of the arterial wall contributes to chronic cerebral vasospasm, and that alteration in properties of smooth muscle takes place after subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage and subsequent chronic vasospasm were induced in dogs by two cisternal injections of autologous blood (on Day 0 and Day 2). Vasospasm was confirmed by angiography performed on Day 0 and Day 7. Animals in the control group underwent angiography only. On Day 8, the mechanical properties of the basilar arteries were studied in vitro. Passive compliance, measured under total inhibition of spontaneous myogenic tone with diltiazem (10(-4) M) plus papaverine (10(-4) M) was smaller in the SAH group. The length-contraction curve was shifted to the left and the optimum length for maximum contraction (Lmax) was significantly shorter in the spastic blood vessels. The spontaneous myogenic tone was augmented in the SAH group, resulting in an increase in resting tension at each length. By contrast, the maximum contractions in response to KCl and uridine 5'-triphosphate were markedly reduced in the SAH group, without changes in sensitivity to these agents. These differences in mechanical properties were observed in rings both with and without endothelium. The results indicate that, in chronic vasospasm, stiffening of the noncontractile component of the vasculature takes place as well as alterations in the contractile component, both of which presumably contribute to the shift in resting length-tension relationship and length-contraction relationship of the artery. The decreased distensibility, the increase in resting tension, and the shortening of the Lmax all favor a smaller diameter of the artery after SAH, possibly contributing to vasospasm.     

Reduced expression of calponin in canine basilar artery after subarachnoid haemorrhage

Summary Calponin, an actin- and tropomyosin-binding protein, has been characterized as an inhibitory factor in the smooth-muscle actomyosin activity. The level of calponin was determined in canine basilar arteries in a double-haemorrhage model. Thirty dogs were assigned to three groups: day 0 group, control; day 2 group, dogs sacrificed 2 days after cisternal injection of blood; and day 7 group, dogs given double cisternal injections of blood and sacrificed 7 days after the first injection. Constriction of the basilar artery was confirmed by arterial angiography. Portions of the affected arteries or the corresponding region in control animals were solubilized for sodium dodecylsulphate-polyacrylamide gel electrophoresis and Western blotting. A major band corresponding to calponin was seen at 34 kD in the basilar artery extracts using chicken gizzard polyclonal antibodies. The densitometer values of the band on Coomassie blue-stained gels were expressed as percentages of day 0 control values. The signals of day 2 and day 7 samples were 47%±20% and 23%±12%, respectively (mean±standard deviation). The proportions of calponin to actin/tropomyosin in the day 0, day 2, and day 7 groups were 13%±6%, 6%±2%, and 4%±2%, respectively. The reduced expression of calponin may be related to sustained contraction during cerebral vasospasm.     

Dissecting aneurysm of basilar artery presenting with recurrent subarachnoid hemorrhage

Spontaneous basilar dissecting aneurysms secondary to subarachnoid hemorrhage are rare, usually presenting with ischemia rather than a subarachnoid hemorrhage (SAH). A 63-year-old man who had SAH repeatedly from a ruptured basilar dissecting aneurysm was treated with endovascular occlusion of the unilateral vertebral artery. Postoperative angiograms 1 month after the procedure showed complete obliteration of the aneurysm. The clinical follow-up at 20 months showed no evidence of recurrent hemorrhage. Received: 24 August 1998 / Accepted: 15 December 1998     

Effects of subarachnoid hemorrhage on platelet-derived vasoconstriction of rabbit basilar artery

The effects of subarachnoid hemorrhage on platelet-derived vasoconstriction of the isolated rabbit basilar artery were examined using an isometric tension recording method. The subarachnoid hemorrhage was induced by injecting arterial blood in the cisterna magna. The following points were confirmed: (1) the maximal contraction produced by the platelets (10⁷/mL) treated with indomethacin or dazoxiben (thromboxane synthetase inhibitor) were suppressed (65% or 70% of the control); (2) the contraction of the arteries treated with ONO-3708 (thromboxane A₂ antagonist) or ketanserin was inhibited (73% or 8.4%), as was contraction after subarachnoid hemorrhage (67% or 14%); (3) platelet-induced contraction was potentiated after subarachnoid hemorrhage; and (4) serotonin-induced contraction was potentiated after subarachnoid hemorrhage. However, synthetic thromboxane A₂-induced contraction was not potentiated.

The present experiments suggest that both serotonin and thromboxane A₂ contribute to vasoconstrictions induced by the platelets, before and after subarachnoid hemorrhage. The platelet-derived contraction response is potentiated after subarachnoid hemorrhage and serotonin is responsible for the increased reactivity.     

Pre-mesencephalic subarachnoid hemorrhage: rupture of tiny aneurysms of the basilar artery perforator

Purpose  

Subarachnoid hemorrhage (SAH) around the midbrain without evidence of aneurysm, a so-called perimesencephalic SAH, has been considered a typical nonaneurysmal SAH. Recently, we have encountered several patients with SAHs that could have been classified as having perimesencephalic SAH, but a common cause of the bleeding was demonstrated. In this article, we describe clinical and radiologic characteristics of these patients.     

Reactivity to vasoactive agents of canine basilar arteries exposed to experimental subarachnoid hemorrhage

Autologous blood was injected into the cisterna magna of mongrel dogs twice with an interval of 48 hours. They were killed 3 days, 1 week, or 4 weeks after the first injection of blood, and helical strips of the basilar artery were prepared. Contractions induced by 5-hydroxytryptamine, noradrenaline, prostaglandin F₂, and oxyhemoglobin were significantly potentiated. Relaxations caused by nicotine, K⁺, arachidonic acid, and prostaglandin I₂ were suppressed, but the relaxant response to calcium ionophore A23187 and substance P did not change significantly. These results suggest that contractions mediated via activation of , 5-hydroxytryptamine, and prostaglandin F₂ receptors are potentiated, and relaxations caused by stimulation of vasodilator nerves and by endogenous and exogenous prostaglandin I₂ are attenuated in dog basilar arteries exposed to subarachnoid clot. On the other hand, certain relaxations possibly mediated by endothelium-derived relaxing factor do not appear to be significantly influenced.     

Effect of subarachnoid hemorrhage on serotonin uptake and release in the rabbit basilar artery

This study analyzes the changes induced by subarachnoid hemorrhage (SAH) on the serotonin (5-hydroxytryptamine, 5-HT) uptake and release evoked in rabbit basilar arteries by tyramine. Rabbits were injected with 5 ml of autologous arterial blood into the cisterna magna to produce SAH. Tritium accumulation in basilar arteries was measured after 30 minutes of incubation with 10(-7) M [3H]5-HT and a subsequent 120-minute superfusion (1 ml/min) period. The uptake of 5-HT by arteries 1, 2, 3, and 7 days after SAH was found to be 109%, 69%, 57% (P less than 0.05), and 67% (P less than 0.05) (n = 4, 4, 9, and 6; P less than 0.05) of control (n = 13; 16.8 +/- 1.2 X 10(2) dpm/mg tissue), respectively. The neuronal (cocaine-sensitive) uptake of 5-HT in the arteries 3 days after SAH decreased to approximately 38% of control, whereas the extraneuronal (cocaine-insensitive) uptake of both groups had almost the same absolute value (n = 6 and 6; 4.4 +/- 0.4 and 4.8 +/- 0.4 X 10(2) dpm/mg). Autoradiographic study disclosed that dense clusters of silver grains in the adventitia were not observed after treatment with cocaine (3 X 10(-5) M), although a diffuse distribution of grains was present throughout the vascular wall. The labeled arteries were stimulated by superfusion of tyramine, which is known to replace amines in the sympathetic nerve ending. Tyramine (10(-6) and 10(-4) M)-induced 3H efflux was significantly potentiated by SAH (n = 6) and was suppressed by treatment with cocaine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Overexpression of cyclooxygenase-2 in rabbit basilar artery endothelial cells after subarachnoid hemorrhage

OBJECTIVE: We investigated the expression in rabbit basilar arteries of cyclooxygenase (COX)-2, which is the inducible isoform of the enzyme of prostaglandin (PG) production, and the concentrations of the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) and representative PGs in the cerebrospinal fluid (CSF) after experimental subarachnoid hemorrhage (SAH). METHODS: Seven sets of basilar arteries were removed from control rabbits and from rabbits killed 1 and 3 days after induced SAH. The arteries were subjected to identical simultaneous immunolabeling for examination with a confocal microscope. One-half of each artery was stained for the constitutive form COX-1 and the other half for COX-2. CSF was sampled in control animals and at 6 hours, 1 day, and 3 days for assays of TNFalpha, PGE2, and 6-keto-PGF1 (metabolite of PGI2). RESULTS: COX-1 immunoreactivity in the endothelial layer was similar in the three groups. Weak endothelial COX-2 immunoreactivity was found in arteries of control animals. COX-2 staining was higher in the group killed at 3 days compared with the control group (P < 0.05). The levels of PGE2 and 6-keto-PGF1alpha in the CSF peaked significantly at 6 hours, then decreased at 3 days to the basal level (PGE2) or significantly lower (6-keto-PGF1). TNFalpha was undetectable in control CSF, significantly higher (P < 0.001) at 6 hours, and undetectable at 3 days. CONCLUSION: After SAH, endothelial COX-1 immunoreactivity does not change, whereas overexpression of COX-2 occurs at 3 days. This induction does not seem linked to TNFalpha production, nor is it responsible for early raised levels of PGE2 and PGI2 in the CSF. We suggest that the role of induced COX-2 may be to modify gene expression and hence alter the properties of the vessel wall after SAH.     

Effect of nicardipine on basilar artery vasoactive responses after subarachnoid hemorrhage.

The effect of the dihydropyridine calcium antagonist, nicardipine, on the vasoactive responses of the basilar artery was investigated after subarachnoid hemorrhage (SAH). Forty-five rabbits were separated into one control group and four groups receiving SAH (nine animals each). The SAH was induced by injecting 5 ml of autologous arterial blood into the cisterna magna. SAH animals were subjected to one of the following: 1) no treatment; 2) intravenous (i.v.) saline infusion (vehicle); 3) i.v. infusion of low-dose nicardipine (0.01 mg/kg/hr), or 4) i.v. infusion of high-dose nicardipine (0.15 mg/kg/hr). The i.v. infusions were started immediately after SAH and continued for 48 hours. Serotonin (5-HT) (10(-8) to 10(-5) mol/L) was used to evoke dose-dependent vasoconstriction of isolated rings of the basilar artery 2 days after SAH. Acetylcholine (ACh) (10(-8) to 10(-4)) and adenosine-triphosphate (ATP) (10(-8) to 10(-4) mol/L) were applied after maximal contraction with 5-HT, evoke a dose-dependent vasodilatation. Compared with controls, in animals subjected to SAH serotonin caused similar or slightly larger contractions; nicardipine infusion did not decrease the amount of contraction observed after SAH. ACh and ATP caused significantly less dilatation in animals submitted to SAH than in controls. After high-dose nicardipine, ACh- and ATP-induced dilatations were significantly more pronounced (57% and 68% of initial contractile tone) than in the other animals receiving SAH (36%-39% and 45%-55%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of nicardipine on vasospasm in rabbit basilar artery after subarachnoid hemorrhage

This study was performed to examine the effect of the dihydropyridine calcium antagonist, nicardipine, on vasospasm after experimental subarachnoid hemorrhage (SAH) in the rabbit. The study was carried out in two parts: 1) effect of intravenous nicardipine (n = 45) and 2) effect of intracisternal nicardipine (n = 21). SAH was induced by injecting 5 ml of autologous arterial blood into the cisterna magna. In the intravenous study, there were five groups: 1) SAH without treatment; 2) SAH with vehicle (saline); 3) SAH and intravenous infusion of low-dose nicardipine (0.01 mg/kg/h); 4) SAH and intravenous infusion of high-dose nicardipine (0.15 mg/kg/h); and 5) controls without SAH. The intravenous infusions were started immediately after SAH and continued for 48 hours until death. In the intracisternal study, there were three groups: 1) SAH without treatment; 2) SAH with intracisternal administration of nicardipine (0.37 mg/h); and 3) controls without SAH. Intracisternal infusions were begun 70 hours after SAH and continued for 2 hours until death. After perfusion-fixation, the basilar artery was removed and processed for morphometric analysis. In the intravenous study, vessels from animals subjected to SAH were significantly narrowed when compared with controls, although after high-dose nicardipine vessel caliber was slightly larger than in the other SAH groups. Animals given intracisternal nicardipine showed a nonsignificant reduction of caliber as compared with controls: only 12% decrease in diameter and 22% decrease in luminal area. In the rabbit SAH model, nicardipine had a very modest effect on vasospasm at the doses tested.     

Effect of subarachnoid hemorrhage on endothelium-dependent vasodilation

The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. The SAH was induced by injecting 5 ml of fresh arterial blood into the cisterna magna. Sixty-two rabbits were separated into four groups according to the timing of sacrifice: control rabbits, and operated rabbits sacrificed on Days 2, 4, and 6 after SAH. Acetylcholine (ACh) (10(-7) M to 10(-4) M) and adenosine triphosphate (ATP) (10(-7) M to 10(-4) M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M serotonin (5-HT). There were no significant differences in the vasodilatory response to ACh among these four groups. Relaxation to approximately 84% of the initial contractile tone occurred with 10(-4) M ACh. On the other hand, the vasodilatory response to ATP was suppressed in the animals sacrificed 2 days after SAH; the relaxation of this group was approximately 52% at 10(-4) M ATP, compared to a relaxation of 87% observed in the other groups of animals. One of the major causes of the impairment of endothelium-dependent vasodilation seems to be an inhibition of the production of endothelium-derived relaxing factor by endothelial cells. After the relaxation studies, the dose-response curves for 5-HT were obtained. Serotonin caused significantly more contraction in the animals sacrificed 2 days after SAH than in the other groups. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH, together with the potentiation of the contractile response to vasoactive agents in cerebral arteries, may play an important role in the pathogenesis of vasospasm.     

Dexamethasone preventing contractile and cytoskeletal protein changes in the rabbit basilar artery after subarachnoid hemorrhage

OBJECT: The aim of this project was to study the perturbations of four smooth-muscle proteins and an extracellular protein, type I collagen, after subarachnoid hemorrhage (SAH) and to examine the possible preventive effects of dexamethasone. METHODS: Using a one-hemorrhage rabbit model, the authors first examined the effects of SAH on the expression of alpha-actin, h-caldesmon, vimentin, smoothelin-B, and type I collagen; second, they studied whether post-SAH systemic administration of dexamethasone (three daily injections) corrected the induced alterations. Measurements were obtained at Day 7 post-SAH. The proteins were studied by performing immunohistochemical staining and using a laser-scanning confocal microscope. Compared with control (sham-injured) arteries, the density of the media of arteries subjected to SAH was reduced for alpha-actin (-11%, p = 0.01) and h-caldesmon (-15%, p = 0.06) but increased for vimentin (+15%, p = 0.04) and smoothelin-B (+53%, p = 0.04). Among animals in which SAH was induced, arteries in those treated with dexamethasone demonstrated higher values of density for alpha-actin (+13%, p = 0.05) and h-caldesmon (+20%, p = 0.01), lower values for vimentin (-55%, p = 0.05), and nonsignificantly different values for smoothelin-B. The density of type I collagen in the adventitia decreased significantly after SAH (-45%, p = 0.01), but dexamethasone treatment had no effect on this decrease. CONCLUSIONS: The SAH-induced alterations in the density of three of four smooth-muscle proteins were prevented by dexamethasone treatment; two of these proteins--alpha-actin and h-caldesmon--are directly related to contraction. This drug may potentially be useful to prevent certain morphological and functional changes in cerebral arteries after SAH.     

Hemoglobin penetration in the wall of the rabbit basilar artery after subarachnoid hemorrhage and intracisternal hemoglobin injection

Summary The ability of hemoglobin (Hb) to penetrate the basilar arterial wallin vivo after experimental subarachnoid hemorrhage was examined using immunohistochemistry. The distribution of anti-Hb antibodies in rabbit basilar artery was studied following the injection of autologous blood in the cisterna magna. Vessels removed two or four days after subarachnoid hemorrhage exhibited varying degrees of vasospasm, and exhibited Hb immuno-fluorescence throughout the vessel wall. Hemoglobin immunofluorescence was most conspicuous in the adventitia but was also seen in the smooth muscle and endothelial cell layers in 7 of 10 animals. The degree of vasoconstriction correlated with the total amount of Hb-fluorescence present in the vessel wall. When Hb solution alone was injected into the subarachnoid space, vasoconstriction was evident but penetration into the vascular layers was not as extensive as that observed after injection of autologous blood.These findings demonstrate that Hb is able to penetrate through the arterial wall after subarachnoid hemorrhage. The results provide direct support for the hypothesis that Hb-induced changes in smooth muscle and/or endothelial function can contribute to the pathogenesis of vasospasm.     

Reactivity of rabbit basilar artery to alterations in extracellular potassium and calcium after subarachnoid hemorrhage

Hemolysis of periarterial clots after subarachnoid hemorrhage may liberate large quantities of K+ into the vicinity of cerebral blood vessels and possibly change their sensitivity to endogenous vasoactive agents. The current study examined the influence of subarachnoid hemorrhage on the sensitivity of rabbit basilar arterial segments to K+ and Ca++. An analysis of K+ and Ca++ dose-response curves demonstrated that incubated arterial segments isolated from animals with subarachnoid hemorrhage were substantially more sensitive to these cations than were corresponding controls. We speculate that chronically elevated K+ levels in areas of periarterial clot lysis or brain ischemia might initiate vascular smooth muscle depolarization and vasospasm. Our data provide additional rationale for the use of calcium channel blockers in preventing or treating vasospasm in cases of subarachnoid hemorrhage.     

Biphasic constriction of rabbit basilar artery following experimental subarachnoid hemorrhage: a morphometric study.

To assess the changes in arterial structure resulting from subarachnoid hemorrhage, morphometric analysis was performed on basilar arteries from rabbits that had received an experimental subarachnoid hemorrhage up to 6 days earlier. For morphometric determination, the cross-sectional area of the media, the area of the lumen, and the length of the internal elastic lamina were measured planimetrically. The morphometric diameter of the lumen, the media-to-radius ratio, and several other morphometric parameters were also calculated. Subarachnoid hemorrhage induced significant biphasic constriction of the basilar artery without any changes in the cross-sectional area of the media. The relative amount of smooth muscle cell decreased significantly in the late stage of hemorrhage.     

Brainstem hypoperfusion in severe symptomatic vasospasm following aneurysmal subarachnoid hemorrhage: role of basilar artery vasospasm

Summary Background. The hemodynamic effects of vertebrobasilar vasospasm are ill defined. The purpose of this study was to determine the effects of basilar artery (BA) vasospasm on brainstem (BS) perfusion. Methods. Forty-five patients with delayed ischemic neurological deficits (DIND) following aneurysmal subarachnoid hemorrhage (SAH) underwent cerebral angiography prior to decision-making concerning endovascular treatment. BA diameter was compared with baseline angiogram. Regional brainstem (BS) cerebral blood flow (CBF) was qualitatively estimated by ^99mTc ethyl cysteinate dimer single photon emission computed tomography (ECD-SPECT). Findings. Delayed BS hypoperfusion was found in 22 (48.9%) of 45 patients and BA narrowing of more than 20% was found in 23 (51.1%). Seventeen of 23 (73.9%) patients with BA narrowing of more than 20% experienced BS hypoperfusion compared to 6 of 22 (27.3%) patients with minimal or no narrowing (p = 0.0072). Patients with severe and moderate BS hypoperfusion had higher degree of BA narrowing compared to patients with normal BS perfusion and mild BS hypoperfusion (p < 0.001). The three-month outcome of patients n-22) with BS hypoperfusion was significantly worse compared to patients (n-23) with unimpaired (p = 0.0377, odd ratio for poor outcome 4, 1.15–13.9 95% confidence interval). Interpretation. These findings suggest that the incidence of BA vasospasm in patients with severe symptomatic vasospasm is high and patients with significant BA vasospasm are at higher risk to experience BS ischemia. Further studies should be done to evaluate the effects of endovascular therapy on BS perfusion and the impact of BS ischemia on morbidity and mortality of patients with severe symptomatic vasospasm.     

Effect of endothelin on the canine basilar artery

Endothelin, a recently discovered peptide produced by endothelial cells, has been shown to have potent constrictor effects on major arteries in vitro. This experiment was performed to determine whether endothelin plays a physiological role in cerebral vasospasm after subarachnoid hemorrhage. A cisternal injection of endothelin (10(-8) mol or 10(-9) mol) caused severe vasoconstriction of the canine basilar artery. The degree of vasoconstriction was dose related and long lasting, persisting for more than 24 hours. This constriction was prevented completely by pretreatment with nicardipine (10(-8) mol). Endothelin produced a marked and transient elevation in blood pressure and might play an important role in cerebral vasospasm. Further investigation will be needed to determine the role of endothelin in the pathogenesis of vasospasm.     

Spontaneous dissecting aneurysms of the basilar artery presenting with a subarachnoid hemorrhage. Report of two cases

A spontaneous dissecting aneurysm of the basilar artery is a rare disorder, usually presenting with ischemia rather than a subarachnoid hemorrhage (SAH). Two cases are described of a dissecting aneurysm of the basilar artery presenting with an SAH. Vertebral angiography revealed a double lumen to the basilar artery. Magnetic resonance (MR) imaging detected the intramural hematoma. One patient was treated conservatively, and the other underwent operative intervention with wrapping of the aneurysm. The usefulness of MR imaging in the diagnosis and the treatment options are discussed.     

Selective hemoglobin inhibition of endothelium-dependent vasodilation of rabbit basilar artery

The effect of hemoglobin on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. Acetylcholine (ACh) (10(-7) - (10(-4) M) evoked a dose-dependent vasodilation of isolated rabbit basilar artery previously contracted by 10(-6) M serotonin. This vasodilating action disappeared after removal of the endothelium. The ACh-induced vasodilation of rabbit basilar artery is thought to be strictly endothelium-dependent. Hemoglobin (10(-7) - 10(-5) M) inhibited this ACh-induced endothelium-dependent vasodilation conditional upon the dose. Adenosine triphosphate (ATP, 10(-7) - 10(-4) M) also relaxed isolated rabbit basilar artery already contracted by 10(-6) M serotonin. This vasodilating action was slightly inhibited by adenosine antagonist, 8-phenyltheophylline (8-PT), and markedly attenuated by removal of the endothelium. This ATP-induced vasodilation is thought to be composed of ATP itself (endothelium-dependent) and ATP degradation products (endothelium-independent) such as adenosine monophosphate or adenosine. Hemoglobin markedly inhibited ATP-induced vasodilation, but there still remained a small vasodilation, which was blocked by 8-PT. Papaverine-induced vasodilation was not affected by removal of the endothelium, and hemoglobin did not inhibit the papaverine-induced vasodilation. These results suggest that rabbit basilar artery has endothelium-dependent vasodilating mechanisms induced by ACh and ATP, and that hemoglobin selectively blocks the endothelium-dependent vasodilation. This finding may relate to the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage: there is a possibility that the presence of hemoglobin released from lysed erythrocytes inhibits the endothelium-dependent vasodilation of cerebral arteries; furthermore, the endothelial degeneration following subarachnoid hemorrhage may impair the vasodilating mechanisms of cerebral artery smooth-muscle cells.     

Ultrastructural changes of the basilar artery following experimental subarachnoid haemorrhage

Summary Recent experimental studies have shown, that the endothelium of cerebral vessels undergoes significant changes after subarachnoid haemorrhage which may lead to biochemical changes at the endothelial surface with disturbance of the delicate homeostasis of vasodilating and vasoconstricting mechanisms which are thought to be responsible for preservation of the tones of the cerebral vasculature. Ultrastructural studies incorporating different forms of microscopic observations of the endothelium after SAH representing a prerequisite for further investigations on the pathogenesis of cerebral vasospasm are scarce. This experimental study was performed in order to investigate and define more precisely the pathomorphological changes at the endothelial surface of the basilar artery of dogs after experimental SAH.Two separate injections of autologous blood into the cisterna magna within 72 hours resulted in extensive angiographic narrowing of the diameter of the basilar artery of all animals. Histological studies of the basilar artery including light microscopic, transmission electron microscopic, scanning electron microscopic and freeze cracking microscopic examinations demonstrated severe pathomorphological changes at the endothelial surface. These consisted mainly of infolding and corrugation of the endothelium, disorientation and desquamation of endothelial cells as well as of vacuolation and ingrowth of fibrous tissue between the endothelial and muscular layer. No pathomorphological changes could be observed in the muscular layer.As the described post-haemorrhagic ultrastructural changes of the endothelium of cerebral vessels in spasm are likely to represent the morphological basis of the delayed form of cerebral vasospasm future research on its pathogenesis should primarily focus on the structural and biochemical changes taking place at the endothelial surface of the cerebral vasculature after SAH.