Effects of indomethacin and prostacyclin on isolated human pial arteries contracted by CSF from patients with aneurysmal SAH

1981 ◽  
Vol 55 (6) ◽  
pp. 877-883 ◽  
Author(s):  
Lennart Brandt ◽  
Bengt Ljunggren ◽  
Karl-Erik Andersson ◽  
Bengt Hindfelt ◽  
Tore Uski
Keyword(s):  
Cerebrospinal Fluid ◽  
Arachidonic Acid ◽  
Vessel Wall ◽  
Cerebral Arteries ◽  
Pial Arteries ◽  
Content Type ◽  
Cerebral Vasoconstriction ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Fine Print

✓ In small human cerebral arteries preincubated with indomethacin, contractions induced by cerebrospinal fluid (CSF), from patients with subarachnoid hemorrhage were markedly increased. Also contractions induced by noradrenaline, but not 5-hydroxytryptamine, were augmented. Prostacyclin and its metabolite 6-keto-prostaglandin (PG)E1 reversed the contractions induced by CSF, as well as by noradrenaline, 5-hydroxytryptamine, and PGF2α. The findings suggest that these substances are able to counteract the influence of vasoconstrictor material in hemorrhagic CSF. If the capacity to synthesize these “protective” arachidonic acid metabolites is reduced, the resulting imbalance between contractile and relaxant forces acting on the vessel wall may lead to sustained cerebral vasoconstriction.

Cerebrospinal fluid may nourish cerebral vessels through pathways in the adventitia that may be analogous to systemic vasa vasorum

1982 ◽  
Vol 56 (4) ◽  
pp. 475-481 ◽  
Author(s):  
Nicholas T. Zervas ◽  
Theodore M. Liszczak ◽  
Marc R. Mayberg ◽  
Peter McL. Black
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Vessels ◽  
Subarachnoid Space ◽  
Cerebral Arteries ◽  
Cerebral Vessels ◽  
Vasa Vasorum ◽  
Cerebral Blood Vessels ◽  
Content Type ◽  
Large Proteins ◽  
Fine Print

✓ Cerebral blood vessels are devoid of vasa vasorum. Therefore, the authors have studied the microarchitecture of the adventitia of large feline cerebral vessels and systemic vessels of the same size, in an effort to determine how the vessels are nourished. The cerebral vessels contain a rete vasorum in the adventitia that is permeable to large proteins and is in continuity with the subarachnoid space. This substructure may be analogous to the systemic vasa vasorum and may contribute to the nutrition of the cerebral arteries.

Potassium and the pathogenesis of cerebral arterial spasm in dog and man

1971 ◽  
Vol 35 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Robert H. Wilkins ◽  
Philip Levitt
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Arterial Spasm ◽  
Content Type ◽  
Blood Clots ◽  
The Individual ◽  
Fine Print

✓ This study investigates the possibility that the intracranial arterial spasm occurring in patients with subarachnoid hemorrhage might be due to potassium released from blood clots surrounding the involved cerebral arteries. Although cerebral arterial spasm could be induced in the dog by the injection of potassium into the chiasmatic cistern, it only occurred with potassium concentrations higher than those expected to result from hemolysis of subarachnoid clots. Furthermore, the potassium concentrations were not elevated in the cerebrospinal fluid of human patients with subarachnoid hemorrhage, and the individual potassium values could not be correlated with the presence or degree of spasm encountered in these patients.

Norepinephrine in cerebrospinal fluid of patients with cerebral vasospasm

1982 ◽  
Vol 56 (3) ◽  
pp. 344-349 ◽  
Author(s):  
Taku Shigeno
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Arteries ◽  
Cerebral Aneurysms ◽  
Fluorometric Method ◽  
Content Type ◽  
Highly Sensitive ◽  
Secondary Phenomenon ◽  
Lumbar Cerebrospinal Fluid ◽  
The Brain ◽  
Fine Print

✓ The content of norepinephrine (NE) in the ventricular, basal cisternal, and lumbar cerebrospinal fluid (CSF) was determined in 19 patients with ruptured cerebral aneurysms at different intervals according to the presence or absence of vasospasm. Twelve were operated on within 3 days after subarachnoid hemorrhage (SAH), prior to the occurrence of vasospasm. Postoperatively, CSF was continuously drained from a basal cistern or lateral ventricle. Norepinephrine was assayed by the highly sensitive automated fluorometric method. The concentration of NE increased in all sites of CSF sampling along with the appearance of vasospasm. Above all, the cisternal CSF of patients with vasospasm contained significantly higher NE (0.246 ± 0.049 ng/ml, mean ± SEM) compared to those without vasospasm (0.075 ± 0.001 ng/ml) (p < 0.001). However, since this increase cannot be considered to be high enough locally to constrict cerebral arteries, this might be only a secondary phenomenon due to release of NE into CSF from various sources in the brain.

Clinicopathological study of cerebral aneurysms

1978 ◽  
Vol 48 (4) ◽  
pp. 505-514 ◽  
Author(s):  
Jiro Suzuki ◽  
Hiro Ohara
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Arteries ◽  
Fibrous Tissue ◽  
Cerebral Aneurysms ◽  
Content Type ◽  
Clinicopathological Study ◽  
The Media ◽  
Fine Print

✓ The origin and mechanism of rupture, repair, and growth of intracranial saccular aneurysms are reported in an investigation of 45 aneurysms (23 unruptured and 22 ruptured) found in 34 brain specimens. Gaps in the media at the bifurcations of cerebral arteries are important for aneurysmal formation. The walls of aneurysms smaller than 3 mm in diameter are mainly composed of endothelial cells, and fibrous tissue. When aneurysms grow larger than 4 mm, the walls become collagenous and extremely thin portions develop in their domes, forming potential rupture points. Immediately after the rupture, bleeding is stopped by clot and a new fibrin layer is formed around the rupture point. It is proposed that the cerebrospinal fluid has a special accelerating action in clot formation. This fibrin layer is weak, and repeat rupture occurs within 3 weeks after the initial hemorrhage. However, after 3 weeks, rebleeding is rare due to the reinforcement of this layer, and capillaries appear in this new wall. Hemorrhages from these capillaries occur within and outside the new wall caused by the constant impingement of blood flow. In severe cases, the aneurysm ruptures again, but when the hemorrhages are slight, the aneurysm grows as the wall is thickened by repeated hemorrhages and their absorption. This may explain the growth mechanism of the aneurysm.

Sign in / Sign up

Export Citation Format

Share Document