Intracranial arterial spasm in the dog

1970 ◽  
Vol 33 (3) ◽  
pp. 260-269 ◽  
Author(s):  
Robert H. Wilkins ◽  
Philip Levitt
Keyword(s):  
Whole Blood ◽  
Cerebral Arteries ◽  
Canine Model ◽  
Circle Of Willis ◽  
Arterial Spasm ◽  
Arterial Tree ◽  
Content Type ◽  
Fine Print

✓ A chronic canine model for the investigation of intracranial arterial spasm was designed and used to study spasm produced by rapid and slow cisternal injections of fresh or heparinized autogenous whole blood, or serum from incubated autogenous blood. Spasm so produced begins within 10 minutes after the injection and lasts from several hours to days. It affects primarily the major arteries of the circle of Willis, especially the proximal anterior cerebral arteries, and it does not seem to involve the extradural arterial tree.

Exposure of the anterior part of the circle of Willis in the dog

1974 ◽  
Vol 41 (1) ◽  
pp. 107-112
Author(s):  
Shigeaki Hori ◽  
Williamina A. Himwich
Keyword(s):  
Anterior Part ◽  
Cerebral Arteries ◽  
Circle Of Willis ◽  
Content Type ◽  
Anatomical Characteristics ◽  
Fine Print

✓ A technique for exposing the vessels in the anterior part of the circle of Willis in the dog is described. Some of the physiological and anatomical characteristics of the anterior communicating and the anterior cerebral arteries are discussed.

Bifurcation geometry and the presence of cerebral artery aneurysms

2004 ◽  
Vol 101 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Tor Ingebrigtsen ◽  
Michael K. Morgan ◽  
Ken Faulder ◽  
Linda Ingebrigtsen ◽  
Trygve Sparr ◽  
...  
Keyword(s):  
Cerebral Artery ◽  
Geometric Model ◽  
Cerebral Arteries ◽  
Multivariate Logistic Regression Analysis ◽  
Circle Of Willis ◽  
Parent Vessel ◽  
Content Type ◽  
Optimality Principles ◽  
The Relationship ◽  
Fine Print

Object. The angles of arterial bifurcations are governed by principles of work minimization (optimality principle). This determines the relationship between the angle of a bifurcation and the radii of the vessels. Nevertheless, the model is predicated on an absence of significant communication between these branches. The circle of Willis changes this relationship because the vessels proximal to the ring of vessels have additional factors that determine work minimization compared with more distal branches. This must have an impact on understanding of the relationship between shear stress and aneurysm formation. The authors hypothesized that normal bifurcations of cerebral arteries beyond the circle of Willis would follow optimality principles of minimum work and that the presence of aneurysms would be associated with deviations from optimum bifurcation geometry. Nevertheless, the vessels participating in (or immediately proximal to) the circle of Willis may not follow the geometric model as it is generally applied and this must also be investigated. Methods. One hundred seven bifurcations of the middle cerebral artery (MCA), distal internal carotid artery (ICA), and basilar artery (BA) were studied in 55 patients. The authors analyzed three-dimensional reconstructions of digital subtraction angiography images with respect to vessel radii and bifurcation angles. The junction exponent (that is, a calculated measure of the division of flow at the bifurcation) and the difference between the predicted optimal and observed branch angles were used as measures of deviation from the geometry thought best to minimize work. The mean junction exponent for MCA bifurcations was 2.9 ± 1.2 (mean ± standard deviation [SD]), which is close to the theoretical optimum of 3, but it was significantly smaller (p < 0.001; 1.7 ± 0.8, mean ± SD) for distal ICA bifurcations. In a multilevel multivariate logistic regression analysis, only the observed branch angles were significant independent predictors for the presence of an aneurysm. The odds ratio (OR) (95% confidence interval) for the presence of an aneurysm was 3.46 (1.02–11.74) between the lowest and highest tertile of the observed angle between the parent vessel and the largest branch. The corresponding OR for the smallest branch was 48.06 (9.7–238.2). Conclusions. The bifurcation beyond the circle of Willis (that is, the MCA) closely approximated optimality principles, whereas the bifurcations within the circle of Willis (that is, the distal ICA and BA) did not. This indicates that the confluence of hemodynamic forces plays an important role in the distribution of work at bifurcations within the circle of Willis. In addition, the observed branch angles were predictors for the presence of aneurysms.

Delayed CSF lavage for arteriographic and morphological vasospasm after experimental SAH

1985 ◽  
Vol 63 (6) ◽  
pp. 949-958 ◽  
Author(s):  
Eben Alexander ◽  
Peter McL. Black ◽  
Theodore M. Liszczak ◽  
Nicholas T. Zervas
Keyword(s):  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Blood Gases ◽  
Canine Model ◽  
Content Type ◽  
Clot Removal ◽  
Wilcoxon Rank Sum Test ◽  
Arterial Vasospasm ◽  
Chronic Vasospasm ◽  
Fine Print

✓ Irrigation of the subarachnoid space after aneurysmal subarachnoid hemorrhage (SAH) has been reported to alleviate subsequent arterial vasospasm. The authors have investigated the effect of lavage of the cerebrospinal fluid (CSF) space in the two-hemorrhage canine model of vasospasm. Twelve dogs had basilar cistern lavage with 120 cc of artificial CSF 24 hours after each of two SAH's, and 12 control dogs had two sequential SAH's without intervening lavage of clot. The amount of clot on the ventral brain stem was evaluated at sacrifice and was graded from 0 (no clot) to 4 (maximum clot) to assess the adequacy of clot removal. Dogs that had undergone lavage had a median grade of 1 (range Grade 0 to 2); control dogs had a median grade of 2 (range Grade 1 to 3.5, p < 0.001, Wilcoxon rank sum test), indicating significant reduction of gross clot by lavage. The neurological findings were graded from 0 to 5, based on meningismus, ataxia, paresis, and cranial nerve deficits. No significant differences in neurological grade were found on any day between the two groups. Satisfactory angiograms were obtained before and 7 days after hemorrhage and were controlled for blood pressure and blood gases; these showed significant spasm in both groups. There was a mean reduction (± standard deviation) of 21.6% ± 16.2% in basilar artery diameter in control dogs, compared to a 28.8% ± 15.1% reduction in dogs with lavage (difference not significant, t-test). There was a strong, but insignificant, trend toward reduction of endothelial desquamation in the basilar and middle cerebral arteries in dogs with lavage compared to control animals (p = 0.06). Corrugation and tearing of the elastica, thickened intima, intimal fibroplasia, vacuolization of the endothelial or smooth-muscle cells, and presence of blood cells in the adventitia occurred similarly in both groups. It appears that cisternal lavage 24 hours after hemorrhage in this model has no effect on the angiographic, neurological, or most morphological sequelae of SAH, in spite of evidence for removal of clot as seen at sacrifice. Any postulated interaction of clot and vessel resulting in chronic vasospasm must occur before this time. Evaluation of the effect of much earlier lavage (for instance, 1 hour after hemorrhage) may elucidate the point at which vasospasm is instigated after SAH, and help in determining what factors cause vasospasm.

Cerebral arterial spasm

1974 ◽  
Vol 40 (4) ◽  
pp. 433-441 ◽  
Author(s):  
George S. Allen ◽  
Lavell M. Henderson ◽  
Shelly N. Chou ◽  
Lyle A. French
Keyword(s):  
Small Volume ◽  
Contractile Activity ◽  
Cerebral Arteries ◽  
Arterial Spasm ◽  
Vasoactive Agents ◽  
Response Curves ◽  
Content Type ◽  
Middle Cerebral Arteries ◽  
Fine Print

✓ In vitro experiments were performed using a small volume chamber to determine the contractile activity of various vasoactive agents on the canine basilar and middle cerebral arteries. Cumulative dose-response curves were obtained for most of the agents tested including serotonin and three different prostaglandins; many of these curves were found to be similar for segments from both arteries. It was concluded from these curves, and the known concentrations in blood, that serotonin is probably the agent in blood responsible for the cerebral arterial spasm that often follows a subarachnoid hemorrhage. This in vitro method is capable of detecting serotonin concentrations as low as 10−12 gm/ml and may prove useful as a quantitative and well-controlled method for studying the etiology of spasm and the receptor mechanisms present in 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.

Failure of intravascular volume expansion without hemodilution to elevate cortical blood flow in region of experimental focal ischemia

1982 ◽  
Vol 56 (1) ◽  
pp. 80-91 ◽  
Author(s):  
James H. Wood ◽  
Lauri L. Snyder ◽  
Frederick A. Simeone
Keyword(s):  
Blood Flow ◽  
Whole Blood ◽  
Volume Expansion ◽  
Cerebral Arteries ◽  
Intravascular Volume ◽  
Cortical Blood Flow ◽  
Content Type ◽  
Autologous Whole Blood ◽  
Cerebral Arterial Occlusion ◽  
Fine Print

✓ Cerebrovascular and cardiac alterations evoked by intravascular volume expansion with whole blood, a popular adjunct in the clinical prevention or therapy of the focal ischemic deficits of cerebral vasospasm and acute stroke, were studied in splenectomized dogs. Clipping of the right distal internal carotid and proximal middle cerebral arteries in eight dogs reduced regional cortical blood flow (rCoBF) by 49% to 58% without altering cardiac output (CO), and produced about 10% hemispheric infarction. Eight dogs underwent similar cerebral arterial occlusion and eight dogs underwent arterial manipulation without clipping. Both latter groups received two autologous whole blood infusions within 2 hours, each equal to 20% of the respective dog's total blood volume. Despite significant CO elevations after the infusions, rCoBF in the middle cerebral arterial territory did not rise. These whole-blood infusions did not significantly alter mean arterial blood pressure, hematocrit, intracranial pressure, or, in dogs with clipped cerebral arteries, the relative size of infarction. These data suggest that nondilutional hypervolemia neither elevates collateral perfusion to ischemic regions of the brain nor reduces infarction. In addition, elevations in CO do not appear to augment blood flow in either ischemic or normal brain.

Delayed cerebral vasospasm is not reversible by aminophylline, nifedipine, or papaverine in a “two-hemorrhage” canine model

1983 ◽  
Vol 58 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Vassilios G. Varsos ◽  
Theodore M. Liszczak ◽  
Dae Hee Han ◽  
J. Philip Kistler ◽  
Juan Vielma ◽  
...  
Keyword(s):  
Calcium Antagonist ◽  
Basilar Artery ◽  
Bolus Injection ◽  
Cerebral Arteries ◽  
Canine Model ◽  
Content Type ◽  
Delayed Cerebral Vasospasm ◽  
Angiographic Vasospasm ◽  
Before And After ◽  
Fine Print

✓ Angiographic spasm of cerebral arteries was produced in dogs by successive injections of cisternal blood 48 hours apart. Angiograms were taken before and after each cisternal injection. There was progressively greater angiographic vasospasm of the basilar artery. Intravenous aminophylline, 10 mg/kg/hr, reversed vessel constriction on the 1st and 3rd day after one injection of cisternal blood. On the 5th day after two blood injections (on Day 1 and Day 3), intravenous aminophylline, nifedipine (1 mg/kg), and intra-arterial bolus injection of 2 mg/kg papaverine failed to reverse the constriction. The intractable constriction produced in this model resembles that found in patients. The calcium antagonist, nifedipine, is as ineffective as the more traditional vasodilators in reversing vasospasm in this model.

Surgical manipulation of primate cerebral arteries in established vasospasm

1991 ◽  
Vol 75 (3) ◽  
pp. 425-432 ◽  
Author(s):  
J. Max Findlay ◽  
R. Loch Macdonald ◽  
Bryce K. A. Weir ◽  
Michael G. A. Grace
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Arteries ◽  
Circle Of Willis ◽  
Content Type ◽  
Increased Risk ◽  
The Right ◽  
Surgical Manipulation ◽  
Fine Print

✓ It is generally believed that surgery in the face of angiographic vasospasm is dangerous due to an increased incidence of postoperative cerebral ischemia. One theory is that arterial narrowing is exacerbated by surgical manipulation of vasospastic vessels during aneurysm dissection and clipping. This theory was tested in a primate model of cerebral vasospasm and the results reported. Six monkeys underwent baseline cerebral angiography, followed by induction of subarachnoid hemorrhage (SAH) on both sides of the circle of Willis. An equal amount of fresh autologous blood clot was placed around each internal carotid, anterior cerebral, and middle cerebral artery. Six days later, angiography was repeated and the right craniectomy was reopened for clot evacuation and surgical manipulation of the right cerebral arteries, including placement of a temporary aneurysm clip on the right middle cerebral artery. The left cerebral arteries were not exposed or manipulated, and served as controls. Twenty-four hours later angiography was repeated, then the animals were killed. Equal and significant vasospasm (> 40% reduction in vessel caliber compared to baseline, p < 0.05) was seen in the middle cerebral arteries on both sides of the circle of Willis in all animals 6 and 7 days after SAH. There was no significant change in the severity of vasospasm on Day 7 compared with Day 6 in the right cerebral arteries. Increased risk of postoperative cerebral ischemia for surgery in the peak vasospasm period may be due to mechanisms other than increased arterial narrowing precipitated by surgical manipulation.

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.

Embolism from intracranial aneurysms

1980 ◽  
Vol 53 (3) ◽  
pp. 300-304 ◽  
Author(s):  
Toshisuke Sakaki ◽  
Kazuhiko Kinugawa ◽  
Tatsuo Tanigake ◽  
Seiji Miyamoto ◽  
Kikuo Kyoi ◽  
...  
Keyword(s):  
Intracranial Aneurysms ◽  
Carotid Arteries ◽  
Internal Carotid ◽  
Cerebral Arteries ◽  
Great Care ◽  
Content Type ◽  
Middle Cerebral Arteries ◽  
Internal Carotid Arteries ◽  
Distal Artery ◽  
Fine Print

✓ Embolism from an aneurysm is one of the mechanisms involved in the pathogenesis of ischemic symptoms associated with intracranial aneurysms. Four cases are reported in which aneurysms of the internal carotid arteries and middle cerebral arteries were the source of emboli resulting in cerebral infarction. In the treatment of these aneurysms, it is best to clip the neck of the aneurysm with great care to avoid embolism due to extrusion of clot into the distal artery.

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