Experimental cerebral vasospasm

1974 ◽  
Vol 41 (3) ◽  
pp. 285-292 ◽  
Author(s):  
Hajime Nagai ◽  
Yoshiaki Suzuki ◽  
Mitsuo Sugiura ◽  
Satoshi Noda ◽  
Hideo Mabe
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Posterior Communicating Artery ◽  
Content Type ◽  
Aneurysmal Rupture ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓The authors describe a model for making an experimental subarachnoid hemorrhage that closely simulates human aneurysmal rupture. A needle previously inserted into the posterior communicating artery is subsequently withdrawn by traction on a thread. Using this model they demonstrate biphasic spasm by measurement of cerebral blood flow and angiography after rupture of the artery; the early spasm lasted 60 minutes and the late spasm began 3 or 4 hours after subarachnoid hemorrhage and continued for several days. The authors discuss the pathogenesis of early and late spasm.

Transcorneal stimulation of trigeminal nerve afferents to increase cerebral blood flow in rats with cerebral vasospasm: a noninvasive method to activate the trigeminovascular reflex

2002 ◽  
Vol 97 (5) ◽  
pp. 1179-1183 ◽  
Author(s):  
Basar Atalay ◽  
Hayrunnisa Bolay ◽  
Turgay Dalkara ◽  
Figen Soylemezoglu ◽  
Kamil Oge ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Vasospasm ◽  
Trigeminal Nerve ◽  
Nerve Endings ◽  
Noninvasive Method ◽  
Direct Stimulation ◽  
Content Type ◽  
Fine Print ◽  
Stimulation Of

Object. The goal of this study was to investigate whether stimulation of trigeminal afferents in the cornea could enhance cerebral blood flow (CBF) in rats after they have been subjected to experimental subarachnoid hemorrhage (SAH). Cerebral vasospasm following SAH may compromise CBF and increase the risks of morbidity and mortality. Currently, there is no effective treatment for SAH-induced vasospasm. Direct stimulation of the trigeminal nerve has been shown to dilate constricted cerebral arteries after SAH; however, a noninvasive method to activate this nerve would be preferable for human applications. The authors hypothesized that stimulation of free nerve endings of trigeminal sensory fibers in the face might be as effective as direct stimulation of the trigeminal nerve. Methods. Autologous blood obtained from the tail artery was injected into the cisterna magna of 10 rats. Forty-eight and 96 hours later (five rats each) trigeminal afferents were stimulated selectively by applying transcorneal biphasic pulses (1 msec, 3 mA, and 30 Hz), and CBF enhancements were detected using laser Doppler flowmetry in the territory of the middle cerebral artery. Stimulation-induced changes in cerebrovascular parameters were compared with similar parameters in sham-operated controls (six rats). Development of vasospasm was histologically verified in every rat with SAH. Corneal stimulation caused an increase in CBF and blood pressure and a net decrease in cerebrovascular resistance. There were no significant differences between groups for these changes. Conclusions. Data from the present study demonstrate that transcorneal stimulation of trigeminal nerve endings induces vasodilation and a robust increase in CBF. The vasodilatory response of cerebral vessels to trigeminal activation is retained after SAH-induced vasospasm.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

Treatment of aneurysmal hemiplegia with dopamine and mannitol

1978 ◽  
Vol 49 (4) ◽  
pp. 525-529 ◽  
Author(s):  
Frederick D. Brown ◽  
Kathryn Hanlon ◽  
Sean Mullan
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Clinical Improvement ◽  
Content Type ◽  
Remarkable Degree ◽  
Induced Hypertension ◽  
Fine Print

✓ Three patients with severe postoperative hemiplegia and one with hemiplegia following a subarachnoid hemorrhage are presented. None had hematomas. All were treated with dopamine-induced hypertension, mannitol, and large quantities of intravascular fluids. All showed a remarkable degree of clinical improvement, presumably secondary to an increase in cerebral blood flow.

Regional cerebral blood flow studies in subarachnoid hemorrhage

1972 ◽  
Vol 37 (1) ◽  
pp. 36-44 ◽  
Author(s):  
M. Peter Heilbrun ◽  
Jes Olesen ◽  
Niels A. Lassen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Regional Cerebral Blood Flow ◽  
Surgical Intervention ◽  
Focal Ischemia ◽  
Regional Cerebral Blood ◽  
Content Type ◽  
Clinical Grading ◽  
Fine Print

✓ Regional cerebral blood flow (rCBF) studies using the intra-arterial 133xenon method were performed on 10 patients with subarachnoid hemorrhage. Both preoperative and postoperative studies showed evidence of decreased flow in the entire hemisphere studied, and, in addition, evidence of focal ischemia, focal hyperemia, focal vasoparalysis, and often global impairment of autoregulation. The degree of flow abnormalities correlated well with the clinical grading of the neurological deficit. It is suggested that analysis of the state of autoregulation might be useful in determining the time for surgical intervention and that rCBF studies are important in defining the effects of drugs used to counteract the ischemic effects of spasm.

Cerebral blood flow following induced subarachnoid hemorrhage in the monkey

1972 ◽  
Vol 37 (3) ◽  
pp. 316-324 ◽  
Author(s):  
K. C. Petruk ◽  
G. R. West ◽  
M. R. Marriott ◽  
J. W. McIntyre ◽  
T. R. Overtone ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Neurological Status ◽  
Neurological Deficits ◽  
Content Type ◽  
Arterial Vasospasm ◽  
Experimental Subarachnoid Hemorrhage ◽  
Angiographic Demonstration

✓ The acute effects of experimental subarachnoid hemorrhage on cerebral blood flow were investigated in 14 adult rhesus monkeys injected with fresh autogenous blood through a needle positioned within the subfrontal subarachnoid space. Cerebral blood flow was measured by the xenon133 tissue clearance method before hemorrhage, and afterward at 30-minute intervals for a 3-hour period. Post-anesthetic neurological status was graded according to Botterell's classification. Twelve monkeys showed a significant decrease in cerebral perfusion, eight displayed focal neurological deficits, and four were moribund. There was a correlation between the degree of impaired circulation and the severity of neurological deficit. Four additional monkeys subjected to subarachnoid acidic saline injection showed no reduction in cerebral blood flow. In three animals cerebral perfusion was increased during the first hour after injection. It is suggested that measurement of cerebral blood flow may be a more valuable prognostic indication of cerebral function and survival than the angiographic demonstration of arterial vasospasm.

Effect of intracarotid nitric oxide on primate cerebral vasospasm after subarachnoid hemorrhage

1995 ◽  
Vol 83 (1) ◽  
pp. 118-122 ◽  
Author(s):  
John K. B. Afshar ◽  
Ryszard M. Pluta ◽  
Robert J. Boock ◽  
B. Gregory Thompson ◽  
Edward H. Oldfield
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Primate Model ◽  
Content Type ◽  
Continuous Release ◽  
Blood Flow Velocities ◽  
The Right ◽  
Fine Print

✓ The continuous release of nitric oxide (NO) is required to maintain basal cerebrovascular tone. Oxyhemoglobin, a putative spasmogen, rapidly binds NO, implicating loss of NO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). If vasospasm is mediated by depletion of NO in the vessel wall, it should be reversible by replacement with NO. To investigate this hypothesis, the authors placed blood clots around the right middle cerebral artery (RMCA) of four cynomolgus monkeys; four unoperated animals served as controls. Arteriography was performed before and 7 days after surgery to assess the presence and degree of vasospasm, which was quantified in the anteroposterior (AP) projection by computerized image analysis. On Day 7, cortical cerebral blood flow (CBF) in the distribution of the right MCA was measured during four to six runs in the right internal carotid artery (ICA) of brief infusions of saline followed by NO solution. Arteriography was performed immediately after completing the final NO infusion in three of the four animals with vasospasm. Right MCA blood flow velocities were obtained using transcranial Doppler before, during, and after NO infusion in two vasospastic animals. After ICA NO infusion, arteriographic vasospasm resolved (mean percent of preoperative AP area, 55.9%); that is, the AP areas of the proximal portion of the right MCA returned to their preoperative values (mean 91.4%; range 88%–96%). Compared to ICA saline, during ICA NO infusion CBF increased 7% in control animals and 19% in vasospastic animals (p < 0.002) without significant changes in other physiological parameters. During NO infusion, peak systolic right MCA CBF velocity decreased (130 to 109 cm/sec and 116 to 76 cm/sec) in two vasospastic animals. The effects of ICA NO on CBF and CBF velocity disappeared shortly after terminating NO infusion. Intracarotid infusion of NO in a primate model of vasospasm 1) increases CBF, 2) decreases cerebral vascular resistance, 3) reverses arteriographic vasospasm, and 4) decreases CBF velocity in the vasospastic artery without producing systemic hypotension. These findings indicate the potential for the development of targeted therapy to reverse cerebral vasospasm after SAH.

Relationship between hemispheric cerebral blood flow, central conduction time, and clinical grade in aneurysmal subarachnoid hemorrhage

1985 ◽  
Vol 62 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Jacob Rosenstein ◽  
Alexander Dah-Jium Wang ◽  
Lindsay Symon ◽  
Mikio Suzuki
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Initial Slope ◽  
Conduction Time ◽  
Clinical Grade ◽  
Content Type ◽  
Significant Difference ◽  
Fine Print

✓ The relationship between central conduction time (CCT) and hemispheric cerebral blood flow (CBF) has been examined in 20 patients presenting with subarachnoid hemorrhage. A total of 63 combined CCT/CBF recordings were performed at various times throughout the hospital course of these patients, and the findings were correlated to clinical status. The initial-slope index of the CBF (CBFisi) was found to correlate well with clinical grade, and a gradation in flow was noted between the different neurological grades. Patients in Grades I and II (Hunt and Hess classification) had the highest flows (mean CBFisi = 47.2 ± 8.1); Grade III patients had intermediate flows (mean CBFisi = 39.6 ± 7.8); and Grade IV patients had the lowest flows (mean CBFisi = 32.0 ± 6.4). While CCT tended to become increasingly prolonged with worsening grade, a significant difference could not be demonstrated between Grade I, II, and III patients. Only when Grade IV status was reached was the CCT significantly prolonged. When CBFisi and CCT were examined, a threshold relationship was noted between CBFisi and CCT prolongation. At flow values above 30, little change was noted in CCT, and CCT remained in the normal range. However, at flow values below 30, CCT became increasingly prolonged as blood flow diminished. The degree of CCT prolongation appeared to be directly proportional to the degree of blood flow diminution at flows below threshold.

Regional cerebral blood flow monitoring in the diagnosis of delayed ischemia following aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 98 (6) ◽  
pp. 1227-1234 ◽  
Author(s):  
Peter Vajkoczy ◽  
Peter Horn ◽  
Claudius Thome ◽  
Elke Munch ◽  
Peter Schmiedek
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Thermal Diffusion ◽  
Regional Cerebral Blood Flow ◽  
High Grade ◽  
Regional Cerebral Blood ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fine Print

Object. The goal of this study was to evaluate regional cerebral blood flow (rCBF) monitoring, performed using thermal-diffusion (TD) flowmetry, as a novel means for the bedside diagnosis of symptomatic vasospasm. Methods. Fourteen patients with high-grade subarachnoid hemorrhage (SAH) who underwent early clip placement for anterior circulation aneurysms were prospectively entered into the study. Thermal-diffusion microprobes were implanted into the white matter of vascular territories that were deemed at risk for developing symptomatic vasospasm. Data on arterial blood pressure, intracranial pressure, cerebral perfusion pressure, rCBF measurement obtained using a TD probe (TD-rCBF), cerebrovascular resistance (CVR), and blood flow velocities were collected at the patient's bedside. The diagnosis of symptomatic vasospasm was based on the manifestation of a delayed ischemic neurological deficit and/or a reduced territorial level of CBF as assessed using stable Xe-enhanced computerized tomography (CT) scanning in combination with vasospasm demonstrated by angiography. Bedside monitoring of TD-rCBF and CVR allowed the detection of symptomatic vasospasm. In the 10 patients with vasospasm the TD-rCBF decreased from 21 ± 4 to 9 ± 1 ml/100 g/min (mean ± standard error of the mean), whereas in the four other patients the TD-rCBF value remained unchanged (mean TD-rCBF = 25 ± 4 compared with 21 ± 4 ml/100 g/min). A comparison of the results of TD-rCBF and Xe-enhanced CT studies, as well as the calculation of sensitivities, specificities, predictive values, and likelihood ratios, identified a TD-rCBF value of 15 ml/100 g/min as a reliable cutoff for the diagnosis of symptomatic vasospasm. In addition, TD flowmetry was characterized by a more favorable diagnostic reliability than transcranial Doppler ultrasonography. Conclusions. Thermal-diffusion flowmetry represents a promising method for the bedside monitoring of patients with SAH to detect symptomatic vasospasm. This is of major clinical interest for patients with high-grade SAH, who often cannot be assessed neurologically.

Abnormal cerebral vasodilation in aneurysmal subarachnoid hemorrhage: use of serial 133Xe cerebral blood flow measurement plus acetazolamide to assess cerebral vasospasm

1993 ◽  
Vol 79 (4) ◽  
pp. 490-493 ◽  
Author(s):  
Yves Roger Tran Dinh ◽  
Guillaume Lot ◽  
Rabah Benrabah ◽  
Oussama Baroudy ◽  
Jean Cophignon ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Artery Aneurysm ◽  
Content Type ◽  
Serial Measurement ◽  
Before And After ◽  
Cerebral Vasodilation

✓ A patient with cerebral vasospasm following subarachnoid hemorrhage (SAH) was investigated by serial measurement of cerebral blood flow (CBF) using the xenon-133 emission tomography method. The CBF was measured before and after acetazolamide injection. On Day 2 after SAH, there was early local hyperperfusion in the middle cerebral artery (MCA) territory, ipsilateral to the left posterior communicating artery aneurysm. The regional CBF of this arterial territory decreased slightly after acetazolamide injection, probably because of vasoplegia and the “steal” phenomenon, and thus surgery was delayed. A right hemiplegia with aphasia and disturbed consciousness occurred 4 days later (on Day 6 after SAH) due to arterial vasospasm, despite treatment with a calcium-channel blocker. The initial hyperemia of the left MCA territory was followed by ischemia. The vasodilation induced by acetazolamide administration was significantly subnormal until Day 13, at which time CBF and vasoreactivity amplitude returned to normal and the patient's clinical condition improved. Surgery on Day 14 and outcome were without complication. It is concluded that serial CBF measurements plus acetazolamide injection are useful for monitoring the development of cerebral vasospasm to determine the most appropriate time for aneurysm surgery.

Delayed cell death related to acute cerebral blood flow changes following subarachnoid hemorrhage in the rat brain

2005 ◽  
Vol 102 (6) ◽  
pp. 1046-1054 ◽  
Author(s):  
Giselle F. Prunell ◽  
Niels-Aage Svendgaard ◽  
Kanar Alkass ◽  
Tiit Mathiesen
Keyword(s):  
Blood Flow ◽  
Cell Death ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Therapeutic Window ◽  
Adequate Treatment ◽  
Doppler Flowmetry ◽  
Content Type ◽  
Delayed Cell Death ◽  
Fine Print

Object. The authors tested the hypotheses that subarachnoid hemorrhage (SAH) leads to delayed cell death with the participation of apoptotic-like mechanisms and is influenced by the degree of acute decrease in the cerebral blood flow (CBF) following hemorrhage. Methods. Subarachnoid hemorrhage was induced in rats by endovascular perforation of the internal carotid artery or injection of blood into the prechiasmatic cistern. Cerebral blood flow was measured using laser Doppler flowmetry for 60 minutes. Brain sections stained with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) showed DNA fragmentation at 2 and 7 days after both methods of inducing SAH in one third to two thirds of the surviving animals in the different experimental groups. More than 80% of the TUNEL-positive cells were neuron-specific nuclear protein—positive (neurons), but immunoreactivity to glial fibrillary acidic protein (astrocytes) and transferrin (oligodendrocytes) were markedly decreased in TUNEL-positive areas. Most of the TUNEL-positive cells displayed chromatin condensation and/or blebs and immunostained for increased Bax; approximately 50% of them were immunoreactive to cleaved caspase-3 and a few to Bcl-2. The duration of the acute CBF decrease below 30% of the baseline level was related to the degree of TUNEL staining. Conclusions. Subarachnoid hemorrhage resulted in delayed cell death in a large proportion, but not all, of the surviving animals. The acute CBF decrease was related to the degree of subsequent cell death. These findings indicated the relevance of apoptotic-like pathways. There appears to be a temporal therapeutic window during which adequate treatment might reduce the final damage following SAH.

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