Time course of the impairment of cerebral autoregulation during chronic cerebral vasospasm after subarachnoid hemorrhage in primates

1992 ◽  
Vol 76 (3) ◽  
pp. 493-501 ◽  
Author(s):  
Yuji Handa ◽  
Minoru Hayashi ◽  
Hiroaki Takeuchi ◽  
Tetsuya Kubota ◽  
Hidenori Kobayashi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Autoregulation ◽  
Time Course ◽  
Blood Clot ◽  
Autologous Blood ◽  
Conduction Time ◽  
Arterial Blood ◽  
The Right ◽  
Chronic Cerebral Vasospasm

✓ The time course of the impairment of cerebral autoregulation during chronic cerebral vasospasm after subarachnoid hemorrhage was studied in 18 monkeys. Changes in cerebral blood flow (CBF) at the regional level and central conduction times during either graded hypo- or hypertension were evaluated in these animals at three stages (3, 7, and 14 days) following the introduction of an autologous blood clot around the right middle cerebral artery (MCA). Angiograms revealed a reduction in vessel caliber (compared to the baseline level in the involved MCA) of 30% at 3 days, 50% at 7 days, and 10% at 14 days. At all stages, CBF remained constant at mean arterial blood pressures (MABP) of 60 to 160 mm Hg in the noninvolved hemisphere. In contrast, at the 3- and 7-day stages, there was an impairment of autoregulation in the involved hemisphere at MABP of 40 to 180 mm Hg. The right hemispheric CBF was significantly (p < 0.05) lower than that in the left throughout the period of investigation at MABP below 120 mm Hg, but rose to exceed the left CBF at MABP above 180 mm Hg at the 7-day stage and 160 mm Hg at the 14-day stage. The right-sided central conduction time showed significant (p < 0.05) prolongation at MABP below 60 mm Hg at the 3-day stage and 40 mm Hg at the 7-day stage. It is suggested that these results may help to develop guidelines for hemodynamic therapy for vasospasm in its various stages.

Impairment of Cerebral Autoregulation during the Development of Chronic Cerebral Vasospasm after Subarachnoid Hemorrhage in Primates

Neurosurgery ◽  
1991 ◽  
Vol 28 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Hiroaki Takeuchi ◽  
Yuji Handa ◽  
Hidenori Kobayashi ◽  
Ilirokazu Kawano ◽  
Minoru Hayashi
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Arterial Blood Pressure ◽  
Cerebral Vasospasm ◽  
Conduction Time ◽  
Arterial Blood ◽  
The Mean ◽  
The Right ◽  
Chronic Cerebral Vasospasm ◽  
The Brain

Abstract We studied the impairment of autoregulation of cerebral blood flow (CBF) and its effect on the electrical activity of the brain during the development of chronic cerebral vasospasm after subarachnoid hemorrhage, using a vasospasm model in primates. Fourteen animals were divided into two groups: a clot group (8) and a sham-operated group (6). To induce subarachnoid hemorrhage, all the animals underwent craniectomy, and in the clot group, the autologous blood clot was located around the arteries dissected free from the arachnoid membrane. Cerebral angiography was performed before subarachnoid hemorrhage and 7 days after (Day 7). On Day 7, regional CBF in the parietal lobe—measured by the hydrogen clearance method—and central conduction time were studied during either graded hypertension or hypotension. In the clot group, the mean vessel caliber of the cerebral arteries on the right side (clot side) of the circle of Willis showed significant (P&lt;0.01) reduction (more than 40%) as compared with the values on the contralateral, non-clot side. The values for the bilateral parietal CBF in the sham-operated group and the left parietal CBF in the clot group were fairly constant when the mean arterial blood pressure (MABP) was in the range of 60 to 160 mm Hg. In the clot group, right parietal CBF was significantly (P &lt; 0.05) smaller than that on the left side at an MABP level of 40 to 100 mm Hg, and increased at an MABP level of 180 mm Hg. The right parietal CBF increased as the arterial blood pressure increased, showing impairment of autoregulation. The central conduction time on the right side in the clot group was significantly (P&lt;0.05) prolonged at an MABP of 40 mm Hg. It is suggested that impairment of autoregulation is strongly affected by the development of cerebral vasospasm and that, in this state, a decrease in cerebral perfusion pressure easily depresses the electrical function of the brain.

Histological studies of intracranial vessels in primates following transluminal angioplasty for vasospasm

1993 ◽  
Vol 78 (3) ◽  
pp. 481-486 ◽  
Author(s):  
Hidenori Kobayashi ◽  
Hisashi Ide ◽  
Hiroshi Aradachi ◽  
Yoshikazu Arai ◽  
Yuji Handa ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Cerebral Artery ◽  
Cell Damage ◽  
Blood Clot ◽  
Autologous Blood ◽  
Transluminal Angioplasty ◽  
Content Type ◽  
Histological Studies ◽  
The Right ◽  
Chronic Cerebral Vasospasm

✓ Percutaneous transluminal angioplasty for treatment of cerebral vasospasm was performed in primates. Chronic cerebral vasospasm was induced by placement of an autologous blood clot over the right internal carotid artery (ICA), middle cerebral artery (MCA), and anterior cerebral artery (ACA). Cerebral angiography on Day 7 showed that the diameters of the ICA, MCA, and ACA were reduced to 55.7% ± 1.3%, 55.3% ± 2.6%, and 59.6% ± 1.3%, respectively, of baseline. The angioplasty was carried out with a silicone microballoon attached to a microcatheter under somatosensory evoked potential (SEP) monitoring on Day 7. The angioplasty for ICA was performed satisfactorily; however, the balloon could be not advanced to the spastic M1 or A1 portions of the cerebral artery. Following angioplasty, the diameters of the ICA, the M1 segment, and the A1 segment were 79.6% ± 2.9% (p < 0.001), 67.6% ± 4.3% (p < 0.05), and 61.7% ± 2.2% (not significant), respectively, of baseline. Histological studies demonstrated that the vessels were well dilated and patent without endothelial cell damage.

Effect of systemic hypotension on cerebral energy metabolism during chronic cerebral vasospasm in primates

1993 ◽  
Vol 78 (1) ◽  
pp. 112-119 ◽  
Author(s):  
Yuji Handa ◽  
Tetsuya Kubota ◽  
Akira Tsuchida ◽  
Masanori Kaneko ◽  
Hakan Caner ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cerebral Vasospasm ◽  
Mr Spectroscopy ◽  
High Energy ◽  
Cerebral Energy Metabolism ◽  
Systemic Hypotension ◽  
Arterial Blood ◽  
The Mean ◽  
The Right ◽  
Chronic Cerebral Vasospasm

✓ The influence of systemic hypotension on cerebral blood flow (CBF) and energy metabolism during chronic cerebral vasospasm after subarachnoid hemorrhage was studied in 15 monkeys. Changes in the phosphorus spectrum, as demonstrated by in vivo phosphorus-31 (31P) magnetic resonance (MR) spectroscopy, or in regional CBF were measured in the parietal cortex during graded hypotension. Sequential changes in the phosphorus spectrum were observed during moderate hypotension in the animals 7 days after the introduction of an autologous blood clot around the right middle cerebral artery (MCA). Angiograms revealed a reduction in vessel caliber by approximately 50% in the right MCA. The mean CBF in the spasm side decreased in parallel with a decrease in the mean arterial blood pressure (MABP) from 120 to 40 mm Hg, indicating the abolition of autoregulation. There were no significant differences in the mean percentage totals of inorganic phosphate (Pi), phosphocreatine (PCr), adenosine triphosphate (ATP), and pH between the hemispheres at baseline MABP before hypotension. The values of PCr, ATP, and pH decreased significantly (p < 0.05) and Pi increased significantly (p < 0.05) at an MABP of less than 60 mm Hg in the involved hemisphere. The ratio of PCr:Pi decreased in parallel with a decrease in MABP. The ATP showed a stepwise decrease during moderate hypotension (MABP 60 mm Hg) and was reduced significantly 20 minutes after the beginning of hypotension (p < 0.05). The results indicate that, during chronic vasospasm, changes in cerebral energy metabolism are coupled with changes in CBF in the state of impaired autoregulation. There exists a critical level for ischemia below which high-energy phosphorus metabolites become markedly depleted. It is suggested that 31P MR spectroscopy may be useful to evaluate the ischemic vulnerability of brain tissue in order to prevent delayed neurological deficit during cerebral vasospasm.

Cerebral perivascular nerves in subarachnoid hemorrhage

1986 ◽  
Vol 65 (4) ◽  
pp. 531-539 ◽  
Author(s):  
Hideaki Hara ◽  
Michael Nosko ◽  
Bryce Weir
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Blood Clot ◽  
Autologous Blood ◽  
Nerve Fibers ◽  
Content Type ◽  
Arterial Blood ◽  
Mild Reduction ◽  
Perivascular Nerves ◽  
Basilar Arteries ◽  
Repeat Angiography

✓ The authors have studied the changes induced by subarachnoid hemorrhage (SAH) in the density and distribution of cerebral perivascular nerves in monkeys and rats. The SAH was induced in monkeys by placement of an autologous blood clot after opening the basal cisterns over the arteries of the circle of Willis on one side. In the rat study, SAH was induced by injection of autologous arterial blood into the cisterna magna. The nerves examined were adrenergic nerves, acetylcholinesterase (AChE)-containing nerves, vasoactive intestinal polypeptide (VIP)-like immunoreactive nerves, and substance P-like immunoreactive nerves. In the monkey study, all animals underwent baseline cerebral angiography, then had repeat angiography just before sacrifice on Day 2, 7, 28, or 70 after SAH. Two sham-operated monkeys underwent the surgical procedure without clot placement and were sacrificed on postoperative Day 7, after repeat angiography. Clot placement in monkeys reduced staining of all middle cerebral artery (MCA) perivascular nerves for between 2 and 28 days post-SAH. The number of stained nerve fibers of MCA's on the non-operated side was slightly reduced on Days 2 and 7 after SAH. Sham-operated monkeys showed a mild reduction of staining in all nerves, but only on the operated side. Cerebral vasospasm was observed on all angiograms taken on Days 2 and 7 following SAH. No vasospasm was found in normal or sham-operated monkeys. The disappearance of nerve staining without associated vasospasm was found on the operated side of the sham-operated monkeys and on the clot side of the animal sacrificed on Day 28 after SAH. Rats sacrificed on Days 2 and 7 post-SAH showed reduction in adrenergic and VIP-like immunoreactive staining around basilar arteries, while nerves containing AChE were not affected. Saline-injected rats exhibited no change in the appearance of perivascular innervation. These results suggest that SAH as well as surgical manipulation of the vessel wall caused a reduction of the studied substances in cerebral perivascular nerves. This reduction in immunoreactive staining of perivascular nerves did not correlate with the development of angiographic vasospasm after SAH.

Prospective, randomized, double-blind trial of BQ-123 and bosentan for prevention of vasospasm following subarachnoid hemorrhage in monkeys

1995 ◽  
Vol 83 (3) ◽  
pp. 503-509 ◽  
Author(s):  
Akihiko Hino ◽  
Bryce K. A. Weir ◽  
R. Loch Macdonald ◽  
Ronald A. Thisted ◽  
Chul-Jin Kim ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Artery ◽  
Internal Carotid ◽  
Blood Clot ◽  
Autologous Blood ◽  
Ommaya Reservoir ◽  
Double Blind ◽  
The Right ◽  
Arterial Diameters

✓ Thirty-one monkeys were randomly divided into three groups to undergo baseline cerebral angiography followed by induction of subarachnoid hemorrhage by placement of autologous blood clot along the right-sided arteries of the anterior circle of Willis (Day 0). The monkeys were then given drug vehicle or one of two endothelin (ET) antagonists, BQ-123 (6 mg/kg/day) or bosentan (5 mg/kg/day) intracisternally. The BQ-123 was administered by continuous infusion from a subcutaneous pump and the bosentan was given by twice-daily injections into an Ommaya reservoir in the subcutaneous space with a catheter along the right middle cerebral artery (MCA). Seven days later (Day 7), angiography was repeated and the animals were killed. Comparison of arterial diameters shown on angiograms between Day 0 and Day 7 groups given placebo and bosentan showed significant reductions in the diameters of the right intradural internal carotid (28% ± 6% and 30% ± 6%, respectively, paired t-test, p < 0.05), anterior cerebral artery (29% ± 8% and 32%, ± 6% respectively ± 6%, respectively) and MCA (34% ± 6% and 46% ± 4%, respectively). Animals injected with BQ-123 had significant narrowing of the right extradural internal carotid artery (7% ± 6%) and the basilar artery (11% ± 3%), but not of the right MCA. Comparison of arterial diameters between groups at Day 7 showed significant variance in the right extradural internal carotid, both intradural internal carotid, right middle cerebral, and left anterior cerebral arteries; the animals injected with BQ-123 developed significantly less arterial narrowing these those receiving bosentan and placebo. Bosentan was not detected in the cerebrospinal fluid aspirated from the cisterna magna on Day 7, whereas BQ-123 was detected in two animals. We can infer from these results that BQ-123 prevents vasospasm following subarachnoid hemorrhage in monkeys, that further investigations of ET antagonists are warranted, and that ET may be an important pathophysiological mediator of vasospasm. The lack of efficacy of bosentan may be related to inadequate cerebrospinal fluid levels obtained by administration twice-daily through an Ommaya reservoir.

Temporal changes in perivascular concentrations of oxyhemoglobin, deoxyhemoglobin, and methemoglobin after subarachnoid hemorrhage

1998 ◽  
Vol 88 (3) ◽  
pp. 557-561 ◽  
Author(s):  
Ryszard M. Pluta ◽  
John K. B. Afshar ◽  
Robert J. Boock ◽  
Edward H. Oldfield
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Blood Clot ◽  
Saline Control ◽  
Control Group ◽  
Content Type ◽  
Delayed Cerebral Vasospasm ◽  
Arterial Blood ◽  
Fine Print

Hemoglobin released from hemolysed erythrocytes has been postulated to be responsible for delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). However, the evidence is indirect and the mechanisms of action are unclear. Cerebrovascular tone is regulated by a dynamic balance of relaxing and contracting factors. Loss of the endothelium-derived relaxing factor—nitric oxide in the presence of oxyhemoglobin and overproduction of endothelin-1 stimulated by oxyhemoglobin have been postulated as causes of delayed cerebral vasospasm after SAH. Object. The authors aimed to investigate this hypothesis using in vivo microdialysis to examine time-dependent changes in the perivascular concentrations of oxyhemoglobin, deoxyhemoglobin, and methemoglobin in a primate model of SAH. Methods. Nine cynomolgus monkeys underwent right-sided frontotemporal craniectomy and placement of a semipermeable microdialysis catheter adjacent to the right middle cerebral artery (MCA). Saline (control group, three animals) or an arterial blood clot (SAH group, six animals) was then placed around the MCA and the catheter. Arteriographically confirmed vasospasm had developed in all animals with SAH but in none of the control animals on Day 7. The dialysate was collected daily for 12 days. Levels of oxyhemoglobin, deoxyhemoglobin, and methemoglobin were measured by means of spectrophotometry. Perivascular concentrations of oxyhemoglobin, deoxyhemoglobin, and methemoglobin peaked on Day 2 in the control monkeys and could not be detected on Days 5 to 12. Perivascular concentrations of oxyhemoglobin and deoxyhemoglobin peaked on Day 7 in the SAH group, at which time the concentrations in the dialysate were 100-fold higher than in any sample obtained from the control animals. Methemoglobin levels increased only slightly, peaking between Days 7 and 12, at which time the concentration in the dialysate was 10-fold higher than in samples from the control animals. Conclusions. This study provides in vivo evidence that the concentrations of oxyhemoglobin and deoxyhemoglobin increase in the cerebral subarachnoid perivascular space during the development of delayed cerebral vasospasm. The results support the hypothesis that oxyhemoglobin is involved in the pathogenesis of delayed cerebral vasospasm after SAH and implicate deoxyhemoglobin as a possible vasospastic agent.

Chronic cerebral vasospasm after large subarachnoid hemorrhage in monkeys

1982 ◽  
Vol 57 (2) ◽  
pp. 224-232 ◽  
Author(s):  
Francisco Espinosa ◽  
Bryce Weir ◽  
Donald Boisvert ◽  
Thomas Overton ◽  
William Castor
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Ct Scan ◽  
Cerebral Vasospasm ◽  
Time Course ◽  
Neurological Status ◽  
Clinical Situation ◽  
Content Type ◽  
Cranial Ct ◽  
Chronic Cerebral Vasospasm ◽  
Fine Print

✓ The authors have developed a model of chronic cerebral vasospasm analogous to the clinical situation, by inducing a large subarachnoid hemorrhage (SAH) in monkeys. With this model, the size of the SAH apparent on the first computerized tomography (CT) scan was correlated with the incidence and severity of cerebral vasospasm that developed. Indices monitored for up to 21 days after SAH included cranial CT scan, cerebral blood flow, vessel caliber, and neurological status. The 18 monkeys studied for 48 hours or more were divided into two groups according to the size of the SAH on CT scan. Vasospasm was more common in the group with large SAH. In this group, on Days 0, 7, and 14, the incidence of vasospasm was significantly higher than at other times (p < 0.001, p < 0.01, and p < 0.05, respectively), and the percentage reduction in vessel caliber was significantly greater than in the group with small/medium SAH (Day 7, p < 0.02; Days 0 and 14, p < 0.05). Delayed neurological deficit developed in two monkeys with large SAH. Apathy was noted from Day 17 to Day 21 in one, and unsteadiness and drowsiness were noted on Days 4 and 5 in the other. Overall, the incidence, degree, and time course of vasospasm reflected the size of the hemorrhage.

The effect of timing of clot removal on chronic vasospasm in a primate model

1987 ◽  
Vol 67 (4) ◽  
pp. 558-564 ◽  
Author(s):  
Yuji Handa ◽  
Bryce K. A. Weir ◽  
Michael Nosko ◽  
Russ Mosewich ◽  
Tsutomu Tsuji ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Blood Clot ◽  
Autologous Blood ◽  
Cerebral Arteries ◽  
Neurological Deficits ◽  
Physiological Status ◽  
Cerebral Vessel ◽  
Clot Removal ◽  
Chronic Cerebral Vasospasm

✓ The effect of complete clot removal at times from 48 to 96 hours after subarachnoid hemorrhage (SAH) on the development of chronic cerebral vasospasm was evaluated to determine whether there is a critical point after which clot removal is ineffective in preventing vasospasm. Thirty cynomolgus monkeys were randomized to one of five groups: sham-operated group, clot removal at 48 hours after SAH (48-hour group), clot removal at 72 hours after SAH (72-hour group), clot removal at 96 hours after SAH (96-hour group), and clot placement only (clot group). Standard microsurgical techniques were used to dissect bilaterally the major cerebral arteries free of arachnoid. An autologous blood clot averaging 4.2 gm was placed around the vessels in the subarachnoid space of the monkeys in the 48-hour, 72-hour, 96-hour, and clot groups. Physiological saline was instilled into the subarachnoid space of the sham-operated animals. Animals in the clot-removal groups underwent surgical clot removal at the determined times for each group. Two animals in each of the sham-operated and clot groups were subjected to reoperation at each of 48, 72, and 96 hours after SAH. The incisions were reopened and then simply reclosed. Neurological status, angiographic cerebral vessel caliber, and physiological status were evaluated before and 7 days after SAH induction. There were no significant neurological deficits in the sham-operated, 48-hour, or 72-hour groups. Two animals in each of the 96-hour and clot groups showed deterioration in level of consciousness developing on Day 4 or 5 after SAH induction. All the major cerebral arteries of the animals in the clot and 96-hour groups showed significant vasospasm (p < 0.01) on Day 7. Animals in the 72-hour group had significant vasospasm (p < 0.05) of the internal carotid and middle cerebral arteries but not the anterior cerebral arteries. There was no significant vasospasm (p > 0.05) in any of the cerebral arteries in the 48-hour group. Severity of vasospasm paralleled the duration of contact between the blood clot and the cerebral vessels. Evacuation of the subarachnoid hematoma later than 48 hours after SAH resulted in no significant reduction in the degree of chronic cerebral vasospasm. It is suggested that clot removal at early operation is likely to be useful only if it is performed within 48 hours of SAH.

scholarly journals Relationship Between Baroreflex and Cerebral Autoregulation in Patients With Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

2022 ◽  
Vol 12 ◽  
Author(s):  
Agnieszka Uryga ◽  
Nathalie Nasr ◽  
Magdalena Kasprowicz ◽  
Karol Budohoski ◽  
Marek Sykora ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Autoregulation ◽  
Cerebral Blood Flow Velocity ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Linear Regression Analysis ◽  
Inverse Correlation ◽  
Arterial Line ◽  
Arterial Blood ◽  
The Impact

Introduction: Common consequences following aneurysmal subarachnoid hemorrhage (aSAH) are cerebral vasospasm (CV), impaired cerebral autoregulation (CA), and disturbance in the autonomic nervous system, as indicated by lower baroreflex sensitivity (BRS). The compensatory interaction between BRS and CA has been shown in healthy volunteers and stable pathological conditions such as carotid atherosclerosis. The aim of this study was to investigate whether the inverse correlation between BRS and CA would be lost in patients after aSAH during vasospasm. A secondary objective was to analyze the time-trend of BRS after aSAH.Materials and Methods: Retrospective analysis of prospectively collected data was performed at the Neuro-Critical Care Unit of Addenbrooke's Hospital (Cambridge, UK) between June 2010 and January 2012. The cerebral blood flow velocity (CBFV) was measured in the middle cerebral artery using transcranial Doppler ultrasonography (TCD). The arterial blood pressure (ABP) was monitored invasively through an arterial line. CA was quantified by the correlation coefficient (Mxa) between slow oscillations in ABP and CBFV. BRS was calculated using the sequential cross-correlation method using the ABP signal.Results: A total of 73 patients with aSAH were included. The age [median (lower-upper quartile)] was 58 (50–67). WFNS scale was 2 (1–4) and the modified Fisher scale was 3 (1–3). In the total group, 31 patients (42%) had a CV and 42 (58%) had no CV. ABP and CBFV were higher in patients with CV during vasospasm compared to patients without CV (p = 0.001 and p &lt; 0.001). There was no significant correlation between Mxa and BRS in patients with CV, neither during nor before vasospasm. In patients without CV, a significant, although moderate correlation was found between BRS and Mxa (rS = 0.31; p = 0.040), with higher BRS being associated with worse CA. Multiple linear regression analysis showed a significant worsening of BRS after aSAH in patients with CV (Rp = −0.42; p &lt; 0.001).Conclusions: Inverse compensatory correlation between BRS and CA was lost in patients who developed CV after aSAH, both before and during vasospasm. The impact of these findings on the prognosis of aSAH should be investigated in larger studies.

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