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.

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.

Nimodipine and Chronic Vasospasm in Monkeys: Part 1 Clinical and Radiological Findings

Neurosurgery ◽  
1985 ◽  
Vol 16 (2) ◽  
pp. 129-136 ◽  
Author(s):  
Michael Nosko ◽  
Bryce Weir ◽  
Christel Krueger ◽  
David Cook ◽  
Susan Norris ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Neurological Status ◽  
Neurological Deficits ◽  
High Dose ◽  
Primate Model ◽  
Cerebral Vessel ◽  
Significant Difference ◽  
Before And After ◽  
The Right ◽  
Chronic Cerebral Vasospasm

Abstract The efficacy of the calcium channel blocker nimodipine in the prevention of chronic cerebral vasospasm (VSP) and delayed ischemia after subarachnoid hemorrhage (SAH) in monkeys was examined in a blind, randomized, placebocontrolled trial. The primate model developed in this laboratory reliably induces chronic cerebral vasospasm and can induce pathologically proven delayed ischemic neurological deficits (DINDs). With standard microsurgical procedures, an average 6.4-ml autologous hematoma was placed directly against the major anterior cerebral vessels in the right basal subarachnoid spaces of 24 monkeys. The monkeys were randomized to one of four groups and were treated orally q8h for 7 days with nimodipine (3, 6, or 12mg/kg) or placebo. An additional 2 monkeys underwent the surgical procedure without clot placement. Drug administration began between 14 and 20 hours after clot placement. Indices monitored before and after SAH included neurological status, angiographic cerebral vessel caliber, and cerebral blood flow. Significant VSP (25 to 100% reduction in vessel caliber) was present on Day 7 on the clot side in 83% of the animals (P ≤ 0.001). There was no significant difference (P &gt; 0.05) in the incidence of VSP among the four groups. Similarly, there was no significant difference (P &gt; 0.05) in the mean vessel caliber reduction after SAH among the four treatment groups. There was no VSP present on Day 7 in the sham-operated animals. One animal receiving high dose nimodipine (12 mg/kg p.o. q8h) developed a DIND on Day 5 after SAH. A second animal in the 12-mg/kg group developed a transient neurological deficit between Days 4 and 7.

Effect of diltiazem on experimental chronic cerebral vasospasm in the monkey

1985 ◽  
Vol 62 (6) ◽  
pp. 912-917 ◽  
Author(s):  
John G. Frazee ◽  
John A. Bevan ◽  
Rosemary D. Bevan ◽  
K. Roy Jones
Keyword(s):  
Cerebral Vasospasm ◽  
Neurological Deficit ◽  
Cerebral Arteries ◽  
Treated Group ◽  
Neurological Deficits ◽  
Primate Model ◽  
Content Type ◽  
Mean Diameter ◽  
The Mean ◽  
Chronic Cerebral Vasospasm

✓ The influence of diltiazem on chronic cerebral vasospasm was studied following subarachnoid hemorrhage (SAH) in a primate model. The model mimics the human experience including the production of neurological deficits. Six monkeys were pretreated with diltiazem (25 mg/kg twice daily) for 2 days prior to surgical production of an SAH and for 5 days after the hemorrhage. This group was compared with six untreated monkeys that also sustained an SAH. The mean diameter of cerebral arteries measured at six angiographic sites was 60.6% of the pre-SAH diameter for the untreated group and 99.7% for the diltiazem-treated group. These values are significantly different (p < 0.0005). There was no neurological deficit in the pretreated animals. The mean diameter of the “most constricted vessel” in each experiment was 22% of the prehemorrhage diameter for the untreated and 84% for the treated group (p < 0.0005). Arterial pressure was unaffected by the dosage regimen. These experiments with this primate model of chronic cerebral vasospasm demonstrate that vascular narrowing and neurological deficit can be markedly attenuated by diltiazem pretreatment.

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.

scholarly journals The Role of Nitric Oxide in Resolution of Vasospasam Corresponding with Cerebral Vasospasms after Subarachnoid Haemorrhage: Animal Model

2008 ◽  
Vol 8 (2) ◽  
pp. 177-182
Author(s):  
Kemal Dizdarević
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Subarachnoid Haemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Control Group ◽  
Blood Products

Intracranial aneurysmal rupture is the common cause of spontaneous subarachnoid haemorrhage (SAH). This haemorrhage is typically diffuse and located in extracerebral subarachnoid space in which main cerebral arterial branches are situated. The intimate and long-term contact of arterial wall and blood products in the closed space causes the cerebral vasospasm as a serious and frequent complication of SAH. It is connected with significant morbidity and mortality due to developing of focal cerebral ischaemia and subsequently cerebral infarction. The aim of our experimental research was to create the animal model of vasospasm using the femoral artery due to examination of reduced basic dilator activity cause in arterial wall after SAH. The important characteristic of major cerebral arteries is their localization in the closed subarachnoid space which enables their to have long-term contact with blood products after haemorrhage. Thirty six femoral arteries (FA) of eighteen female rats weighing about 300 g were used. In vivo, femoral arteries are microsurgically prepared in both inguinal regions in all rats. Eighteen arteries were encompassed by polytetrafluoroethylene (PTFE) material forming closed tube and autologous blood was injected in the tube around the arterial wall. Additional eighteen arteries, as a control group, were also put in PTFE tube but without exposing to the blood. All rats are left to live for eight days. Afterwards, rats were sacrificed and their arteries were in vitro examined including an isometric tension measurement and histological changes analysis. The tension was measured during application of vasoconstrictors and vasodilatators (nitric oxide, NO). FA exposed to periadventitial blood exhibit hyper reactivity to constrictors (KCl, phenylephrine, acetylcholine) compared to control group. It was also found that NO donor (sodium nitroprusside) diminished arterial spasm induced by blood and vasoconstrictors. In conclusion, FA can be used as a model for vasospasm correlating with cerebral vasospasm after SAH and therefore this model can be utilized in future experiments assessing cerebral vasospasm. The reduced basic dilator activity of spastic femoral artery is caused by an absence of gaseous messenger NO next to the arteries but not by diminished response vasculature to NO. Absence of NO after SAH probably causes the reduced basic dilator activity of cerebral arteries as well. The guanylate-cyclase level in the arterial wall is consequently reduced after SAH primary due to absence of NO but not due to direct reduction of enzyme activities caused by process of blood degradation inside of subarachnoid space.

Cerebral vasospasm: contractile activity of hemoglobin in isolated canine basilar arteries

1980 ◽  
Vol 53 (6) ◽  
pp. 787-793 ◽  
Author(s):  
Takeo Tanishima
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Contractile Activity ◽  
Cerebral Arteries ◽  
Adenosine Monophosphate ◽  
Active Species ◽  
Exchange Chromatography ◽  
Basilar Arteries ◽  
Chronic Cerebral Vasospasm

✓ Recent studies suggest the possible role of the red blood cell (RBC) in causing chronic cerebral vasospasm. However, the basic action of hemoglobin (Hb), the major component of the RBC, on cerebral arteries remains unknown. The present study was undertaken to analyze the contractile effects of human Hb (purified by ion-exchange chromatography) on canine arteries in vitro. The contractile activity of lysed RBC was shown to be derived from Hb. Hemoglobin in oxygenated form (oxyHb) caused a maximum contraction equal to about 70% of that induced by serotonin in the basilar artery. Ferrous Hb's (oxyHb and carboxyHb) produced much greater contraction than ferric Hb's (methemoglobin and cyanmethemoglobin), suggesting that superoxide radicals, an active species of oxygen, may be related to the contractile activity of Hb. Neither methysergide, phentolamine, mepyramine, nor aspirin inhibited the vasoconstrictive activity of oxyHb. This finding indicates that the activation of serotonergic, alpha-adrenergic, or histaminergic H1 receptors, or prostaglandin synthesis may not be involved in the mechanism of action of oxyHb. The constituents of Hb caused little or no contraction as compared with Hb as a whole. The basilar artery was more highly sensitive to Hb than arteries from other anatomical locations. Cyclic adenosine monophosphate caused a very slight decrease in the Hb-induced contraction. It is concluded that oxyHb can contract cerebral arteries in vitro. These results, coupled with recent reports on the participation of the RBC in producing chronic vasospasm, strongly suggest that oxyHb released from RBC's plays an important role in the pathogenesis of chronic cerebral vasospasm.

Pharmacological alterations after clot removal in monkey chronic cerebral vasospasm

1995 ◽  
Vol 2 (4) ◽  
pp. 333-338
Author(s):  
Tsutomu Tsuji ◽  
David A Cook ◽  
Bryce K.A Weir ◽  
Yuji Handa
Keyword(s):  
Cerebral Vasospasm ◽  
Clot Removal ◽  
Chronic Cerebral Vasospasm

Blood Component Induction of Cerebral Vasospasm

Neurosurgery ◽  
1990 ◽  
Vol 27 (2) ◽  
pp. 252-256 ◽  
Author(s):  
Tsutomu Harada ◽  
Yoshio Suzuki ◽  
Shin-ichi Satoh ◽  
Ichiro Ikegaki ◽  
Toshio Asano ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Whole Blood ◽  
Subarachnoid Space ◽  
Platelet Rich Plasma ◽  
Blood Clot ◽  
Clot Formation ◽  
Blood Component ◽  
Dependent Manner ◽  
Blood Components ◽  
Chronic Vasospasm

Abstract The role of blood components in cerebral vasospasm was evaluated using an in vivo canine model. An intracisternal injection of 5 ml of washed red blood cells (RBCs) and platelet-rich plasma (PRP) resulted in acute vasospasm of the basilar artery as seen by angiography. This was comparable with the degree of vasospasm induced by an injection of the same amount of whole blood. Repeated injections of blood components or whole blood on Days 1 and 3 induced chronic vasospasm. as shown by angiography on Day 7. Results clearly indicate that chronic vasospasm was produced by RBCs and PRP. and it was in a dose-dependent manner with increasing concentrations of RBCs (hematocrit: 30, 50. and 70%). The vasospasm induced by both components closely reproduced that seen with whole blood. Neither acute nor chronic vasospasm induced by blood component injection was associated with clot formation in the subarachnoid space, as confirmed by an autopsy. These results suggest that the extravasation of RBCs and PRP into the subarachnoid space produces cerebral vasospasm by mechanisms independent of blood clot formation.

Intracarotid slow bolus injection of nimodipine during angiography for treatment of cerebral vasospasm after SAH

1984 ◽  
Vol 61 (2) ◽  
pp. 231-240 ◽  
Author(s):  
J. Andre Grotenhuis ◽  
Winfried Bettag ◽  
B. J. Othmar Fiebach ◽  
Khosrow Dabir
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Calcium Antagonist ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Bolus Injection ◽  
Neurological Deficits ◽  
Cerebral Vessel ◽  
Content Type ◽  
Venous Infusion ◽  
Fine Print

✓ Nimodipine was given as an intracarotid slow bolus injection in six patients with subarachnoid hemorrhage (SAH) due to rupture of a cerebral aneurysm, with angiographically demonstrated vasospasm. The patients were followed by serial angiograms for demonstration of the effect of nimodipine on vasospasm. After angiography, all patients were treated with a constant venous infusion of this new calcium antagonist. Although the therapeutic regimen was started only a few hours after onset of vasospasm, there was no change in cerebral vessel caliber detectable on angiograms following the intracarotid injection. Three patients died, two patients finally recovered with neurological deficits due to cerebral ischemia, and one patient with asymptomatic vasospasm remained symptom-free. Although nimodipine may act to prevent cerebral vasospasm after SAH, the authors believe that the intracarotid application is not effective after vasospasm has occurred.

scholarly journals Cerebral Vasospasm: A Review

2015 ◽  
Vol 43 (1) ◽  
pp. 15-32 ◽  
Author(s):  
J. Max Findlay ◽  
Joshua Nisar ◽  
Tim Darsaut
Keyword(s):  
Cerebral Vasospasm ◽  
Blood Clot ◽  
Cerebral Arteries ◽  
Aneurysm Rupture ◽  
Best Management ◽  
Randomized Controlled ◽  
Complex Interactions ◽  
Patient Morbidity ◽  
Improve Patient ◽  
Potential Opportunity

AbstractCerebral vasospasm is a prolonged but reversible narrowing of cerebral arteries beginning days after subarachnoid hemorrhage. Progression to cerebral ischemia is tied mostly to vasospasm severity, and its pathogenesis lies in artery encasement by blood clot, although the complex interactions between hematoma and surrounding structures are not fully understood. The delayed onset of vasospasm provides a potential opportunity for its prevention. It is disappointing that recent randomized, controlled trials did not demonstrate that the endothelin antagonist clazosentan, the cholesterol-lowering agent simvastatin, and the vasodilator magnesium sulfate improve patient outcome. Minimizing ischemia by avoiding inadequate blood volume and pressure, administering the calcium antagonist nimodipine, and intervention with balloon angioplasty, when necessary, constitutes current best management. Over the past two decades, our ability to manage vasospasm has led to a significant decline in patient morbidity and mortality from vasospasm, yet it still remains an important determinant of outcome after aneurysm rupture.

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