Cerebral damage caused by interrupted, repeated arterial occlusion versus uninterrupted occlusion in a focal ischemic model

1994 ◽  
Vol 81 (4) ◽  
pp. 554-559 ◽  
Author(s):  
Gary K. Steinberg ◽  
Nariman Panahian ◽  
Go-Hua Sun ◽  
Carolina M. Maier ◽  
David Kunis
Keyword(s):  
Neuronal Damage ◽  
Rabbit Model ◽  
Total Duration ◽  
Arterial Occlusion ◽  
Focal Ischemia ◽  
Global Ischemia ◽  
Cerebral Injury ◽  
Content Type ◽  
Temporary Occlusion ◽  
Fine Print

✓ Temporary intracranial arterial occlusion is often utilized during the surgical treatment of intracranial aneurysms. Although numerous experimental studies have suggested that repetitive, brief periods of global ischemia cause more severe cerebral injury than a similar single period of global ischemia, this issue has not been extensively studied in relation to focal ischemia. It remains controversial whether it is safer to use brief periods of interrupted, temporary occlusion separated by reperfusion periods, or a more prolonged, single temporary occlusion. This question is addressed in studies on a rabbit model of transient, focal cerebral ischemia. Sixteen anesthetized rabbits underwent transorbital occlusion of the left internal carotid, middle cerebral, and anterior cerebral arteries, with one of two paradigms: uninterrupted occlusion (1 hour of temporary occlusion followed by 5 hours of reperfusion in eight rabbits), or interrupted occlusion (three separate 20-minute periods of occlusion, with 10 minutes of reperfusion between occlusions, followed by 4 hours, 40 minutes of reperfusion in eight rabbits). Histopathological evaluation for ischemic neuronal damage and magnetic resonance imaging studies for ischemic edema were conducted 6 hours after the initial arterial occlusion. The animals in the interrupted, repeated occlusion group showed a 59% decrease in the area of cortical ischemic neuronal damage (mean ± standard error of the mean 10.0% ± 1.7%) compared with the uninterrupted occlusion group (24.4% ± 5%, p = 0.016). There was no difference between the groups in the extent of striatal ischemic damage or area of ischemic edema. These results suggest that interrupted, repeated focal ischemia causes less cortical ischemic injury than uninterrupted transient ischemia of a similar total duration. Although caution should be exercised in extrapolating from these results to the clinical situation, they may have important implications for temporary arterial occlusion during intracranial surgery.

Cerebral protection by intermittent reperfusion during temporary focal ischemia in the rat

1996 ◽  
Vol 85 (5) ◽  
pp. 923-928 ◽  
Author(s):  
Carlos A. David ◽  
Ricardo Prado ◽  
W. Dalton Dietrich
Keyword(s):  
Arterial Occlusion ◽  
Focal Ischemia ◽  
Global Ischemia ◽  
Cerebral Injury ◽  
Histopathological Analysis ◽  
Content Type ◽  
Group I ◽  
Group Ii ◽  
Temporary Clipping ◽  
Fine Print

✓ Temporary arterial occlusion has been routinely used as an adjunct in intracranial aneurysm surgery. This has commonly been performed using a protocol of multiple short periods of occlusion alternating with periods of restoration of normal circulation. Recently, the logical basis of this method has come under scrutiny. There is extensive experimental evidence to suggest that repetitive, brief periods of global ischemia may cause more severe cerebral injury than an equivalent single period of global ischemia. Only recently has this issue begun to be addressed with regard to focal ischemia. Hence, despite the common use of temporary clipping, little experimental data are available regarding the ischemic consequences of temporary arterial occlusion with periods of reperfusion versus uninterrupted temporary occlusion. To investigate this issue, a protocol of occlusion/reperfusion that simulates the temporal profile that occurs during surgery was performed in a rat model of focal ischemia. Sixteen anesthetized Sprague—Dawley rats were divided into two groups. The animals in Group I underwent 60 minutes of uninterrupted middle cerebral artery occlusion and the animals in Group II were subjected to six separate 10-minute occlusion periods with 5 minutes of reperfusion between occlusions. Histopathological analysis was performed 72 hours postischemia. Group I had significantly increased mean infarction volumes (50.0 ± 12.1 mm3) compared to Group II (8.7 ± 3.1 mm3) (p = 0.008). Injuries in Group I occurred in both the cortex and striatum, whereas Group II showed only striatal injuries. Furthermore, the extent of the injuries in Group II was less severe, characterized by ischemic neuronal injury rather than frank infarction. The results indicate that intermittent reperfusion is neuroprotective during temporary focal ischemia and support the hypothesis that intermittent reperfusion is beneficial if temporary clipping is required during aneurysm repair.

Neuronal damage in gerbils caused by intermittent forebrain ischemia

1999 ◽  
Vol 91 (5) ◽  
pp. 835-842 ◽  
Author(s):  
Takatoshi Sorimachi ◽  
Hiroshi Abe ◽  
Shigekazu Takeuchi ◽  
Ryuichi Tanaka
Keyword(s):  
Neuronal Damage ◽  
Cerebral Arteries ◽  
Ischemic Insult ◽  
Content Type ◽  
Ischemic Episode ◽  
Temporary Occlusion ◽  
Ischemic Depolarization ◽  
The Brain ◽  
Severe Ischemia ◽  
Fine Print

Object. The purpose of this study was to investigate the possibility of preventing cumulative neuronal damage after repetitive severe ischemia.Methods. The authors monitored ischemic depolarization in the gerbil hippocampus, which has recently been shown to be a good experimental model of the effects of brief ischemia on the brain, and evaluated neuronal damage in the CA1 subregion 7 days after the ischemic insult. In a single-ischemia paradigm, the results indicate that induction of ischemia-induced neuronal damage depended on the duration of ischemic depolarization. Neuronal damage can be detected in the CA1 subregion after a period of depolarization lasting 210 seconds. Using a double-ischemia paradigm in which the animals were subjected to two periods of ischemia, there was apparently no accumulation of neuronal damage from the first ischemic episode to the second, provided the duration of the first period of ischemic depolarization did not exceed 90 seconds. Neuronal damage accumulated when the duration of the first ischemia episode exceeded 90 seconds, regardless of the duration of the reperfusion interval between the two ischemic insults. Finally, when the ischemic insult was spread over four separate episodes, each lasting 90 seconds (with a reperfusion interval of 5 minutes), neuronal damage was not found when the total depolarization period was less than 420 seconds.Conclusions. The authors conclude that cumulative neuronal damage may be avoided by adopting an intermittent ischemia approach. The implications of these results for human surgery requiring temporary occlusion of the cerebral arteries are discussed.

Temporary occlusion of the middle cerebral artery in intracranial aneurysm surgery: time limitation and advantage of brain protection

1997 ◽  
Vol 87 (6) ◽  
pp. 817-824 ◽  
Author(s):  
Sean D. Lavine ◽  
Lena S. Masri ◽  
Michael L. Levy ◽  
Steven L. Giannotta
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Arterial Occlusion ◽  
Brain Protection ◽  
Content Type ◽  
Multiple Aneurysms ◽  
Temporary Occlusion ◽  
The Mean ◽  
Mca Aneurysm ◽  
Fine Print

✓ The risk of focal infarction secondary to the induced reversible arrest of local arterial flow during microsurgical dissection of middle cerebral artery (MCA) aneurysms was evaluated further to define the optimal approach to temporary arterial occlusion. To compare the effectiveness of potential brain-protection anesthetics, a group of patients treated with the intravenous agents propofol, etomidate, and pentobarbital, administered individually or in combination, was compared to a group treated with the inhalational agent isoflurane. Forty-nine consecutive MCA aneurysm surgeries involving the temporary clipping of the parent vessel were retrospectively reviewed. Thirty-eight patients received intravenous brain-protection (IVBP) anesthesia. Groups of patients with and without infarctions, and receiving and not receiving IVBP anesthesia, were compared based on the duration and nature of temporary arterial occlusion. Postoperative radiographic evidence of new infarction was used as the threshold for failure of occlusion tolerance. The overall infarction rate was 22.4% (11 of 49 patients), including 15.8% (six of 38 patients) in the IVBP group versus 45.5% (five of 11 patients) in the group that did not receive brain protection (NBP). In the NBP group, the mean duration of temporary occlusion was 3.9 ± 2.2 minutes for patients without infarction versus 12.2 ± 4.3 minutes for patients with focal infarction (p < 0.01). In contrast, the mean duration was 13.6 ± 10.6 minutes for patients without infarction and 18.5 ± 9.9 minutes for patients with infarction in the IVBP group. All patients (four of four) in the NBP group who underwent occlusion lasting 10 minutes or longer suffered an infarction versus five of 23 patients in the IVBP group (p < 0.0001). Patients with multiple aneurysms were found to be at increased risk of developing focal infarction, whereas those treated with intermittent temporary clip application were at decreased risk. It is concluded that patients in whom focal iatrogenic ischemia is induced during MCA aneurysm clip ligation have a significant advantage compared with those receiving isoflurane when they are given pentobarbital as the primary neuroprotective agent or when they receive propofol or etomidate titrated to achieve electroencephalographic burst suppression, particularly if more than 10 minutes of occlusion time is required. It is also concluded that 10 minutes is a general guideline for safe, temporary occlusion of the MCA. The use of intermittent temporary arterial occlusion and its use in patients with multiple aneurysms need further evaluation before specific recommendations can be made.

Activation of complement by tissue plasminogen activator, but not acute cerebral ischemia, in a rabbit model of thromboembolic stroke

1997 ◽  
Vol 86 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Martin M. Bednar ◽  
Cordell E. Gross ◽  
Sheila R. Russell ◽  
David Short ◽  
Patricia C. Giclas
Keyword(s):  
Cerebral Ischemia ◽  
Plasminogen Activator ◽  
Complement Activation ◽  
Rabbit Model ◽  
Thromboembolic Stroke ◽  
Content Type ◽  
Acute Cerebral Ischemia ◽  
Tissue Plasminogen ◽  
Before And After ◽  
Fine Print

✓ Although complement activation is associated with tissue injury during inflammatory and ischemic states, complement activation in states of acute cerebral ischemia before and after administration of tissue plasminogen activator (TPA) has not yet been examined and is the focus of this investigation. Twenty-four New Zealand White rabbits weighing 3 to 3.5 kg were used for this study. Of these, 20 were subjected to intracranial autologous clot embolization via the internal carotid artery. Three hours postembolization, rabbits received an intravenous infusion of TPA (6.3 mg/kg, 20% bolus with the remainder infused over a 2-hour interval; 12 animals) or vehicle (eight animals). All animals were observed for a total of 7 or 8 hours postembolization. These two groups were compared to a cohort undergoing sham operation with subsequent TPA infusion (four animals). Plasma samples to quantify complement component C5 hemolytic activity (C5H5O) were obtained at the following time points: 30 minutes before and after clot embolization; 1 hour before and 1 hour after the initiation of therapy with TPA or vehicle and at the completion of the protocol; 7 to 8 hours after clot embolization. The C5 activation was not detected as the result of acute cerebral ischemia. However, animals receiving TPA with or without concomitant clot embolization exhibited C5 activation as assessed by a reduction in C5 hemolytic function, both 1 hour after initiation of TPA infusion (78.7 ± 10.3% and 77.5 ± 9.9% of baseline value, respectively; mean ± standard error of the mean [SEM]) and at the end of the protocol, 2 hours after the completion of the TPA infusion (72.5 ± 8.8% and 53.3 ± 8.1%, respectively; mean ± SEM, p < 0.05, each group). This study supports the conclusion that TPA, but not acute cerebral ischemia, may activate the complement cascade in this rabbit model of thromboembolic stroke.

Upper basilar artery aneurysms: oculomotor outcomes in 163 cases

2005 ◽  
Vol 102 (3) ◽  
pp. 482-488 ◽  
Author(s):  
Hisham Al-Khayat ◽  
Haitham Al-Khayat ◽  
Jonathan White ◽  
David Manner ◽  
Duke Samson
Keyword(s):  
Basilar Artery ◽  
Nerve Palsy ◽  
Arterial Occlusion ◽  
Oculomotor Nerve ◽  
Oculomotor Nerve Palsy ◽  
Stepwise Logistic Regression ◽  
Categorical Data Analysis ◽  
Content Type ◽  
History Of ◽  
Fine Print

Object. The purpose of this study was to identify factors predictive of postoperative oculomotor nerve palsy among patients who undergo surgery for distal basilar artery (BA) aneurysms. The data can be used to estimate preoperative risk in this population. The natural history of oculomotor nerve palsy in patients with good outcomes is also defined. Methods. The cases of 163 patients with distal BA aneurysms, who were treated surgically between 1996 and 2002, were retrospectively studied to identify factors contributing to oculomotor nerve palsy. After the data had been collected, stepwise logistic regression procedures were used to determine the predictive effects of each variable on the development of oculomotor nerve palsy and to create a scoring system. Factors that interfered with resolution of oculomotor dysfunction in patients with good outcomes were also studied. Postoperative oculomotor nerve palsy occurred in 86 patients (52.8%) with distal BA aneurysms. The following factors were associated with postoperative oculomotor dysfunction, as determined by a categorical data analysis: 1) younger patient age (p < 0.001); 2) poor admission Hunt and Hess grade (p < 0.001); 3) use of temporary arterial occlusion (p < 0.001); 4) poor Glasgow Outcome Scale score (p < 0.001); and 5) the presence of a BA apex aneurysm that projected posteriorly (p < 0.001). For patients with good outcomes, postoperative oculomotor nerve palsy resolved completely within 3 months in 31 patients (52%) and within 6 months in 47 patients (80%). The projection of the BA aneurysm was associated with incomplete oculomotor recovery at 6 months postoperatively (p = 0.019). Conclusions. The results of this study can help identify patients with a high risk for the development of oculomotor nerve palsy. This may help neurosurgeons in preoperative planning and discussions.

Cerebral oxygen and microdialysis monitoring during aneurysm surgery: effects of blood pressure, cerebrospinal fluid drainage, and temporary clipping on infarction

2002 ◽  
Vol 96 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Rupert Kett-White ◽  
Peter J. Hutchinson ◽  
Pippa G. Al-Rawi ◽  
Marek Czosnyka ◽  
Arun K. Gupta ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Total Duration ◽  
Wilcoxon Test ◽  
Fisher Exact Test ◽  
Content Type ◽  
The Impact ◽  
Temporary Clipping ◽  
Fine Print

Object. The aim of this study was to investigate potential episodes of cerebral ischemia during surgery for large and complicated aneurysms, by examining the effects of arterial temporary clipping and the impact of confounding variables such as blood pressure and cerebrospinal fluid (CSF) drainage. Methods. Brain tissue PO2, PCO2, and pH, as well as temperature and extracellular glucose, lactate, pyruvate, and glutamate were monitored in 46 patients by using multiparameter sensors and microdialysis. Baseline data showed that brain tissue PO2 decreased significantly, below a mean arterial pressure (MAP) threshold of 70 mm Hg. Further evidence of its relationship with cerebral perfusion pressure was shown by an increase in mean brain tissue PO2 after drainage of CSF from the basal cisterns (Wilcoxon test, p < 0.01). Temporary clipping was required in 31 patients, with a mean total duration of 14 minutes (range 3–52 minutes), causing brain tissue PO2 to decrease and brain tissue PCO2 to increase (Wilcoxon test, p < 0.01). In patients in whom no subsequent infarction developed in the monitored region, brain tissue PO2 fell to 11 mm Hg (95% confidence interval 8–14 mm Hg). A brain tissue PO2 level below 8 mm Hg for 30 minutes was associated with infarction in any region (p < 0.05 according to the Fisher exact test); other parameters were not predictive of infarction. Intermittent occlusions of less than 30 minutes in total had little effect on extracellular chemistry. Large glutamate increases were only seen in two patients, in both of whom brain tissue PO2 during occlusion was continuously lower than 8 mm Hg for longer than 38 minutes. Conclusions. The brain tissue PO2 decreases with hypotension, and, when it is below 8 mm Hg for longer than 30 minutes during temporary clipping, it is associated with increasing extracellular glutamate levels and cerebral infarction.

Selection and combination of various endovascular techniques in the treatment of giant aneurysms

1992 ◽  
Vol 77 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Waro Taki ◽  
Shogo Nishi ◽  
Kohsuke Yamashita ◽  
Akiyo Sadatoh ◽  
Ichiro Nakahara ◽  
...  
Keyword(s):  
Arterial Occlusion ◽  
The Other ◽  
Parent Artery ◽  
Endovascular Techniques ◽  
Detachable Balloon ◽  
Content Type ◽  
Ethylene Vinyl Alcohol ◽  
Complete Occlusion ◽  
Giant Aneurysms ◽  
Fine Print

✓ Between April, 1989, and January, 1991, a total of 19 cases of giant aneurysm were treated by the endovascular approach. The patients included seven males and 12 females aged 15 to 72 years. Detachable balloons, occlusion coils, and ethylene vinyl alcohol copolymer liquid were used as embolic materials. In seven cases, thrombosis of the aneurysmal sac and/or base was achieved while sparing the parent arterial flow; complete obliteration of the aneurysm was achieved in four of these. Of these four patients, the thrombotic material was a detachable balloon in two, a combination of a detachable balloon and coils in one, and occlusion liquid in one. In the other three cases, complete occlusion was not achieved; one aneurysm was occluded with a detachable balloon and two with coils. In 11 patients, the parent artery was occluded either by trapping or by proximal arterial occlusion, and all patients showed complete occlusion of the aneurysms. In one patient, a combined bypass procedure and parent artery occlusion was performed. Among the 19 cases in this series there were four transient ischemic attacks, one reversible ischemic neurological deficit, and one death due to aneurysmal rupture during the procedure. Two patients died in the follow-up period, one from pneumonia 2 months postoperatively and the other from acute cardiac failure 2 weeks following surgery. Both deaths were unrelated to the endovascular procedure. It is concluded that the endovascular treatment of giant aneurysms remains difficult because of the large and irregular shape of the aneurysmal base and thrombus in the aneurysmal sac. The proper selection and combination of the available endovascular techniques is therefore of critical importance.

Suppression of secondary generalization of limbic seizures by stimulation of subthalamic nucleus in rats

2005 ◽  
Vol 102 (6) ◽  
pp. 1122-1129 ◽  
Author(s):  
Naotaka Usui ◽  
Satoshi Maesawa ◽  
Yasukazu Kajita ◽  
Otone Endo ◽  
Shigenori Takebayashi ◽  
...  
Keyword(s):  
Subthalamic Nucleus ◽  
Total Duration ◽  
Control Group ◽  
Limbic Seizures ◽  
Content Type ◽  
Focal Seizures ◽  
Stn Dbs ◽  
Fine Print ◽  
Secondary Generalization ◽  
Stimulation Of

Object. Deep brain stimulation (DBS) of subcortical nuclei such as the subthalamic nucleus (STN) or the substantia nigra pars reticulata (SNR) may provide an alternative therapy for intractable epilepsy. The authors attempted to evaluate the antiepileptic effects of DBS to these structures in an experimental seizure model. Methods. Three groups of rats were prepared. In the first two groups, the rats underwent unilateral implantation of stimulation electrodes in the STN (six rats) or the SNR (six rats). A control group received no electrodes (six rats). Kainic acid (KA) was systemically administered to induce limbic seizures, which started with focal seizures and became generalized secondarily. High-frequency electrical stimulation of the STN or SNR was begun immediately after KA administration, and changes on electroencephalography (EEG) and the magnitude of clinical seizures were evaluated. Results showed that STN stimulation significantly reduced the duration of generalized seizures on EEG, although the total duration of seizures (generalized plus focal seizures) was unchanged. The duration of focal seizures on EEG was prolonged by STN DBS, a result possibly due to the suppression of secondary generalization. In addition, STN DBS reduced the severity of clinical seizures. On the other hand, stimulation of the SNR demonstrated no effect. Conclusions. Unilateral STN DBS showed significant suppression of the secondary generalization of limbic seizures. Note, however, that SNR DBS was less effective, which implies that in addition to the nigral control of the epilepsy system, another antiepileptic mechanism such as antidromic stimulation of the corticosubthalamic pathway should be considered.

Barbiturate protection against hypoxic neuronal damage in vitro

1986 ◽  
Vol 65 (2) ◽  
pp. 230-232 ◽  
Author(s):  
Peter G. Aitken ◽  
Steven J. Schiff
Keyword(s):  
Neuronal Damage ◽  
Pyramidal Cells ◽  
Perfusion Medium ◽  
Tissue Slices ◽  
Content Type ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Tissue ◽  
Barbiturate Protection ◽  
Fine Print

✓ Hippocampal tissue slices in vitro were exposed to periods of hypoxia of different durations. Addition of pentobarbital to the perfusion medium significantly increased the duration of hypoxia that was survived by CA1 pyramidal cells.

Platelet-activating factor and progressive brain damage following focal brain injury

1990 ◽  
Vol 73 (2) ◽  
pp. 223-233 ◽  
Author(s):  
Kai U. Frerichs ◽  
Perttu J. Lindsberg ◽  
John M. Hallenbeck ◽  
Giora Z. Feuerstein
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Neuronal Death ◽  
Hippocampal Neurons ◽  
Neuronal Damage ◽  
Platelet Activating Factor ◽  
Secondary Brain Damage ◽  
Content Type ◽  
Focal Brain Injury ◽  
Fine Print

✓ The effects of a platelet-activating factor (PAF) antagonist on brain edema, cortical microcirculation, blood-brain barrier (BBB) disruption, and neuronal death following focal brain injury are reported. A neodymium:yttrium-aluminum-garnet (Nd:YAG) laser was used to induce highly reproducible focal cortical lesions in anesthetized rats. Secondary brain damage in this model was characterized by progressive cortical hypoperfusion, edema, and BBB disruption in the vicinity of the hemispheroid lesion occurring acutely after injury. The histopathological evolution was followed for up to 4 days. Neuronal damage in the cortex and the hippocampus (CA-1) was assessed quantitatively, revealing secondary and progressive loss of neuronal tissue within the first 24 hours following injury. Pretreatment with the PAF antagonist BN 50739 ameliorated the severe hypoperfusion in 12 rats (increasing local cerebral blood flow from a mean ± standard error of the mean of 40.5% ± 8.3% to 80.2% ± 7.8%, p < 0.01) and reduced edema by 70% in 10 rats (p < 0.05) acutely after injury. The PAF antagonist also reduced the progression of neuronal damage in the cortex and the CA-1 hippocampal neurons (decrease of neuronal death from 88.0% ± 3.9% to 49.8% ± 4.2% at 24 hours in the cortex and from 40.2 ± 5.0% to 13.2% ± 2.1% in the hippocampus in 30 rats; p < 0.05). This study provides evidence to support progressive brain damage following focal brain injury, associated with secondary loss of neuronal cells. In this latter process, PAF antagonists may provide significant therapeutic protection in arresting secondary brain damage following cerebral ischemia and neurological trauma.

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