A New Model for Chronic Reversible Cerebral Ischemia

Spetzler, Robert F.; Selman, Warre N R.; Weinstein, Philip; Townsend, Jeannette J.; Mehdorn, H. Maximilian; Telles, D.

doi:10.1007/978-1-4612-6090-5_5

Cited by 4 publications

(2 citation statements)

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“…128 In 1976, at the request of Dr. R. F. Spetzler, I summa rized in a letter my personal experience in microneuro surgery, which was later published in the 1985 monograph Cerebral Revascularization for Stroke. 95 This monograph consists of 618 pages, with 82 original articles related to a conference in Phoenix. In my previously mentioned let ter, which was used as the monograph's forward, I gave an account of my experiences in microsurgery, with some indications of my specific interest and future program in the field of microneurosurgery.…”

Section: Conferences For Microsurgery and Microneurosurgerymentioning

confidence: 99%

Editorial

Mg¹

2010

JNS

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Section: Conferences For Microsurgery and Microneurosurgerymentioning

confidence: 99%

Editorial

Mg¹

2010

JNS

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“…General anesthesia and controlled ventilation might have had a protective effect, and ischemia might have been aggravated by vasospasm after vascular dissection and clipping. 1 In this study, we used a modified version of an implantable occluder system previously tested in baboons 6 to perform temporary MCA occlusion followed by reperfusion in unanesthetized cats. We then correlated the severity of neurological deficit during and after occlusion with infarct size and the occurrence of hemorrhage.…”

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Neurological deficit and cerebral infarction after temporary middle cerebral artery occlusion in unanesthetized cats.

Weinstein¹,

Anderson²,

Telles³

1986

Stroke

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SUMMARY Forty-four unanesthetized cats underwent temporary middle cerebral artery (MCA) occlusion with an implanted, externally controlled balloon cuff occluder. The occlusion was reversed to allow reperfusion of the MCA after 2 min to 24 hr of ischemia. Fourteen cats had temporary occlusions lasting 2 mln to 3 hr; their neurological deficits improved or resolved after reperfusion, and brain sections showed only scattered microscopic areas of necrosis. After a 4-hr occlusion, five of nine cats (55%) recovered completely within 24 hr; two had persistent deficit when sacrificed, 10 days later, and each had a circumscribed infarct. All 18 cats undergoing 5-, 6-, 8-, and 24-hr occlusions sustained permanent neurological deficits. Three 3-hr occlusions at 2-day intervals in three cats resulted in permanent deficits and infarcts that were 25% larger than those after single 8-hr occlusions. Ten cats underwent permanent MCA occlusion; three deteriorated neurologically and died, and the survivors showed no improvement. Infarcts after 5-, 6-, and 8-hr occlusions followed by reperfusion were 66% smaller (p < 0.05) than those after permanent occlusion; reperfusion after 24 hr of occlusion did not reduce infarct size. Hemorrhagic infarction occurred after two permanent occlusions, but after only one 5-hr temporary occlusion. The results obtained with this method of temporary regional ischemia indicate that restoration of flow after 1-8 hr, but not after 24 hr, of MCA occlusion resulted in less severe neurological deficit and smaller infarcts than did permanent occlusion. The Infarct size correlated with the duration of MCA occlusion (p < 0.05) rather than with the degree of deficit during occlusion. Stroke Vol 17, No 2, 1986 ALTHOUGH the degree and duration of blood flow reduction have been related to the occurrence of neuronal damage, 5 it is not known how soon after the onset of neurological deficit resuscitation of ischemic brain by reperfusion becomes impossible.l3 Studies of blood flow restoration after regional cerebral ischemia is induced by temporary clipping of the middle cerebral artery (MCA) in cats and monkeys have shown that the mortality rate is lower, the neurological deficit less severe, and infarct size smaller after 6-hr occlusion than after permanent ligation, despite the occurrence of hyperemia and edema following reperfusion, 12Those experiments, however, were done immediately after surgical exposure of the MCA in anesthetized animals. General anesthesia and controlled ventilation might have had a protective effect, and ischemia might have been aggravated by vasospasm after vascular dissection and clipping. 1In this study, we used a modified version of an implantable occluder system previously tested in baboons 6 to perform temporary MCA occlusion followed by reperfusion in unanesthetized cats. We then correlated the severity of neurological deficit during and after occlusion with infarct size and the occurrence of hemorrhage. Because the cats remained conscious, neurological function was not influenc...

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Naloxone therapy during focal cerebral ischemia evaluation in a primate model.

Zabramski¹,

Spetzler²,

Selman³

et al. 1984

Stroke

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Conflicting reports have appeared in the literature regarding the effect of the opiate antagonist naloxone on ischemic neurologic deficits. We report the results of a study using naloxone in our model of focal cerebral ischemia in the awake primate. A total of 14 adult baboons were subjected to six-hour occlusion of the left middle cerebral artery (MCA). Seven animals served as controls and seven received treatment with naloxone (5 mg/kg) beginning 30 min after MCA occlusion and continuing until two hours after reperfusion. All animals developed profound hemiparesis and homonymous hemianopsia within seconds of inflating the MCA occluder. Acutely, therapy with naloxone partially reversed ischemic neurologic deficits in five of the seven treatment animals. Within minutes of receiving the loading dose of naloxone, responding animals were more alert and demonstrated improvements in motor function. Naloxone did not affect mortality: Three animals in the treatment group and two in the naloxone group died secondary to malignant intracranial pressure within 48 hours of the ischemic episode. In animals surviving the ischemic insult however, treatment with naloxone significantly improved neurologic outcome at 10 days (p less than 0.05). Neuropathologic examinations in these animals revealed amelioration of ischemic tissue damage, with three of the five suffering only small focal areas of infarction. (All control animals suffered large infarcts of the MCA territory.) Our results verify that naloxone can reverse ischemic deficits, and more importantly may improve the outcome from focal ischemic insults.

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A New Model for Chronic Reversible Cerebral Ischemia

Cited by 4 publications

References 9 publications

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Neurological deficit and cerebral infarction after temporary middle cerebral artery occlusion in unanesthetized cats.

Naloxone therapy during focal cerebral ischemia evaluation in a primate model.

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