The role of the prostacyclin-thromboxane system in cerebral vasospasm following induced subarachnoid hemorrhage in the rabbit

Chan, Richard C.; Durity, Felix; Thompson, Gordon; Nugent, Robert A.; Kendall, Marie

doi:10.3171/jns.1984.61.6.1120

Cited by 86 publications

(24 citation statements)

References 39 publications

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“…> 22 In my study, however, the level of PGF 2a , a classical cerebrovascular contractile agonist, did not increase after subarachnoid hemorrhage. Furthermore, TxB 2 , the stable metabolite of another contractile agent, although elevated in untreated compared with treated dogs, was found to be negatively correlated with the degree of angiographic vasospasm.…”

Section: Discussionmentioning

confidence: 83%

Prevention of chronic cerebral vasospasm in dogs with ibuprofen and high-dose methylprednisolone.

Chyatte

1989

Stroke

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Severe chronic cerebral vasospasm was produced in dog basilar arteries by two injections, 2 days apart, of autologous blood into the cisterna magna of 25 dogs. Treatment with ibuprofen (ra=8) or high-dose methylprednisolone (n=8) after the first injection of blood prevented or reduced angiographic vasospasm. Cerebrospinal fluid concentrations of prostaglandin E 2 , prostaglandin F 2a , 6-ketoprostaglandin F l a (a metabolite of prostacyclin), and thromboxane B 2 (a metabolite of thromboxane A 2 ) were measured in both treated and untreated (n=7) dogs. In untreated dogs, the level of prostaglandin E 2 increased 94-fold by Day 8 after the first injection of blood and was strongly and positively correlated with the degree of angiographic vasospasm. Treatment with ibuprofen and high-dose methylprednisolone prevented or significantly reduced this increase in prostaglandin E 2 concentration. Smaller increases in cerebrospinal fluid concentrations of thromboxane B 2 and 6-ketoprostaglandin ¥ la occurred after experimental subarachnoid hemorrhage; the magnitude of these increases was also reduced by ibuprofen or high-dose methylprednisolone treatment. In contrast, prostaglandin F 2a levels were not significantly altered during the study. These data show that enhanced prostaglandin E 2 synthesis occurs during experimental subarachnoid hemorrhage, and the by-products generated in its synthesis may play a role in the pathogenesis of cerebral vasospasm.

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Section: Discussionmentioning

confidence: 83%

Prevention of chronic cerebral vasospasm in dogs with ibuprofen and high-dose methylprednisolone.

Chyatte

1989

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“…The rabbit is a relatively inexpensive, easily available experimental animal; however, it has been used infrequently in experimental studies of SAH [5,8,13,15,20]. Its size allows angiography of the cerebral vessels to be performed adequately without too much sophistication needed in the technique.…”

Section: Discussionmentioning

confidence: 99%

“…Several animal models of SAH have been reported in the literature. The aim of the present study was to assess the validity of a new model of SAH in rabbit, an animal seldom used in SAH experiments [5,8,15,19].…”

Section: Introductionmentioning

confidence: 99%

Cerebral vasospasm in a double-injection model in rabbit

Spallone

Pastore

1989

Surgical Neurology

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Spallone A, Pastore FS. Cerebral vasospasm in a double-injection model in rabbit. Surg Neurol 1989;32:408-17.The present study was designed to assess the occurrence of cerebral vasospasm following an experimental subarachnoid hemorrhage model in rabbits. Sixty-nine New Zealand albino rabbits were used in this study. One milliliter of fresh arterial blood was injected through the surgically exposed atlanto-occipital membrane over a period of 20 seconds. The procedure was then repeated 24 hours later. Fifty animals underwent digital subtraction angiography at one of the following prefixed intervals: 1, 3, or 8 days after the second injection hemorrhage. Nineteen animals underwent one angiographic examination prior to the instillation of the intracisternal blood. This procedure was followed by a repeated angiography 3 days after the second experimental subarachnoid hemorrhage. For the purpose of evaluation, the films were magnified 10-fold and the diameter of the basilar artery as well as that of the extracranial vertebral artery at three different levels were measured. We assessed the diameter of the basilar artery as well as the mean ratio extracranial vertebral artery/basilar artery diameters. This ratio was considered to minimize anatomical and technical variabilities. The results in the first 50 animals showed a trend suggesting that spasmogenic activity reaches a peak at about the third day after subarachnoid hemorrhage. These results were confirmed in the latter 19 animals. However, mortality in this group was high: 50%. This double-injection model of subarachnoid hemorrhage in rabbits consistently reproduced cerebral vascular spasm 3 days after repeated subarachnoid hemorrhage. However, its usefulness as an experimental model for subarachnoid hemorrhage is limited practically by the high animal mortality in the protocols where repeated angiographic studies are necessary.

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“…16,17 Therefore, the animals were killed 72 hours after the surgeries and underwent in situ perfusion-fixation. Anesthesia was induced as described above, and a 200-mg/kg intraperitoneal injection of sodium pentobarbital was administered.…”

Section: Histological Assessmentmentioning

confidence: 99%

Prevention of Experimental Cerebral Vasospasm by Intracranial Delivery of a Nitric Oxide Donor From a Controlled-Release Polymer

Gabikian

Clatterbuck

Eberhart

et al. 2002

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Background and Purpose-A reduction in the local availability of nitric oxide (NO) may play a role in the etiology of chronic cerebral vasospasm after subarachnoid hemorrhage (SAH). We investigated the toxicity and efficacy of a locally delivered NO donor from a controlled-release polymer in preventing experimental cerebral vasospasm in rats and rabbits, respectively. Methods-Diethylenetriamine/NO (DETA/NO) was incorporated into controlled release ethylene-vinyl acetate (EVAc) polymers. Twenty-eight rats were used in a dose-escalation toxicity study to establish a maximally tolerated dose of DETA/NO-EVAc polymer. In the efficacy experiment, 20 rabbits were assigned to 4 experimental groups (nϭ5 per group): sham operation; SAH only; SAHϩempty EVAc polymer; and SAHϩDETA/NO-EVAc polymer. Treatment was initiated 30 minutes after blood deposition. Basilar artery lumen patency was assessed 72 hours after hemorrhage to evaluate the efficacy of DETA/NO in preventing cerebral vasospasm. Results-In the toxicity study, a dose of 3.4 mg/kg was identified as the LD 20 (dose with 20% mortality during the study period) of this DETA/NO formulation. Brain histology revealed hemorrhage and ischemic changes at the implantation site associated with high concentrations of DETA/NO. In the efficacy study, treatment with DETA/NO-EVAc polymer resulted in a significant decrease in basilar artery vasospasm compared with no treatment (

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The role of the prostacyclin-thromboxane system in cerebral vasospasm following induced subarachnoid hemorrhage in the rabbit

Cited by 86 publications

References 39 publications

Prevention of chronic cerebral vasospasm in dogs with ibuprofen and high-dose methylprednisolone.

Prevention of chronic cerebral vasospasm in dogs with ibuprofen and high-dose methylprednisolone.

Cerebral vasospasm in a double-injection model in rabbit

Prevention of Experimental Cerebral Vasospasm by Intracranial Delivery of a Nitric Oxide Donor From a Controlled-Release Polymer

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