The effect of thiocolchicoside on cerebral vasospasm following experimental subarachnoid hemorrhage in the rabbit

Kertmen, Hayri; Gürer, Bora; Yı́lmaz, Erdal; Arıkök, Ata Türker; Demirci, Adnan; Gökyaprak, Salih Metin; Şekerci, Zeki

doi:10.1007/s00701-012-1420-3

Cited by 9 publications

(5 citation statements)

References 20 publications

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“…The underlying pathological mechanism of SAH-induced vasospasm is multifactorial, complex, and not fully understood. Various recent studies have focused on strategies for preventing or treating both SAH-induced EBI and vasospasm (Gürer et al 2014;Kertmen et al 2012Kertmen et al , 2014Miller et al 2014).…”

Section: Discussionmentioning

confidence: 99%

“…The model used in this study is one of the most commonly used protocols for establishing SAH in rabbits (Gürer et al 2014;Kertmen et al 2012Kertmen et al , 2014. With the rabbit in the prone position, its head was flexed and the atlanto-occipital membrane was exposed via a midline nuchal incision and dissection of the paravertebral muscles.…”

Section: The Cerebral Vasospasm Modelmentioning

confidence: 99%

“…The hippocampus of each rabbit was embedded in paraffin, sectioned into 4-6 μm thick slices and stained with H&E. Morphological signs of neuronal degeneration, such as neuronal shrinkage, hyperchromasia, and nuclear pyknosis were evaluated under a light microscope. The presence and extent of hippocampal degeneration in the CA1, CA3, and dentate gyrus regions were semiquantitatively scored as follows: 1, normal appearance; 2, a few degenerated neurons among normal neurons; 3, a large number of degenerated neurons with some scattered normal neurons; 4, complete degeneration with no residual normal neurons (Gürer et al 2014;Kertmen et al 2012Kertmen et al , 2014. The sum of the scores for the three regions of the hippocampus was considered to be the degeneration score, and the mean values were used in statistical analysis.…”

Section: Hippocampal Degenerationmentioning

confidence: 99%

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The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits

et al. 2019

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The neuroprotective and vasodilatory effects of cinnamaldehyde have been widely studied and documented. On the basis of these findings, we hypothesized that cinnamaldehyde exhibits therapeutic effects on subarachnoid hemorrhage-induced early brain injury and cerebral vasospasm. Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits: control, subarachnoid hemorrhage, subarachnoid hemorrhage + vehicle, and subarachnoid hemorrhage + cinnamaldehyde. An intraperitoneal dose of 50 mg/kg cinnamaldehyde was administered 5 min following an intracisternal blood injection, followed by three further daily injections at identical doses. The animals were sacrificed 72 h after subarachnoid hemorrhage was induced. The crosssectional areas and arterial wall thicknesses of the basilar artery were measured and hippocampal degeneration scores were evaluated. Treatment with cinnamaldehyde was effective in providing neuroprotection and attenuating cerebral vasospasm after subarachnoid hemorrhage in rabbits. It effectively increased the cross-sectional areas of the basilar artery and reduced the arterial wall thickness; in addition, hippocampal degeneration scores were lower in the cinnamaldehyde group. The findings of this study showed, for the first time to our knowledge, that cinnamaldehyde exhibits neuroprotective activity against subarachnoid hemorrhage-induced early brain injury and that it can prevent vasospasm. Potential mechanisms underlying the neuroprotection and vasodilation were discussed. Cinnamaldehyde could play a role in subarachnoid hemorrhage treatment.

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Section: Discussionmentioning

confidence: 99%

Section: The Cerebral Vasospasm Modelmentioning

confidence: 99%

Section: Hippocampal Degenerationmentioning

confidence: 99%

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The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits

et al. 2019

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“…Group 2 (SAH Group; n= 8): SAH was induced as previously described (15,17,18). No treatment was administered.…”

Section: Experimental Groupsmentioning

confidence: 99%

“…Mean ± SD value obtained from each artery was used as the final value for a particular vessel. All measurements were repeated twice for each artery, in a blind fashion by two pathologists, and the final values corresponded to the average of these measurements (10,14,17,18). The levels of inter-and intra-observer reliability are presented in Table I.…”

Section: Histological Morphometric Analysis Of the Basilar Arterymentioning

confidence: 99%

Vasorelaxant and neuroprotective effects of mildronate in a rabbit subarachnoid hemorrhage model

Eser

Bektaşoğlu²,

Gürer³

et al. 2018

Turkish Neurosurgery

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the early 1980s (46). The drug was firstly used as a carnitine biosynthesis inhibitor to inhibit fatty acid oxidation thus reducing the production of cytotoxic products and blocking the high oxygen use in ischemic conditions (38). In addition to carnitine biosynthesis inhibition, mildronate inhibits carnitine acyltransferase and attenuates carnitine incorporation into the mitochondria (32). Collectively, mildronate prevents the accumulation of ischemic precursors and toxic acylcarnitine products, by inhibiting carnitine █ INTRODUCTION C erebral ischemia is the most important cause of mortality and morbidity following subarachnoid hemorrhage (SAH)-related vasospasm (2,13). Despite numerous studies investigating treatments for SAH-induced vasospasm, effective prevention and therapy are still lacking. Mildronate (2,2,2 triethylhydrazinium, Quaterine, Meldonium, MET-88) is an anti-ischemic drug first produced in Lithuania in AIM: To investigate the effects of an anti-ischemic agent, mildronate, on subarachnoid hemorrhage-induced vasospasm. MATERIAL and METHODS: Rabbits were randomly divided into four groups: control, subarachnoid hemorrhage (SAH), vehicle, and mildronate (n = 8 animals per group). In the treatment group, 200 mg/kg of mildronate were intraperitoneally administered 5 min after the procedure and continued for 3 days as daily administrations of the same dose. At the end of the third day, the cerebrum, cerebellum, and brain stem were perfused, fixated, and removed for histopathological examination. Tissues were examined for arterial wall thickness, luminal area, and hippocampal neuronal degeneration. RESULTS: Mildronate group showed significantly increased luminal area and reduced wall thickness of the basilar artery compared with the subarachnoid hemorrhage group. In addition, the hippocampal cell degeneration score was significantly lower in the mildronate group than in the SAH and vehicle groups. CONCLUSION: These results show that mildronate exerts protective effects against SAH-induced vasospasm and secondary neural injury.

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The comparative effects of recombinant human erythropoietin and darbepoetin-alpha on cerebral vasospasm following experimental subarachnoid hemorrhage in the rabbit

et al. 2014

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The effect of thiocolchicoside on cerebral vasospasm following experimental subarachnoid hemorrhage in the rabbit

Cited by 9 publications

References 20 publications

The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits

The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits

Vasorelaxant and neuroprotective effects of mildronate in a rabbit subarachnoid hemorrhage model

The comparative effects of recombinant human erythropoietin and darbepoetin-alpha on cerebral vasospasm following experimental subarachnoid hemorrhage in the rabbit

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