Journals / Ulusal Travma ve Acil Cerrahi Dergisi / 2015 / Cilt: 21 - Sayı: 6

Effects of decompressive craniectomy, hypertonic saline solution and mannitol on an experimental model of cerebral ischemia

Pages
425–431
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Combined treatment approaches performed to decrease infarction volume also resulted in favorable outcomes

📌 3 Key Takeaways

🎯
Objective & Hypothesis:BACKGROUND: Cerebral ischemia is a cause of serious morbidity and mortality.
📊
Key Findings & Data:Strategies that would protect cerebral tissue against ischemic injury are important.
💡
Conclusion & Impact:Combined treatment approaches performed to decrease infarction volume also resulted in favorable outcomes
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

BACKGROUND: Cerebral ischemia is a cause of serious morbidity and mortality. Strategies that would protect cerebral tissue against ischemic injury are important. The present study aimed to evaluate effects of surgical and medical treatments, either alone or in combination, on infarction area in an experimental rat model of cerebral ischemia.METHODS: Adult male Sprague-Dawley rats (n=30) were divided into 6 groups, each including 5 experimental animals. Cerebral ischemia was created by right common carotid artery occlusion (CCAO) under anesthesia. Decompressive craniectomy (DC) was performed in the relevant groups at the 12th hour following CCAO, whereas medical treatments were performed in the relevant groups at the 1st, 12th, and 24th hours following CCAO. After CCAO, the control group received 1 mL/kg physiological saline, hypertonic saline (HS) group received 3% hypertonic saline (1 mL/kg), and mannitol (MAN) group received 20% mannitol (1 g/kg). While only DC was performed following CCAO in the DC group, DC+HS group underwent DC together with hypertonic saline treatment and DC+MAN group underwent DC together with mannitol treatment. The rats were decapitated at the end of the 24th hour following ischemia. Cerebral sections were stained with 2% 2,3,5-triphenyltetrazolium chloride (TTC). The ratio of infarction area to the total area of section was calculated as percentage.RESULTS: Mean infarction areas were 27.9% in the control group, 13.7% in the HS group, 15.1% in the MAN group, 10.6% in the DC group, 8.1% in the DC+HS group, and 9.7% in the DC+MAN group. Mean infarction areas were significantly lower in all groups than in the control group. While the mean infarction area did not differ between the HS and MAN groups, it was lower in the groups undergoing DC as compared to these two groups. The best outcome was observed in the DC+HS group.CONCLUSION: Both medical and surgical treatments were effective in decreasing cerebral ischemic infarction. There was no difference between medical treatments groups in terms of efficacy, whereas DC led to a substantial decrease in ischemic infarction volume as compared with the medical treatment groups. Combined treatment approaches performed to decrease infarction volume also resulted in favorable outcomes

🔖

Cite This Article

ÇALIKOĞLU, Ç., AKGÜL, M. H., AKGÜL, O., KARATAŞ, A. (2015). Effects of decompressive craniectomy, hypertonic saline solution and mannitol on an experimental model of cerebral ischemia. Ulusal Travma ve Acil Cerrahi Dergisi, Cilt: 21 - Sayı: 6, 425–431. https://ajindex.com/articles/323764

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (12)

  1. Mukherjee D, Patil CG. Epidemiology and the global burden of stroke. World Neurosurg 2011;76(6 Suppl):85-90.
  2. Norrving B, Kissela B. The global burden of stroke and need for a con- tinuum of care. Neurology 2013;80(3 Suppl 2):5-12.
  3. Truelsen T, Begg, S, Mathers C. Global burden of cerebrovascular dis- ease. 2000. Retrieved from: http://www.who.int/healthinfo/statistics/ bod_cerebrovasculardiseasestroke.pdf. Last Access: 22 October 2014. Raichle ME. The pathophysiology of brain ischemia. Ann Neurol 1983;13:2-10. Ginsberg MD. Adventures in the pathophysiology of brain ischemia: penumbra, gene expression, neuroprotection: the 2002 Thomas Willis Lecture. Stroke 2003;34:214-23.
  4. Jivan K, Ranchod K, Modi G. Management of ischaemic stroke in the acute setting: review of the current status. Cardiovasc J Afr 2013;24:86- 92. Bhardwaj A, Ulatowski JA. Hypertonic saline solutions in brain injury. Curr Opin Crit Care 2004;10:126-31.
  5. Honeybul S, Ho KM. The current role of decompressive craniectomy in the management of neurological emergencies. Brain Inj 2013;27:979- 91. Rice JE 3rd, Vannucci RC, Brierley JB. The influence of immaturity on hypoxic-ischemic brain damage in the rat. Ann Neurol 1981;9:131-41.
  6. Bederson JB, Pitts LH, Germano SM, Nishimura MC, Davis RL, Bart- kowski HM. Evaluation of 2,3,5-triphenyltetrazolium chloride as a stain for detection and quantification of experimental cerebral infarction in rats. Stroke 1986;17:1304-8.
  7. Kawamura S, Li Y, Shirasawa M, Yasui N, Fukasawa H. Reversible mid- dle cerebral artery occlusion in rats using an intraluminal thread tech- nique. Surg Neurol 1994;41:368-73.
  8. LeBlanc MH, Li XQ, Huang M, Patel DM, Smith EE. AMPA antagonist LY293558 does not affect the severity of hypoxic-ischemic injury in new- born pigs. Stroke 1995;26:1908-15.
  9. Childs AM, Evans RH, Watkins JC. The pharmacological selectivity of three NMDA antagonists. Eur J Pharmacol 1988;145:81-6.
  10. Franke CL, Palm R, Dalby M, Schoonderwaldt HC, Hantson L, Er- iksson B, et al. Flunarizine in stroke treatment (FIST): a double-blind, placebo-controlled trial in Scandinavia and the Netherlands. Acta Neurol Scand 1996;93:56-60.
  11. Cho S, Park EM, Febbraio M, Anrather J, Park L, Racchumi G, et al. The class B scavenger receptor CD36 mediates free radical production and tissue injury in cerebral ischemia. J Neurosci 2005;25:2504-12.
  12. Adibhatla RM, Hatcher JF, Dempsey RJ. Cytidine-5'-diphosphocholine affects CTP-phosphocholine cytidylyltransferase and lyso-phosphatidyl- choline afte