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Sıçanlarda Deneysel Kafa Travması Sonrası Kan Şekeri Değişikliklerinin İstatistiksel Analizi

Year 2024, , 1623 - 1629, 15.09.2024
https://doi.org/10.31466/kfbd.1527755

Abstract

Travmaya bağlı santral sinir sistemi hasarları önemli ölüm ve sakatlık sebebidir. Ancak travma sonucu oluşan hasardan sadece primer beyin harabiyeti değil bunu takip eden kompleks fizyopatolojik sekonder olaylar da sorumludur. Travma sonrası beyin dokusunun sistemik bozukluklara daha duyarlı hale geldiği tespit edilmiştir. Travma sonrası ortaya çıkan hipoksi ve iskemik olaylar sereberal enerji metabolizmasını belirgin şekilde etkileyerek yaygın beyin harabiyeti oluştururlar. Ağır kafa travmasını takiben erken dönmede hipergliseminin mevcut olduğu, kan glikoz düzeyi ile travmayı takiben iyileşme arasında negatif ilişki olduğu gösterilmiştir. Deneyde toplam 42 adet 250/350 gram ağırlığında erkek Wistar albino sıçan kullanıldı. Sıçanların 36 tanesinde yukarıda belirtildiği şekilde kafa travması oluşturuldu. Altı tanesinde travma oluşturulmadı, kontrol grubu olarak ölçümleri yapıldı. Çalışmamızda travma grubundaki sıçanlarda travma sonrası yapılan tüm ölçümlerde belirgin hiperglisemi tespit edildi (P<0.0001). Hiperglisemi ilk 24 saat içerisinde en yüksek seviyede seyretti. 48 saatten sonra azalmakla birlikte 7. günde kan şekeri değerleri travma öncesi değerlerin üzerinde görüldü (P<0.0001). Kontrol grubunda tüm ölçümlerde kan şekeri değerleri normal seyretti.

References

  • Becker DP, Gudeman SK.,(1980) Acute head injury: Assessment, management, and prognosis.In: Hardy JD(ed), Critical surgical illness (2nd ed). WB Saunders, Philadelphia pp 110-134.
  • Chesnut RM, Marshall LF, Klauber MR, Blunt BA, et al,(1993) The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 34:216-22.
  • Davalos A,Cendra E,Teruel J, et al.(1990) Deteriorating ischemic stroke: Risk factors and prognosis. Neurology 40:1865-1869.
  • De Salles AA, Muizelar JP, Young HF.(1987) Hyperglycemia, cerebrospinal fluid lactic acidosis, and cerebral blood flow in severely head-injured patients. Neurosurgery. 21:45-50.
  • Dixon CE, Lyeth BG, Povlishock JT, et al.(1987) A fluıd percussion model of experimental brain injury in the rat. J Neurosurg 67:110-119.
  • Falkowska A, Gutowska I, Goschorska M, et al.(2015). Energy metabolism of the brain, including the cooperation between astrocytes and neurons, especially in the context of glycogen metabolism. Int J Mol Sci. 16:25959-81.
  • Foda MAA, Marmarou A. (1994) A new model of diffuse brain injury in rats. Part 2: Morphological Characterization. J Neurosurg 80:301-313.
  • Gardiner M, Smith ML, Kågström E, et al.(1982) Influence of blood glucose concentration on brain lactate accumulation during severe hypoxia and subsequent recovery of brain energy metabolism. J Cereb Blood Flow Metab. 2:429-38.
  • Generalli TA.(1990) Mechanism of cerebral concussion,consition and other effects of head injury. İn: Youmans JR(ed), Neurological surgery. Vol.3(vascular disease and trauma)WB Saunders, Philadelphia. pp1953-1964.
  • Hamilton MG, Tranmer BI, Auer RN.(1995) Insulin reduction of cerebral infarction due to transient focal ischemia. J Neurosurg. 82:262-8.
  • Hawkins RA, Mans AM.(1982) Intermediary metabolism of carbohydrates and other fuels,In: Lajtha A(ed) Handbook of Neurochemistry. Vol 3. Plenium Press, New York pp259-294.
  • Jenkins LW, Moszynski K, Lyeth BG, et al.(1989) Increased vulnerability of the mildly traumatized rat brain to cerebral ischemia: The use of controlled secondary ischemia as a research tool to identify common or different mechanisms contributing to mechanical and ischemic brain injury. Brain Res. 477:211-24.
  • Jennett B, Galbraith S.,(1983) Head İnjuries: Pathology and history of head injury.An introduction to Neurosurgery(4th ed). William Heinemann, London pp 214-223.
  • Kerby JD, Griffin RL, MacLennan P, et al.(2012) 3rd. Stress-induced hyperglycemia, not diabetic hyperglycemia, is associated with higher mortality in trauma. Ann Surg. 256: 446-52.
  • King LR, Knowles HC, Mc Laurin RL, et al.(1971) Glucose tolerance and plasma insülin in cranial trauma. Ann Surg 173:337-343.
  • Lying-Tunell U, Lindblad BS, Malmlund HO, et al.(1980) Cerebral blood flow and metabolic rate of oxygen, glucose, lactate, pyruvate, ketone bodies, and amino acids. Acta Neurol Scand 62:265-275.
  • Marmarou A, Foda MA, van den Brink W, et al.(1994) K. A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. J Neurosurg. 80:291-300.
  • Mc Intosh TK, Vink R, Noble L, et al(1989). Traumatic brain injury in the rat: Characterization of lateral fluid- percussion model. Neuroscience 28:233-244.
  • Pulsinelli WA, Waldman S, Rawlinson D, et al (1982). Moderate hyperglycemia augments ischemic brain damage: a neuropathologic study in the rat. Neurology. 32:1239-46.
  • Rehenora S,Rosen I, Siesjö BK.(1981) Brain lactic acidosis and ischemic cell damage. Biochemistry and Neurophysiology. J Cereb Blood Flow Metab 1:297-311.
  • Roberson CS, Goodman JC, Narayan RK, et al.(1991) The effect of glucose administration on carbohydrate metabolism after head injury. J Neurosurg 74:43-50.
  • Rosner MJ, Newsome HH, Becker DP.(1984) Mechanical brain injury: The sympathoadrenal response. J Neurosurg 61:76-86.
  • Shi J, Dong B, Mao Y, et al.2016)( Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor. Onco Target. 7:71052-71061.
  • Siemkowicz E, Hansen AJ.(1978) Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic rats. Acta Neurol Scand. 58: 1-8.
  • Sullivan HG, Martinez J, Becker DP, et al.(1976) Fluid percussion of mechanical brain injury in the cat. J Neurosurg 45:520-534.

Statistical Analysis of Blood Glucose Changes After Experimental Head Trauma in Rats

Year 2024, , 1623 - 1629, 15.09.2024
https://doi.org/10.31466/kfbd.1527755

Abstract

Trauma-related central nervous system injuries are an important cause of death and disability. However, not only primary brain damage but also complex physiopathological secondary events are responsible for the damage caused by trauma. It has been determined that brain tissue becomes more sensitive to systemic disorders after trauma. Post-traumatic hypoxia and ischaemic events markedly affect cerebral energy metabolism and cause widespread brain damage. It has been shown that hyperglycemia is present in early recovery following severe head trauma and that there is a negative correlation between blood glucose level and recovery following trauma. A total of 42 male Wistar albino rats weighing 250/350 grams were used in the experiment. Head trauma was induced in 36 rats as described above. Six rats were not traumatized and measured as a control group. In our study, significant hyperglycemia was detected in all measurements made after trauma in rats in the trauma group (P<0.0001). Hyperglycaemia was at the highest level in the first 24 hours. Although it decreased after 48 hours, blood glucose values were above the pre-trauma values on the 7th day (P<0.0001). In the control group, blood glucose values were normal in all measurements.

References

  • Becker DP, Gudeman SK.,(1980) Acute head injury: Assessment, management, and prognosis.In: Hardy JD(ed), Critical surgical illness (2nd ed). WB Saunders, Philadelphia pp 110-134.
  • Chesnut RM, Marshall LF, Klauber MR, Blunt BA, et al,(1993) The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 34:216-22.
  • Davalos A,Cendra E,Teruel J, et al.(1990) Deteriorating ischemic stroke: Risk factors and prognosis. Neurology 40:1865-1869.
  • De Salles AA, Muizelar JP, Young HF.(1987) Hyperglycemia, cerebrospinal fluid lactic acidosis, and cerebral blood flow in severely head-injured patients. Neurosurgery. 21:45-50.
  • Dixon CE, Lyeth BG, Povlishock JT, et al.(1987) A fluıd percussion model of experimental brain injury in the rat. J Neurosurg 67:110-119.
  • Falkowska A, Gutowska I, Goschorska M, et al.(2015). Energy metabolism of the brain, including the cooperation between astrocytes and neurons, especially in the context of glycogen metabolism. Int J Mol Sci. 16:25959-81.
  • Foda MAA, Marmarou A. (1994) A new model of diffuse brain injury in rats. Part 2: Morphological Characterization. J Neurosurg 80:301-313.
  • Gardiner M, Smith ML, Kågström E, et al.(1982) Influence of blood glucose concentration on brain lactate accumulation during severe hypoxia and subsequent recovery of brain energy metabolism. J Cereb Blood Flow Metab. 2:429-38.
  • Generalli TA.(1990) Mechanism of cerebral concussion,consition and other effects of head injury. İn: Youmans JR(ed), Neurological surgery. Vol.3(vascular disease and trauma)WB Saunders, Philadelphia. pp1953-1964.
  • Hamilton MG, Tranmer BI, Auer RN.(1995) Insulin reduction of cerebral infarction due to transient focal ischemia. J Neurosurg. 82:262-8.
  • Hawkins RA, Mans AM.(1982) Intermediary metabolism of carbohydrates and other fuels,In: Lajtha A(ed) Handbook of Neurochemistry. Vol 3. Plenium Press, New York pp259-294.
  • Jenkins LW, Moszynski K, Lyeth BG, et al.(1989) Increased vulnerability of the mildly traumatized rat brain to cerebral ischemia: The use of controlled secondary ischemia as a research tool to identify common or different mechanisms contributing to mechanical and ischemic brain injury. Brain Res. 477:211-24.
  • Jennett B, Galbraith S.,(1983) Head İnjuries: Pathology and history of head injury.An introduction to Neurosurgery(4th ed). William Heinemann, London pp 214-223.
  • Kerby JD, Griffin RL, MacLennan P, et al.(2012) 3rd. Stress-induced hyperglycemia, not diabetic hyperglycemia, is associated with higher mortality in trauma. Ann Surg. 256: 446-52.
  • King LR, Knowles HC, Mc Laurin RL, et al.(1971) Glucose tolerance and plasma insülin in cranial trauma. Ann Surg 173:337-343.
  • Lying-Tunell U, Lindblad BS, Malmlund HO, et al.(1980) Cerebral blood flow and metabolic rate of oxygen, glucose, lactate, pyruvate, ketone bodies, and amino acids. Acta Neurol Scand 62:265-275.
  • Marmarou A, Foda MA, van den Brink W, et al.(1994) K. A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. J Neurosurg. 80:291-300.
  • Mc Intosh TK, Vink R, Noble L, et al(1989). Traumatic brain injury in the rat: Characterization of lateral fluid- percussion model. Neuroscience 28:233-244.
  • Pulsinelli WA, Waldman S, Rawlinson D, et al (1982). Moderate hyperglycemia augments ischemic brain damage: a neuropathologic study in the rat. Neurology. 32:1239-46.
  • Rehenora S,Rosen I, Siesjö BK.(1981) Brain lactic acidosis and ischemic cell damage. Biochemistry and Neurophysiology. J Cereb Blood Flow Metab 1:297-311.
  • Roberson CS, Goodman JC, Narayan RK, et al.(1991) The effect of glucose administration on carbohydrate metabolism after head injury. J Neurosurg 74:43-50.
  • Rosner MJ, Newsome HH, Becker DP.(1984) Mechanical brain injury: The sympathoadrenal response. J Neurosurg 61:76-86.
  • Shi J, Dong B, Mao Y, et al.2016)( Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor. Onco Target. 7:71052-71061.
  • Siemkowicz E, Hansen AJ.(1978) Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic rats. Acta Neurol Scand. 58: 1-8.
  • Sullivan HG, Martinez J, Becker DP, et al.(1976) Fluid percussion of mechanical brain injury in the cat. J Neurosurg 45:520-534.
There are 25 citations in total.

Details

Primary Language Turkish
Subjects Biochemistry and Cell Biology (Other)
Journal Section Articles
Authors

Mehmet Meral 0000-0003-3814-3528

Publication Date September 15, 2024
Submission Date August 3, 2024
Acceptance Date September 11, 2024
Published in Issue Year 2024

Cite

APA Meral, M. (2024). Sıçanlarda Deneysel Kafa Travması Sonrası Kan Şekeri Değişikliklerinin İstatistiksel Analizi. Karadeniz Fen Bilimleri Dergisi, 14(3), 1623-1629. https://doi.org/10.31466/kfbd.1527755