Model of Closed He ad Injury in Rats – Experimental Study

Czech version

Authors: M. Bláha ^1,2; J. Schwab ^1,2; O. Vajnerová ²; M. Bednář ³; R. Pádr ⁴; P. Bittner ²; M. Tichý ^1,2
Authors‘ workplace: Ne urochirurgické oddělení FN Motol, Praha, 2Ústav fyzi ologi e 2. LF UK v Praze, 3Anesteziologicko‑resuscitační oddělení, CLINICUM, a. s., Praha, sup>4Klinika zobrazovacích metod FN Motol a 2. LF UK v Praze ¹
Published in: Cesk Slov Neurol N 2009; 72/105(3): 235-241
Category: Original Paper

Overview

Objective:
The objective of this study is to create a reproducible model of closed head injury in rats using the acceleration-deceleration mechanism. The model should result in increased intracranial pressure (ICP) and neurological deterioration animals, and generate graded brain injury. Material and method: In order to provoke cranial traumas we constructed an impactor with selectable weights and a mobile impact surface. Within the first pilot group of 40 rats, we tested only its basic setup. Afterwards, within the second group of 21 rats, we provoked an experimental cranial trauma using a weight of 400 grams dropped from a height ranging from 30 to 100 centimetres at a constant surface elasticity. Within the third control group of 15 rats, we measured physiological parameters including ICP. Results: According to the height of fall, four types of brain injuries were established – lethal, severe, moderate, and mild. With the lethal injury (45–100 cm), an immediate convulsions with subsequent death occurred in all the rats. A severe injury (40 cm) showed 50% mortality. Neurological deterioration and an average ICP of 9.3 ± 3.76 mmHg was recorded in the surviving animals. A moderate brain injury (35 cm) resulted in lower mortality, the neurological deficit occurred in half of the survivors and ICP achieved 7.6 ± 3.54 mmHg. Within the group of mild brain injury (30 cm), all animals survived without any neurological and behavioral deterioration with an ICP of 5.5 ± 0.74 mmHg. The control group without any injury had an ICP of 2.9 ± 0.81 mmHg. Conclusion: The described model of closed head injury in rats using a modified impactor with adjustable weights is suitable for both single-stage and two-stage experiments examining craniocerebral injuries. By simply changing the fall height of the impactor, reproducible severe, moderate, or mild brain injury can be created. The intracranial pressure elevation and the neurological deterioration correlate with these grades of brain injury.

Key words:
brain injury – intracrani al pressure – animal models

Sources

1. Česák T, Hobza V. Epidemi ologi e mozkových tra umat. In: Česák T, Hobza V (eds). Poranění mozku. 1st ed. Praha: Grada Publishing 2001: 19– 28.

2. Marmaro u A. Incre ased intracrani al pressure in he ad injury and influence of blo od volume. J Ne urotra uma 1992; 9 (Suppl 1): S327– S332.

3. Marshall LF, Smith RW, Shapiro RM. The o utcome with aggressive tre atment in severe he ad injuri es. Part I:the significance of intracrani al pressure monitoring. J Ne urosurg 1979; 50(1): 20– 25.

4. Brain Tra uma Fo undati on; American Associ ati on of Ne urological Surge ons; Congress of Ne urological Surge ons; Jo int Secti on on Ne urotra uma and Critical Care, AANS/ CNS. Guidelines for the management of severe tra umatic brain injury. IX. Cerebral perfusi on thresholds. J Ne urotra uma 2007; 24 (Suppl 1): S59– S64.

5. Smrčka M. Patofyzi ologi e poranění mozku. In: Česák T, Hobza V (eds). Poranění mozku. 1st ed. Praha: Grada Publishing 2001: 29– 52.

6. Blaha M, Aaslid R, Do uville CM, Correra R, Newell DW. Cerebral blo od flow and dynamic cerebral a utoregulati on during ethanol intoxicati on and hypercapni a. J Clin Ne urosci 2003; 10(2): 195– 198.

7. Marmaro u A, Foda MA, van den Brink WA, Campbeell J, Kita H, Demetri ado u K. A new model of diffuse brain injury in rats. Part I: pathophysi ology and bi omechanics. J Ne urosurg 1994; 80(2): 291– 300.

8. Engelborghs K, Verlo oy J, Van Reempts J, van De uren B, van de Ven M, Borgers M. Temporal changes in intracrani al pressure in a modifi ed experimental model of closed he ad injury. J Ne urosurg 1998; 89(5): 796– 806.

9. Ro oker S, Jorens PG, Van Reempts J, Borgers M, Verloy J. Continuo us me asurement of intracrani al pressure in awake rats after experimental closed he ad injury. J Ne urosci Methods 2003; 131(1– 2): 75– 81.

10. Ro oker S, de Visscher G, Van De uren B, Borgers M, Jorens PG, Reneman RS et al. Comparison of intracrani al pressure me asured in the cerebral cortex and cerebellum of the rat. J Ne urosci Methods 2002; 119(1): 83– 88.

11. Cla usen F, Hillered L. Intracrani al pressure changes during fluid percussi on, controlled cortical impact and weight drop injury in rats. Acta Ne urochir (Wi en) 2005; 147(7): 775– 780.

12. Smith DH, Chen XH, Xu BN, McIntosh TK, Gennarelli TA, Me aney DF. Characterizati on of diffuse axonal pathology and selective hippocampal damage following inerti al brain tra uma in the pig. J Ne uropathol Exp Ne urol 1997; 56(7): 822– 834.

13. James HE, Schneider S. Cryogenic brain oedema: loss of cerebrovascular a utoregulati on as a ca use of intracrani al hypertensi on. Implicati ons for tre atment. Acta Ne urochir Suppl (Wi en) 1990; 51: 79– 81.

14. Todd MM, Weeks JB, Warner DS. A focal cryogenic brain lesi on does not reduce the minimum alve olar concentrati on for halothane in rats. Anesthesi ology 1993; 79(1): 139– 143.

15. Faltusová K, Němecek S. A model of mild spinal cord injury in rats – dynamics of changes in motor functi on. Sb Ved Pr Lek Fak Karlovy Univerzity Hradci Kralove Suppl 1992; 35(1): 25– 41.

16. Otevřel F, Smrčka M, Kuchtičková Š, Mužík J. Korelace ptiO2 a apoptózy u fokální mozkové ischemi e a vliv systémové hypertenze. Cesk Slov Ne urol N 2007; 70/ 103(2): 168– 173.

17. Palecek F. Me asurement of ventilatory mechanics in the rat. J Appl Physi ol 1969; 27(1): 149– 156.

18. Jo u IM, Tsai YT, Tsai CL, Wu MH, Chang HY, Wang NS. Simplifi ed rat intubati on using a new oropharynge al intubati on wedge. J Appl Physi ol 2000; 89(5): 1766– 1770.