Traumatic Brain Injuries – Effects of Alcohol and Coffein on Intracranial Pressure and Cerebral Blood Flow

Česká verzia

Authors: M. Bláha; O. Vajnerová ¹; M. Bednář ²; L. Vajner ³; M. Tichý
Authors place of work: Neurochirurgické oddělení FN Motol, Ústav fyziologie 2. LF UK Praha, primář doc. MUDr. M. Tichý, CSc. ; Ústav fyziologie 2. LF UK Praha, prof. MUDr. J. Herget, DrSc. ¹; Anesteziologicko-resuscitační oddělení CLINICUM a. s., Praha, primář MUDr. M. Bednář ²; Ústav histologie a embryologie 2. LF UK Praha, doc. MVDr. L. Vajner, CSc. ³
Published in the journal: Rozhl. Chir., 2009, roč. 88, č. 11, s. 682-686.
Category: Monothematic special - Original

Summary

Introduction:
Alcohol and caffeine is intermittently or regularly used by majority of people. These drugs may have acute or chronic effects on patients with traumatic brain injury. Alcohol intoxication increases cerebral blood flow from 8 to 24%. Caffeine decreases cerebral blood flow from 10 to 20%. These facts create a theoretical hypothesis that the decrease of CBF may reduce incranial pressure. The aim of this study was to investigate the effect of caffeine on intracranial pressure in rats following traumatic brain injury.

Methods:
Ten Wistar male rats underwent weight drop closed head injury. The second stage of the experiment was done 12 to 18 hours later. Intracranial pressure, respiration, heart rate and the mean arterial pressure was monitored. Intraperitoneal injection of caffeine (20mg/kg) was administered and repetitive measurement of vital signs and intracranial pressure was done.

Results:
The baseline ICP after head injury was 8.5 ± 2.9 mm Hg. Ten minutes after intraperitoneal caffeine administration ICP dropped to 7.6 ± 3.1 mm Hg (p < 0.05). This represents a 11% decrease from baseline value. Mean arterial pressure, respiration and heart rate were stable.

Conclusion:
Intracranial pressure decrease of 11 % from baseline value. This drop was compatible with our hypothesis. The exact dosage of caffeine, its form and rate, should be more precisely specified in further studies.

Key words:
traumatic brain injury – caffeine – alcohol – intracranial pressure – rats

Zdroje

1. Galasko, G. T., Furman, K. I., Alberts, E. The caffeine contents of non-alcoholic beverages. Food Chem. Toxicol., 1989; 27(1): 49–51.

2. Nehlig, A., Daval, J.L., Debry, G. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res. Rev., 1992; 17(20): 139–170.

3. Marmarou, A. Increased intracranial pressure in head injury and influence of blood volume. J. Neurotrauma, 1992 Mar; vol. 9, Suppl. 1: 327–332.

4. Marshall, L. F., Smith, R. W., Shapiro, R. M. The outcome with agressive treatment in severe head injuries. Part I: The significance of intracranial pressure monitoring. J Neurosurg., 1979; 50: 20–25.

5. Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS, Bratton, S.L., Chestnut, R.M., Ghajar, J. et al.: Guidelines for the management of severe traumatic brain injury. XIV.Hyperventilation. Intracranial pressure tresholds. J Neurotrauma., 2007; 24 Suppl 1: S55-58.

6. Sioutos, P. J., Orozco, J. A., Carter, L. P., et al. Continuous regional cerebral blood flow monitoring in head-injured patients. Neurosurgery, 1995; 36(5): 949–950.

7. Bouma, G. J., Muizelaar, J. P., Stringer, W. A., et al. Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. J. Neurosurg., 1992; 77(3): 360–368.

8. Bouma, G. J., Muizelaar, J. P. Cerebral blood flow, cerebral blood flow volume, and cerebrovascular reactivity after severe head injury. J Neurotrauma, 1992; 9 Suppl 1: S333–348.

9. Aygok, G. A., Marmarou, A., Fatouros, P., et al. Assessment of mitochondrial impairment and cerebral blood flow in severe brain injured patients. Acta Neurochir. Suppl., 2008; 102: 57–61.

10. Hattori, N., Huang, S. C., Wu, H. M., et al. PET investigation of post-traumatic cerebral blood volume and blood flow. Acta Neurochir. Suppl., 2003; 86: 49–52.

11. Weber, B. B., Kerr, M. E., Wechsler, L. R., et al. Absence of diastolic velocity notch does not indicate hyperemia in traumatic brain injured patients without elevated cerebral blood flow velocity. J. Neurosurg. Anesthesiol., 2002; 14(4): 279–286.

12. Ojha, B. K., Jha, D. K., Kale, S. S., et al. Trans-cranial Doppler in severe head injury: evaluation of pattern of changes in cerebral blood flow velocity and its impact on outcome. Surg. Neurol., 2005; 62(2): 174–179.

13. Wintermark, M., van Melle, G., Schnyder, P., et al. Admission perfusion CT: prognostic value in patients with severe head trauma. Radiology, 2004; 232(1): 211–220.

14. Marion, D. W., Darby, J., Yonas, H. Acute regional cerebral blood flow changes caused by severe head injuries. J. Neurosurg., 1991; 74(3): 407–414.

15. van Santbrink, H., Schouten, J. W., Steyerberg, E. W., et al. Serial transcranial Doppler measurements in traumatic brain injury with special focus on the early posttraumatic period. Acta Neurochir. (Wien), 2002; 144(11): 1141–1149.

16. Soustiel, J. F., Sviri, G. E. Monitoring of cerebral metabolism: non-ischemic impairment of oxidative metabolism following severe traumatic brain injury. Neurol. Res., 2007; 29(7): 654–660.

17. Rivara, F. P., Jurkovich, G. J., Gurney, J. G., et al. The magnitude of acute and chronic alcohol abuse in trauma patients. Arch. Surg., 1993; 128(8), 907–913.

18. Gurney, J. G., Rivara, F. P., Mueller, B. A., et al. The effects of alcohol intoxication on the initial treatment and hospital course of patients with acute brain injury. J. Trauma., 1992; 33(5): 709–713.

19. Pories, S. E., Gamelli, R. L., Vacek, P., et al. Intoxication and injury. J. Trauma., 1992; 32(1): 60–64.

20. Zink, B. J., Maio, R. F., Chen, B. Alcohol, central nervous system injury, and time to death in fatal motor vehicle crashes. Alcohol Clin. Exp. Res., 1996; 20(9): 1518–1522.

21. Jurkovich, G. J., Rivara, F. P., Gurney, J. G., et al. The effect of acute alcohol intoxication and chronic alcohol abuse on outcome from trauma. JAMA, 1993; 7, 270(1): 93–94.

22. Zink, B. J., Sheinberg, M. A., Wang, X., et al. Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response. J. Neurosurg., 1998; 89: 983–990.

23. Zink, B. J., Walsh, R. F., Feustel, P. J. Effects of ethanol in traumatic brain injury. J. Neurotrauma., 1993; 10(3): 275–286.

24. Kelly, D. F., Kozlowski, D. A., Haddad, E., et al. Ethanol reduces metabolic uncoupling following experimental head injury. Journal of Neurotrauma., 2000; 17(4): 261–272.

25. Sano, M., Wendt, P. E., Wirsen, A., et al. Acute effects of alcohol on regional cerebral blood flow in man. J. of Studies on Alcohol, 1993; May: 369–376.

26. Tiihonen, J., Kuikka, J., Hakola, P., et al. Acute ethanol-induced changes in cerebral blood flow. Am. J. Psychiatry, 1994; 151(10): 1505–1508.

27. Blaha, M., Aaslid, R., Douville, C. M., et al. Cerebral blood flow and dynamic cerebral autoregulation during ethanol intoxication and hypercapnia. J. Clin. Neurosci., 2003: 10(2): 195–198.

28. Ngai, A. C., Coyne, E. F., Meno, J. R., et al. Receptor subtypes mediating adenosine-induced dilation of cerebral arterioles. Am. J. Physiol. Heart Circ. Physiol., 2001; 280(5): 2329–2335.

29. Phillis, J. W., DeLong, R. E. An involvement of adenosine in cerebral blood flow regulation during hypercapnia. Gen. Pharmacol.,1987; 18(2): 133–139.

30. West, G. A., Meno, J. R., Nguyen, T. S., et al. cGMP-dependent and not cAMP-dependent kinase is required for adenosine-induced dilation of intracerebral arterioles. J. Cardiovasc. Pharmacol., 2003; 41(3): 444–451.

31. Meno, J. R., Nguyen, T. S., Jensen, E. M., et al. Effect of caffeine on cerebral blood flow response to somatosensory stimulation. J. Cereb. Blood Flow Metab., 2005; 25(6): 775–784.

32. Mathew, R. J., Wilson, W. H. Substance abuse and cerebral blood flow. Am. J. Psychiatry, 1991; 148(3): 292–305.

33. Blaha, M., Benes, V., Douville, C. M. et al. The effect of caffeine on dilated cerebral circulation and on diagnostic CO2 reactivity testing. J. Clin. Neurosci., 2007; 14 (5): 464–467.

34. Bláha, M., Ostrý, S. Vliv kofeinu na průtok krve mozkem. Cesk. Slov. Neurol. N., 2003; 5: 335–337.

35. Mathew, R. J., Wilson, W. H. Caffeine induced changes in cerebral circulation. Stroke., 1985; 16: 814–817.

36. Mathew, R. J., Barr, D. L., Weinman, M. L. Caffeine and cerebral blood flow. Br. J. Psychiatry, 1983; 143: 604–608.

37. Cameron, O. G., Modell, J. G., Hariharan, M. Caffeine and human cerebral blood flow: a positron emission tomography study. Life Sci., 1990; 47(13): 1141–1146.

38. Aronowski, J., Strong, R., Shirzadi, A., et al. Ethanol plus caffeine (caffeinol) for treatment of ischemic stroke: preclinical experience. Stroke, 2003; 34(5): 1246–1251.

39. Strong, R., Grotta, J. C., Aronowski, J. Combination of low dose ethanol and caffeine protects brain from damage produced by focal ischemia in rats. Neuropharmacology, 2000; 39(3): 515–522.

40. Zhao, X., Liu, S. J., Zhang, J., et al. Combining insulin-like growth factor derivatives plus caffeinol produces robust neuroprotection after stroke in rats. Stroke, 2005; 36(1): 129–134.

41. Piriyawat, P., Labiche, L. A., Burgin, W. S., et al. Pilot dose escalation study of caffeine plus ethanol (caffeinol) in acute ischemic stroke. Stroke, 2003; 34: 1242–1245.

42. Dash, P. K., Moore, A. N., Moody, M. R., et al. Post-trauma administration of caffeine plus ethanol reduces contusion volume and improves working memory in rats. J. Neurotrauma., 2004; 21(11): 1573–1583.

43. Bláha, M., Schwab, J., Vajnerová, O., et al. Model zavřeného poranění hlavy u potkana – experimentální studie. Cesk. Slov. Neurol N., 2009; 72/105(3): 235–241.