Hostname: page-component-848d4c4894-4rdrl Total loading time: 0 Render date: 2024-06-23T11:51:44.902Z Has data issue: false hasContentIssue false
  • English
  • Français

Quantitative analysis of influence of sevoflurane on the reactivity of microglial cells in the course of the experimental model of intracerebral haemorrhage

Published online by Cambridge University Press:  24 May 2006

Z. Karwacki ,
P. Kowiański ,
J. Dziewiatkowski ,
B. Domaradzka-Pytel ,
B. Ludkiewicz ,
S. Wójcik ,
O. Narkiewicz  and
J. Moryś
Z. Karwacki
Affiliation:
Medical University of Gdańsk, Department of Neuroanaesthesiology, Gdańsk, Poland
P. Kowiański
Affiliation:
Medical University of Gdańsk, Department of Anatomy and Neurobiology, Gdańsk, Poland
J. Dziewiatkowski
Affiliation:
Medical University of Gdańsk, Department of Anatomy and Neurobiology, Gdańsk, Poland
B. Domaradzka-Pytel
Affiliation:
Medical University of Gdańsk, Department of Anatomy and Neurobiology, Gdańsk, Poland
B. Ludkiewicz
Affiliation:
Medical University of Gdańsk, Department of Anatomy and Neurobiology, Gdańsk, Poland
S. Wójcik
Affiliation:
Medical University of Gdańsk, Department of Anatomy and Neurobiology, Gdańsk, Poland
O. Narkiewicz
Affiliation:
Medical University of Gdańsk, Department of Anatomy and Neurobiology, Gdańsk, Poland
J. Moryś
Affiliation:
Medical University of Gdańsk, Department of Anatomy and Neurobiology, Gdańsk, Poland
Get access

Abstract

Summary

Backgrounds: Microglial cells play an important role in the pathophysiology of intracerebral haemorrhage. We have examined the possible influence of sevoflurane on the reactivity of microglial cells during intracranial haemorrhage. Methods: Forty adult male rats were divided into two groups. All animals were anaesthetized with fentanyl, dehydrobenzperidol and midazolam. In the experimental group animals additionally received sevoflurane 2.2 vol% end-tidal concentration. Intracranial haemorrhage was produced through infusion of blood into the striatum. The microglial cell population (numerical density of immunoreactive cells and their distribution) was assessed on days 1, 3, 7, 14 and 21 after producing a haematoma using antibodies OX42 and OX6. Results: In the control group significant differences in the density of OX42-ir cells between 3rd and 7th (81.86 vs. 129.99) (95% CI: −77.99 to −18.25, P = 0.0035) and between 14th and 21st (105.36 vs. 63.81) (95% CI: 13.21 to 69.89, P = 0.006) survival days were observed. However, significant increase of percentage of amoeboid OX42-ir cells between 3rd and 7th (0.98 vs. 48.71) (95% CI: −52.17 to −43.30, P = 0.0001) and between 7th and 14th (48.71 vs. 58.47) (95% CI: −13.96 to −5.55, P = 0.0002) and then their decrease – between 14th and 21st (58.47 vs. 31.74) (95% CI: 22.52 to 30.93, P = 0.0001) days of observation were noted. In the sevoflurane groups OX42-ir cells were not found. On the 3rd day the density of OX6-ir cells in the sevoflurane group was significantly lower than that in the control group (12.39 vs. 34.57) (95% CI: −49.78 to −2.96, P = 0.02). The percentage of an amoeboid form of OX6-ir cells was significantly lower in the sevoflurane group than that in the control group (27.31 vs. 82.03) (95% CI: −72.52 to −36.92, P = 0.0001) (58.76 vs. 82.37) (95% CI: −38.81 to −8.41, P = 0.003) (42.87 vs. 81.55) (95% CI: −53.23 to −24.10, P = 0.0001) respectively for 3rd, 7th and 14th days of survival. Conclusion: Administration of sevoflurane during anaesthesia in animals with intracerebral haemorrhage evoked a decrease of activation of the microglial cells.

Keywords

ANAESTHETICS INHALATIONAL, sevofluraneMICROGLIARATCEREBRAL HAEMORRHAGE
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 23 , Issue 10 , October 2006 , pp. 874 - 881
Copyright
2006 European Society of Anaesthesiology

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Altumbabic M, Peeling J, Del Bigio MR. Intracerebral hemorrhage in the rat: effects of hematoma aspiration. Stroke 1998; 29: 1917–1923.Google Scholar
Jellinger K. Pathology and aetiology of supratentorial haemorrhage. In: Pia HW, Langmaid C, Zierski J, eds. Spontaneous Intracerebral Haematomas. Advances in Diagnosis and Therapy.Berlin, Heidelberg, New York: Springer-Verlag, 1980: 131–135.
Nath FP, Kelly PT, Jenkins A, Mendelov AD, Graham DI, Teasdale GM. Effects of experimental intracerebral hemorrhage on blood flow, capillary permeability, and histochemistry. J Neurosurg 1987; 66: 555–562.Google Scholar
Nehls DG, Mendelow AD, Graham DI, Sinar EJ, Teasdale GM. Experimental intracerebral hemorrhage: progression of hemodynamic changes after production of a spontaneous mass lesion. Neurosurgery 1988; 23: 439–444.Google Scholar
Hickenbottom SL, Grotta JC, Strong R, Denner LA, Aronowski J. Nuclear factor-kappa B and cell death after experimental intracerebral hemorrhage in rats. Stroke 1999; 30 (11): 2472–2477.Google Scholar
Megyeri P, Abraham CS, Temesvari P. Recombinant human tumor necrosis factor a constrics pial arterioles and increases blood–brain barrier permeability in newborn piglets. Neurosci Lett 1992; 148: 137–140.Google Scholar
Xi G, Hua Y, Bhasin R, Emis SR, Keep RF, Hoff JT. Mechanisms of edema formation after intracerebral hemorrhage. Effects of extravasatad red blood cells on blood flow and blood–brain barrier integrity. Stroke 2001; 32: 2932–2938.Google Scholar
Xi G, Hua Y, Keep RF, Younger JG, Hoff JT. Systemic complement depletion diminishes perihematomal brain edema in rats. Stroke 2001; 32: 162–168.Google Scholar
Stence N, Waite M, Dailey ME. Dynamic of microglial activation a confocal time-lapse analysis in hipocampal slices. Glia 2001; 33: 256–266.Google Scholar
Silva Y, Leira R, Tejada J, Lainez JM, Castillo J, Davalos A. Molecular signatures of vascular injury are associated with early growth of intracerebral hemorrhage. Stroke 2005; 36: 86–91.Google Scholar
Holmin S, Mathiesen T. Intracerebral administration of interleukin-1beta and induction of inflammation, apoptosis and vasogenic edema. J Neurosurg 2000; 92: 108–120.Google Scholar
Gong C, Hoff JT, Keep RF. Acute inflammatory reaction following experimental intracerebral hemorrhage in rat. Brain Res 2000; 871: 55–65.Google Scholar
Koeppen AH, Dickson AC, McEvoy JA. The cellular reactions to experimental intracerebral hemorrhage. J Neurol Sci (Suppl)1995; 134: 102–112.Google Scholar
Kowiański P, Karwacki Z, Dziewiatkowski Jet al. Evolution of microglial and astroglial response during experimental intracerebral haemorrhage in the rat. Folia Neuropathol 2003; 41 (3): 123–130.Google Scholar
Saver JL, Hankey G, Hon CS. Surgery for primary intracerebral hemorrhage: meta-analysis of CT-era studies. Stroke 1998; 29: 1477–1478.Google Scholar
Auer LM, Deinsberger W, Neiderkorn Ket al. Endoscopic surgery versus medical treatment for spontaneous intracerebral hematoma: a randomized study. J Neurosurg 1989; 70: 530–535.Google Scholar
Bundgaard H, von Oettingen G, Larsen KMet al. Effects of sevoflurane on intracranial pressure, cerebral blood flow and cerebral metabolism. A dose-response study in patients subjected to craniotomy for cerebral tumors. Acta Anaesthesiol Scand 1998; 42 (6): 621–627.Google Scholar
Nakajima Y, Moriwaki G, Ikeda K, Fujise Y. The effects of sevoflurane on recovery of brain energy metabolism after cerebral ischemia in the rat: a comparison with isoflurane and halothane. Anesth Analg 1997; 85 (3): 593–599.Google Scholar
Heindl B, Reihle FM, Zhler S, Conzen PF, Becker BF. Sevoflurane and isoflurane protect the reperfused guinea pig heart by reducing postischemic adhesion of polymorphonuclear neutrophils. Anesthesiology 1999; 91: 521–530.Google Scholar
Horn NA, de Rossi L, Robitzsch T, Hecker KE, Hutschenreuter G, Rossaint R. Sevoflurane inhibits unstimulated and agonist-induced platelet antigen expression and platelet function in whole blood in vitro. Anesthesiology 2001; 95: 1220–1225.Google Scholar
Kowalski Ch, Zahler S, Becker BFet al. Halothane, isoflurane, and sevoflurane reduce postischemic adhesion of neutrophils in the coronary system. Anesthesiology 1997; 86: 188–195.Google Scholar
Mobert J, Zahler S, Becker BF, Conzen PF. Inhibition of neutrophil activation by volatile anesthetic decreases adhesion to cultured human endothelial cells. Anesthesiology 1999; 90: 1372–1381.Google Scholar
Otten U, Marz P, Hesse K, Hock C, Kunz D, Rose-John S. Signals regulating neurotrophin expression in glial cells. In: Castellano-Lopez B, Nieto-Sampedro M, eds. Glial Cell Function.Amsterdam, London, New York, Oxford, Paris, Shanon, Tokyo: Elsevier, 2001: 545–565.
Mitsuhata H, Shimizu R, Yokoyama MM. Suppressive effects of volatile anesthetics on cytokine release in human peripheral blood mononuclear cells. Int J Immunopharmacol 1995; 17: 529–534.Google Scholar
Gimenez y Ribotta M, Menet V, Privat A. The role of astrocytes in axonal regeneration in the mannalian CNS. In: Castellano-Lopez B, Nieto-Sampedro M, eds. Glial Cell Function.Amsterdam, London, New York, Oxford, Paris, Shanon, Tokyo: Elsevier, 2001: 588–610.[net]
Brugger B, Bauer A, Finsterer U, Bernasconi P, Kreimeier U, Christ F. Microvasular changes during anesthesia: sevoflurane compared with propofol. Acta Anaesthesiol Scand 2002; 46: 481–487.Google Scholar
Chi OZ, Anwar M, Sinha AK, Wei H, Klein SL, Weiss HR. Effects of isoflurane on transport across the blood–brain barrier. Anesthesiology 1992; 76: 426–431.Google Scholar
Oshima T, Karasawa F, Okazaki Y, Wada H, Sato T. Effects of sevoflurane on cerebral blood flow and cerebral metabolic rate of oxygen in human beings: a comparison with isoflurane. Eur J Anaesthesiol 2003; 20: 543–547.Google Scholar
Vinje ML, Moe MC, Valo ET, Berg-Johnsen J. The effect of sevoflurane on glutamate release and uptake in rat cerebrocortical presynaptic terminals. Acta Anaesthesiol Scand 2002; 46: 103–108.Google Scholar
Engelhard K, Werner C, Eberspacher Eet al. Sevoflurane and propofol influence the expression of apoptosis-regulating proteins after cerebral ischaemia and reperfusion in rats. Eur J Anaesthesiol 2004; 21: 530–537.Google Scholar