Effects of Anaesthetic Agents on Cerebral Blood Flow and Brain Oedema from a Focal Lesion in Rabbit Brain

  • R. Murr
  • L. Schürer
  • S. Berger
  • R. Enzenbach
  • A. Baethmann
Conference paper
Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 51)


Anaesthetic agents reduce cerebral metabolism and may impair coupling of cerebral blood flow and metabolism. We analyzed the effects of isoflurane (I) (1 MAC), fentanyl (F), thiopental (T) (32.5 mg/ kg × hr) and α-chloralose (C) on rCBF and brain oedema formation after a focal cerebral injury (cold lesion) in rabbits (n = 6 per group). In the isoflurane group, angiotensin II (0.15 µg/kg × min) was given to maintain blood pressure. rCBF of cerebral cortex was measured 3 times per hr by H2-clearance with needle electrodes placed at different distances to the lesion during 6 hrs after induction of trauma. Thereafter, samples of white matter were obtained near the focal lesions and from corresponding areas of the contralateral hemisphere for measurement of specific gravity (SG) by a linear density column (Percoll R). Blood pressure was 78, 86, 72, and 88 mmHg for groups I, F, T, and C, respectively. After induction of the lesion, hyperemia of approximately 1 hr was observed in all groups. This was most pronounced distant to the lesion. Close to the lesion rCBF remained unchanged in groups C and T, but fell significantly below control in I and F. The blood flow response distant to the trauma was characterized by a moderate increase (C), or no alteration (T), while isoflurane animals had a pronounced secondary hyperemia for about 3 hrs. With fentanyl, however, rCBF was markedly reduced in this area. SG of white matter close to the lesion decreased significantly to values of 1.032 g/cm3 (I, F, T), or 1.031 (C), indicative of oedema. Specific gravity was 1.034 in the contralateral hemisphere (control). The differences in SG adjacent to the lesion between groups I, F, and T were statistically not significant. Further, no significant differences were observed between the specific gravity of group C and the other groups. It is concluded, that with an open skull preparation formation of posttraumatic brain oedema from a focal cerebral lesion does not seem to be markedly affected by either hyperemia, or a blood flow reduction from various anaesthetic agents, at least during the first hours after trauma.


Cerebral Blood Flow Specific Gravity Anaesthetic Agent Brain Oedema Focal Lesion 
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  1. 1.
    Cucchiara RF, Theye RA, Michenfelder JD (1974) The effects of isoflurane on canine cerebral metabolism and blood flow. Anaesthesiology 40: 571–574CrossRefGoogle Scholar
  2. 2.
    DeWitt DW, Jenkins LW, Wei EP, Lutz HJ, Becker DP, Kontos HA (1986) Effects of fluid percussion brain injury on regional cerebral blood flow and pial arterial diameter. J Neurosurg 64: 787–794PubMedCrossRefGoogle Scholar
  3. 3.
    Frei HJ, Wallenfang W. Pöll H, Reulen HJ, Schubert R, Brock M (1973) Regional cerebral blood flow and regional metabolism in cold induced oedema. Acta Neurochir (Wien) 29: 15–28CrossRefGoogle Scholar
  4. 4.
    Grosslight K, Foster R, Colohan AR, Bedford RF (1985) Isoflurane for neuroanaesthesia: risk factors for increases in intra-cranial pressure. Anaesthesiology 63: 533–536CrossRefGoogle Scholar
  5. 5.
    Kaieda R, Todd MM, Weeks JB, Warner DS (1989) A comparison of the effects of halothane, isoflurane, and pentobarbital anaesthesia on intracranial pressure and cerebral oedema formation following brain injury in rabbits. Anaesthesiology 71: 571–579CrossRefGoogle Scholar
  6. 6.
    Klatzo I, Piraux A, Laskowski EJ (1959) The relationship between oedema, blood-brain barrier and tissue elements in a local brain injury. J Neuropath Exp Neurol 17: 548–564CrossRefGoogle Scholar
  7. 7.
    Michenfelder JD (1980) The cerebral circulation. In: Prys-Roberts C (ed) The circulation in anaesthesia. Blackwell Scient Publ, OxfordGoogle Scholar
  8. 8.
    Murr R, Berger S, Schürer L, Baethmann A (1989) Regional cerebral blood flow and tissue pO2 after focal trauma: effects of isoflurane and fentanyl. In: Hammersen F, Messmer K (eds) Cerebral microcirculation. Progr Appl Microcirc. Karger, Basel, pp 61–70Google Scholar
  9. 9.
    Pappius HM (1981) Local cerebral glucose utilization in thermally traumatized brain. Ann Neurol 9: 484–491PubMedCrossRefGoogle Scholar
  10. 10.
    Smith AL, Marque JJ (1976) Anaesthetics and cerebral oedema. Anaesthesiology 45: 64–72CrossRefGoogle Scholar
  11. 11.
    Yamamoto L, Soejima T, Meyer E, Feindel W (1976) Early haemodynamic changes at the microcirculatory level following cryogenic injury over the cortex. In: Pappius HM, Feindel W (eds) Dynamics of brain oedema. Springer, Berlin Heidelberg New York, pp 59–62CrossRefGoogle Scholar

Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • R. Murr
    • 2
  • L. Schürer
    • 3
  • S. Berger
    • 3
  • R. Enzenbach
    • 1
  • A. Baethmann
    • 3
  1. 1.Institute AnesthesiologyLMU Munich, Klinikum GroßhadernMünchenFederal Republic of Germany
  2. 2.Institute AnaesthesiologyLMU Munich, Klinikum GroßhadernMünchen 70Federal Republic of Germany
  3. 3.Institute Surgical ResearchLMU Munich, Klinikum GroßhadernMünchenFederal Republic of Germany

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