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Morphometrical Evaluation of Triflusal in Brain Infarction

  • N. Heye
  • A. Campos
  • S. Sampaolo
  • J. Cervos-Navarro
Conference paper
Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 57)

Abstract

MCA occlusion in animals is a common model for experimental stroke. In previous studies we have shown that one of the factors, which influence evolution of an infarct is microthrombosis in the area of infarction and in the surrounding brain tissue.

The present study was undertaken for assessment of the number of microthrombi and of the size of brain infarcting in rats treated with the antiaggregatory substance Triflusal.

7 groups of Sprague-Dawley rats, each group consisting of 6 animals, underwent transsphenoidal MCA occlusion. The animals received Triflusal in various amounts from day 2 till day 6. At day 7 animals were decapitated and the brains were fixed in formaldehyde. The brain was dissected at the level of the optic chiasm and embedded in paraffin. Fresh microthrombi were detected py PTAH (Phosphotungstic acid hematoxylin) staining. In each animal the hemisphere with the ischemic lesion as well as the contralateral hemisphere were examined. The area of both hemispheres was calculated by subtraction of the ventricle area from the total brain area of a section. Infarct was defined as the region of necrosis which was sharply demarcated from normal brain. The infarcted area was planimetrically measured to obtain a ratio of infarcted to normal brain.

A correlation between the effect of Triflusal, number of microthrombi and size of the infarcted area could be demonstrated. The pathogenetic role of the microthrombi in the evolution of cerebral infarction as well as the effect of Triflusal in different dosages on the number of microthrombi could be clearly assessed by quantitative morphometry.

Keywords

Cerebral infarction microthrombosis antiaggregatory therapy triflusal 

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References

  1. 1.
    Benderson JB, Pitts LH, Tsuji M,Nishimura MC, Davis RL, Bartowski H (1986) Rat middle cerebral arteryocclusion: evaluation of the model and development of a neurologicalexamination. Stroke 17: 472–476CrossRefGoogle Scholar
  2. 2.
    Castellarnau de C, Sancho MJ, Vila L, Albors M, Rutllant MLL (1988)Effects and interaction studies of triflusal and other salicylic derivates oncyclooxygenase in rats. Prostaglandins Leukotrienes and Essential Fatty Acids31: 83–89CrossRefGoogle Scholar
  3. 3.
    DietrichWD, Prado R, Watson BD, Nakayama H (1988) Middle cerebral artery thrombosis:acute blood-brain barrier consequences. J Neuropath Exp Neurol 47: 443–451PubMedCrossRefGoogle Scholar
  4. 4.
    Duverger D, Lecoffre C, MacKenzie ET (1985)Histological quantification of cerebral infarction following middle cerebral arteryocclusion in various rat strains. J Cerebral Blood Flow Metabol 5 [Suppll]:415–416Google Scholar
  5. 5.
    Rubino GJ, Young W (1988) Ischemiccortical lesions after permanent occlusion of individual middle cerebral arterybranches in rats. Stroke 19: 870–877PubMedCrossRefGoogle Scholar
  6. 6.
    Sampaolo S, Cervós-Navarro J, Djouchadar D, Figols J (1987) Clinicaland experimental evidence of microthrombosis in cerebral ischemia. In: Hartmann A,Kuschinsky W (eds) Cerebral ischemia and hemorheology. Springer, BerlinHeidelberg New York, pp 386–393CrossRefGoogle Scholar
  7. 7.
    Shah AB, Beamer N,Coull BM (1985) Enhanced in vivoplatelet activation in subtypes ofischemic stroke. Stroke 16: 643–647PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 1993

Authors and Affiliations

  • N. Heye
    • 1
  • A. Campos
    • 1
  • S. Sampaolo
    • 1
  • J. Cervos-Navarro
    • 1
  1. 1.Institute of Neuropathology, Klinikum SteglitzFreie Universität BerlinBerlinFederal Republic of Germany

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