Acute administration of oestradiol or progesterone in a spinal cord ischaemia-reperfusion model in rats

Carregando...
Imagem de Miniatura
Citações na Scopus
9
Tipo de produção
article
Data de publicação
2018
Título da Revista
ISSN da Revista
Título do Volume
Editora
OXFORD UNIV PRESS
Citação
INTERACTIVE CARDIOVASCULAR AND THORACIC SURGERY, v.26, n.2, p.196-201, 2018
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
OBJECTIVES: Despite research into protective pharmacological adjuncts, paraplegia persists as a dreaded complication after thoracic and thoracoabdominal aortic interventions. Reports on gender-related neurological outcomes after ischaemic and traumatic brain injuries have led to increased interest in hormonal neuroprotective effects and have generated other studies seeking to prove the neuroprotective effects of the therapeutic administration of 17 beta-oestradiol and of progesterone. We hypothesised that acute administration of oestradiol or progesterone would prevent or attenuate spinal cord ischaemic injury induced by occlusion of the descending thoracic aorta. METHODS: Male rats were divided into groups receiving 280 A mu g/kg of 17 beta-oestradiol or 4 mg/kg of progesterone or vehicle 30 min before transitory endovascular occlusion of the proximal descending thoracic aorta for 12 min. Hindlimb motor function was assessed by a functional grading scale (that of Basso, Beattie and Bresnahan) for 14 days after reperfusion. On the 14th day, a segment of the thoracolumbar spinal cord was harvested and prepared for histological and immunohistochemical analyses. RESULTS: There was significant impairment of the motor function of the hindlimb in the 3 study groups, with partial improvement noticed over time, but no difference was detected between the groups. On Day 1 of assessment, the 17 beta-oestradiol group had a functional score of 9.8 (0.0-16.5); the progesterone group, a score of 0.0 (0-17.1) and the control group, a score of 6.5 (0-16.9); on the 14th day, the 17 beta-oestradiol group had a functional score of 18.0 (4.4-19.4); the progesterone group had a score of 7.5 (0-18.5) and the control group had a score of 17.0 (0-19.9). Analysis of the grey matter showed that the number of viable neurons per section was not different between the study groups on the 14th day. Immunostaining of the spinal cord grey matter was also similar among the 3 groups. CONCLUSIONS: Acute administration of oestradiol or of progesterone 30 min before transitory occlusion of the proximal descending thoracic aorta of male rats could not prevent or attenuate spinal cord ischaemic injury based on an analysis of functional and histological outcomes.
Palavras-chave
Animal model, Aortic operation, Ischaemia-reperfusion injury, Spinal cord, Paraplegia, Related subjects, Surgery, Complication
Referências
  1. BASSO DM, 1995, J NEUROTRAUM, V12, P1, DOI 10.1089/neu.1995.12.1
  2. Breithaupt-Faloppa AC, 2014, SHOCK, V41, P208, DOI 10.1097/SHK.0000000000000092
  3. Brown CM, 2009, SEMIN REPROD MED, V27, P240, DOI 10.1055/s-0029-1216277
  4. Elkabes S, 2014, EXP NEUROL, V259, P28, DOI 10.1016/j.expneurol.2014.01.008
  5. Gibson CL, 2005, EXP NEUROL, V193, P522, DOI 10.1016/j.expneurol.2005.01.009
  6. Gibson CL, 2009, NEUROSCIENTIST, V15, P324, DOI 10.1177/1073858409333069
  7. Gravereaux EC, 2001, J VASC SURG, V34, P997, DOI 10.1067/mva.2001.119890
  8. Institute of Laboratory Animal Resources Commission on Life Sciences National Research Council, 1996, GUIDE CARE USE LAB A
  9. Ishrat T, 2012, NEUROSCIENCE, V210, P442, DOI 10.1016/j.neuroscience.2012.03.008
  10. Jacobs MJ, 2015, EUR J VASC ENDOVASC, V49, P410, DOI 10.1016/j.ejvs.2015.01.003
  11. Jiang N, 1996, BRAIN RES, V735, P101, DOI 10.1016/0006-8993(96)00605-1
  12. Judas GI, 2014, INTERACT CARDIOV TH, V18, P757, DOI 10.1093/icvts/ivu021
  13. Kanellopoulos GK, 1997, STROKE, V28, P2532, DOI 10.1161/01.STR.28.12.2532
  14. Khalaj L, 2011, NEUROCHEM RES, V36, P268, DOI 10.1007/s11064-010-0314-0
  15. KOYANAGI I, 1993, NEUROSURGERY, V33, P277
  16. Maeda T, 2012, J ANESTH, V26, P805, DOI 10.1007/s00540-012-1434-2
  17. Messe SR, 2008, NEUROCRIT CARE, V9, P344, DOI 10.1007/s12028-008-9104-9
  18. Morishita K, 2003, ANN THORAC SURG, V76, P1967, DOI 10.1016/S0003-4975(03)01254-2
  19. Ramsey JBG, 2010, J NEUROTRAUM, V27, P1709, DOI 10.1089/neu.2010.1382
  20. Saito T, 2011, ANESTH ANALG, V113, P565, DOI 10.1213/ANE.0b013e318224ac35
  21. Simon FHP, 2016, J VASC SURG, V64, P1797, DOI 10.1016/j.jvs.2015.10.011
  22. Singer CA, 1996, NEUROSCI LETT, V212, P13, DOI 10.1016/0304-3940(96)12760-9
  23. Sousa PTR, 2017, J VASC SURG, DOI [10.1016/j.jvs.2016.12.125., DOI 10.1016/J.JVS.2016.12.125]
  24. Suzuki S, 2009, FRONT NEUROENDOCRIN, V30, P201, DOI 10.1016/j.yfrne.2009.04.007
  25. Taira Y, 1996, STROKE, V27, P1850, DOI 10.1161/01.STR.27.10.1850
  26. Toung TJK, 1998, STROKE, V29, P1666, DOI 10.1161/01.STR.29.8.1666
  27. Umehara S, 2010, ANESTH ANALG, V110, P1133, DOI 10.1213/ANE.0b013e3181cdb06b
  28. Vandenberk N, 2013, AM J EMERG MED, V31, P581, DOI 10.1016/j.ajem.2012.09.025
  29. Wilson ME, 2002, MOL BRAIN RES, V102, P48, DOI 10.1016/S0169-328X(02)00181-X
  30. Wise PM, 2000, BIOL REPROD, V63, P982, DOI 10.1095/biolreprod63.4.982
  31. Wynn M, 2016, J VASC SURG, V64, P289, DOI 10.1016/j.jvs.2015.12.060