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Lesão de isquemia e reperfusão hepáticas em cães: estudos histológicos sobre necrose hepatocítica, conteúdo de glicogênio hepático e contagem tecidual de polimorfonucleares

Hepatic ischaemia and reperfusion lesion in the dog: investigations of hepatocellular necrosis, hepatic glycogen content and polymorphonuclear tissue cells counting

Resumos

No transplante hepático, a fisiopatologia da lesão de isquemia e reperfusão do fígado não é completamente conhecida. Várias preparações experimentais têm sido usadas para estudos de tal lesão. Para tal fim, no presente trabalho, um modelo modificado foi proposto e avaliado. Vinte cães mestiços, pesando 15,25 ± 1,21 kg, sob anestesia geral, foram distribuídos em dois grupos de investigação: 1. Grupo Teste (n = 10) - os animais foram submetidos a desvascularização de 70% da massa hepática, por período de noventa minutos, seguida de revascularização do fígado. Durante o período de isquemia, a descompressão venosa esplâncnica foi realizada através dos lobos caudado e lateral direito; 2. Grupo Controle (n = 10) - os cães foram submetidos a operação simulada. Em todos os animais foram realizadas biópsias do fígado. O método foi avaliado através de determinações de Necrose Hepatocítica (NH), Conteúdo de Glicogênio Hepático (CGH) e Contagem Tecidual de Polimorfonucleares (CTPMN), realizadas aos cinco minutos antes da isquemia (To) cinco minutos antes da reperfusão (T1) e uma hora (T2) e cinco horas (T3) após a reperfusão. Os resultados permitiram concluir com uma confiança de 95% que: I. Houve aumento progressivo de intensidade de NH e diminuição do CGH durante os estágios de isquemia e de reperfusão hepáticas; 2. Não foi comprovada diferença significativa na CTPMN entre os grupos investigados. As alterações histológicas verificadas são indicativas de NH efetiva, decorrente de isquemia e reperfusão do fígado.

Fígado; Isquemia normotérmica; Reperfusão; Necrose hepatocítica; Glicogênio hepático; Neutrófilos polimorfonucleares; Cães


In the liver transplantation pathophysiology of hepatic ischaemia and reperfusion lesion is not completely understood. Several experimental models have been used to perform studies on tissue hipoxia and reperfusion of the liver. The present work, presents a modified model proposed to evaluate this kind of lesion. Twenty mongrel dogs, weighting 15.25 ± 1.21 kg, under general anesthesia, were referred to the following investigation groups: 1. Test Group (n = 10) - Animals were submitted to devascularization of 70 per cent of hepatic mass during a ninety minutes period, followed by liver reperfusion. During the time of ischaemia, splancnic venous decompression was provided through the right lateral and caudate lobes; 2. Control Group (n = 10) - The dogs were submitted to a sham operation. Liver samples were taken at 5 minutes before ischaemia (T0) 5 minutes before reperfusion (T1) and I hour (T2) and 5 hours (T3) after hepatic reperfusion. The method was evaluated by hepatic cells necrosis (HCN), hepatic glycogen content (HGC) and tissue polymorphonuclear cells counting (PMNCC). The results showed with a 95 per cent of confidence that: I. There was a progressive rise in HCN intensity and a fall in HGC, during the hepatic ischaemia and reperfusion stages; 2. There was no evidence of significant differences in PMNCC between the investigated groups. The verified histologic change are expression of effective HCN derived from liver isquemia and reperfusion.

Liver; Normothermic ischaemia; Reperfusion; Hepatic necrosis; Hepatic glycogen; Polymorphonuclear cells; Dogs


ARTIGOS ORIGINAIS

Lesão de isquemia e reperfusão hepáticas em cães. Estudos histológicos sobre necrose hepatocítica, conteúdo de glicogênio hepático e contagem tecidual de polimorfonucleares

Hepatic ischaemia and reperfusion lesion in the dog. Investigations of hepatocellular necrosis, hepatic glycogen content and polymorphonuclear tissue cells counting

Renato Dornelas Câmara Neto, TCBC-PEI; Silvia Limongi LopesII; Antônio Roberto de Barros CoelhoI; Ayrton Ponce de Souza, TCBC-PEIII; Álvaro Antônio Bandeira Ferraz, TCBC-PEI; Edmundo Machado Ferraz, TCBC-PEIV

IProfessor Adjunto, Doutor do Departamento de Cirurgia do Centro de Ciências da Saúde, Hospital das Clínicas - UFPE

IIProfessor Adjunto, Doutor do Departamento de Patologia do Centro de Ciências da Saúde da UFPE

IIIProfessor dos Cursos de P6s-Graduação em Cirurgia, Doutor, Livre-Docente do Departamento de Cirurgia do Centro de Ciências da Saúde do Hospital das Clínicas - UFPE

IVProfessor Titular, Doutor, Livre-Docente do Deptartamento de Cirurgia do Centro de Ciências da Saúde do Hospital das Clínicas da UFPE

Endereço para correspondência Endereço para correspondência: Prof. Edmundo Machado Ferraz Rua Dom Sebastião Leme, 173/2.501 52011-160 - Recife-PE

RESUMO

No transplante hepático, a fisiopatologia da lesão de isquemia e reperfusão do fígado não é completamente conhecida. Várias preparações experimentais têm sido usadas para estudos de tal lesão. Para tal fim, no presente trabalho, um modelo modificado foi proposto e avaliado. Vinte cães mestiços, pesando 15,25 ± 1,21 kg, sob anestesia geral, foram distribuídos em dois grupos de investigação: 1. Grupo Teste (n = 10) - os animais foram submetidos a desvascularização de 70% da massa hepática, por período de noventa minutos, seguida de revascularização do fígado. Durante o período de isquemia, a descompressão venosa esplâncnica foi realizada através dos lobos caudado e lateral direito; 2. Grupo Controle (n = 10) - os cães foram submetidos a operação simulada. Em todos os animais foram realizadas biópsias do fígado. O método foi avaliado através de determinações de Necrose Hepatocítica (NH), Conteúdo de Glicogênio Hepático (CGH) e Contagem Tecidual de Polimorfonucleares (CTPMN), realizadas aos cinco minutos antes da isquemia (To) cinco minutos antes da reperfusão (T1) e uma hora (T2) e cinco horas (T3) após a reperfusão. Os resultados permitiram concluir com uma confiança de 95% que: I. Houve aumento progressivo de intensidade de NH e diminuição do CGH durante os estágios de isquemia e de reperfusão hepáticas; 2. Não foi comprovada diferença significativa na CTPMN entre os grupos investigados. As alterações histológicas verificadas são indicativas de NH efetiva, decorrente de isquemia e reperfusão do fígado.

Unitermos: Fígado; Isquemia normotérmica; Reperfusão; Necrose hepatocítica; Glicogênio hepático; Neutrófilos polimorfonucleares; Cães.

ABSTRACT

In the liver transplantation pathophysiology of hepatic ischaemia and reperfusion lesion is not completely understood. Several experimental models have been used to perform studies on tissue hipoxia and reperfusion of the liver. The present work, presents a modified model proposed to evaluate this kind of lesion. Twenty mongrel dogs, weighting 15.25 ± 1.21 kg, under general anesthesia, were referred to the following investigation groups: 1. Test Group (n = 10) - Animals were submitted to devascularization of 70 per cent of hepatic mass during a ninety minutes period, followed by liver reperfusion. During the time of ischaemia, splancnic venous decompression was provided through the right lateral and caudate lobes; 2. Control Group (n = 10) - The dogs were submitted to a sham operation. Liver samples were taken at 5 minutes before ischaemia (T0) 5 minutes before reperfusion (T1) and I hour (T2) and 5 hours (T3) after hepatic reperfusion. The method was evaluated by hepatic cells necrosis (HCN), hepatic glycogen content (HGC) and tissue polymorphonuclear cells counting (PMNCC). The results showed with a 95 per cent of confidence that: I. There was a progressive rise in HCN intensity and a fall in HGC, during the hepatic ischaemia and reperfusion stages; 2. There was no evidence of significant differences in PMNCC between the investigated groups. The verified histologic change are expression of effective HCN derived from liver isquemia and reperfusion.

Key words: Liver; Normothermic ischaemia; Reperfusion; Hepatic necrosis; Hepatic glycogen; Polymorphonuclear cells; Dogs.

Texto completo disponível apenas em PDF.

Full text available only in PDF format.

REFERÊNCIAS

1. Aggarwal S, Kang Y, Freeman JA, et al. Post-reperfusion syndrome: cardiovascular collapse following hepatic reperfusion during liver transplantation. Transplant Proc 1987;19(4) supl 3:54-55.

2. Aggarwal S, Kang Y, Freeman JA, et al. Post-reperfusion syndrome: hypotension after reperfusion of the transplanted liver. J Crit Care 1993;8(3): 154.

3. Arll S, Monden K., Adachi Y, et al. Pathogenic role of Kupffer cell activation in the reperfusion injury of cold-preserved liver. Transplantation, 1994;58(10):1072-1077.

4. Blanot 5, Gillon MC, Lopes I, et al. Circulating endotoxins and postreperfusion syndrome during orthotopic liver transplantation. Transplantation 1 995;60( I): 103-106.

5. Fukuzawa K., Emre S, Senyuz O, et al. N-acetylcysteine ameliorates reperfusion injury after warm hepatic ischemia. Transplanfation, 1995;59(1):6-9.

6. Kahn D, Hickman R, Dent DM, et al. For how long can the liver tolerate ischaemia? Eur Surg Res 1986;18:277-282.

7. Ontell SI, Makowka L, Trager J, et al. Pharmacologic modulation of experimental postischemic hepatic function. Ann Surg 1989; 209 (2): 200-210.

8. Peng XX, Currin RT, Thunnan RG, et al. Protection by pentoxiflylline against normothermic liver ischemia/reperfusion in rats. Transplantation 1995;59(11):1537-1541.

9. Piratvisuth T, Dunne JB, Williams R, et al. Amlodipine improves hepatic hemodynamic and metabolic function in the isolated perfused rat liver after sequential cold and warm ischemia. Transplanlalíon 1995; 60(1):23-28.

10. Suehiro T, Boros P, Emre P, et al. Value of caval effluent in predicting early graft function after orthotopic liver transplantation. Transplanl Proc 1997;29(1/2):469-470.

11. Harris KA, Wallace C, Wall WJ. Tolerance of the liver to ischemia in the pig. J Surg Res 1982;33:524-530.

12. Hasselgren P. Prevention and treatment of ischemia of the liver. Surg Gynecol Obstet 1987;164:187-196.

13. Mays E Truman. Simpósio sobre cirurgia hepática: Oclusão vascular. Clín Cír Am N 1977;57(2):291-323.

14. Barbieri A, Zonta F, Saracino ML, et al. Evaluation of the reperfusion syndrome after liver ischemia in the rat. J. Surg Res New York NY , 1996; 62(suppl. 2): 153-158.

15. DeWeese MS, Lewis Jr. C, Mich AA. Partial hepatectomy in the dog: an experimental study. Surgery 1951;30(4):642-651.

16. Emond J, Wachs ME, Renz JF, et al. Total vascular exclusion for major hepatectomy in patients with abnormal liver parenchyma. Arch Surg 1995;130:824-831.

17. Furnival CM, Mackenzie RJ, Blumgart LH. The mechanism of impaired coagulation after partial hepatectomy in in the dogs. Surg Gynecol Obstet 1976;143: 81-86.

18. Huguet C, Gavelli A, Chieco PA, et al. Liver ischemia for hepatic resection: Where is the limit? Surgery 1992;111:251-259.

19. Huguet C, Nordlinger B, Bloch P, et al. Tolerance of the human liver to prolonged normothermic ischemia. Arch Surg 1978;113:1448-.1451.

20. Child III CG - The liver and Shock – cap. 9. In: The hepatic circulation and portal hypertension. Philadelphia PA, W.B. Saunders Company, 1954. p. 122-126.

21. Fonkalsrud EW. Common mechanisms of hypotension in irreversible shock and liver transplantation. Surg Gynecol Obstet 1969; 128(3): 601-602.

22. Rappaport AM, MacDonald MH, Borowy ZJ. Hepatic coma following ischemia of the liver. Surg Gynecol Obstet 1953;97:748-762.

23. Ito Y, Takahashi T, Saro K, et al. Effects of oxigenation during initial perfusion of the liver on hepatic metabolism and morphology following simple hypothermic storage in brain-dead rabbits. Transplant Proc 1997;29(1/2):359-361.

24. Kootstra G. The asystolic, or non-heartbeating donor. Transplantalíon 1997;63(7):917-921.

25. Kusano T, Shiraishi M, Miyaguni T, et al. Organ preserving effect of lidocaine administration in the model of orthotopic liver trans- plantation from non-heartbeating donors. Transplant Proc 1996; 28(3):1928-1929.

26. Lindell SL, Southard JH, Vreugdenhil P, et al. Kupffer cells depress hepatocyte protein synthesis on cold storage of the rat liver. Transplantation 1994;58(8):869-874.

27. Nauta RJ, Tsimoyiannis E, Uribe M, et al. Oxigen-derived free radicaIs in the hepatic ischemia and reperfusion injury in the rat. Surg Gynecol Obstet 1990;171:120-125.

28. Schon MR, Hunt CJ, Pegg DE, et al. The possibility of resuscitating livers after warm ischemic injury. Transplantation 1993;56(1): 24-31.

29. Takada Y, Taniguchi H, Fukunaga K, et al. Hepatic allograft procurement from non-heartbeating donors. Limits of warm ischemia in porcine liver transplantation. Transplantation 1997;63(3):369-373.

30. Garcia- Valdecasas JC, Rull R, Grande L, et al. Prostacyclin, thromboxane, and oxigen free radicals and postoperative liver function in human liver transplantation. Transplantation 1995; 60(7):662-667.

31. Ikeda T, Yanaga K, Kishikawa K, et al. Ischemic injury in liver transplantation: Difference in injury sites between warm and cold ischemia in rats. Hepatology 1992;16(2):454-465.

32. Isai H, Nakajima Y, Kimura J, et al. Calcium mobilization in porcine orthotopic liver transplantation. Transplant Proc 1996;28(3): 1.780- 1.781.

33. Ishine N, Tanaka N, Yagi T, et al - Postreperfusion syndrome in swine liver transplantation: Comparison between orthotopic liver transplantation and total hepatectomy with portacaval shunt using aortic graft. Transplant Proc 1996;28(3): 1.756-1.758.

34. Ishine N, Yagi T, Ishikawa T, et al. Hemodynamic analysis of post- reperfusion syndrome and the effect of preventing this syndrome using thromboxane A, synthetase inhibitor (OKY -046) in swine liver transplantation. Transplant Proc 1997;29(1/2):378-381.

35. Jugan E, Albaladejo P, Jayais p, et al. The failure of venovenous bypass to prevent graft liver postreperfusion syndrome. Transplantation 1992; 54(1):81-84.

36. Kamachi H, Nakajima Y, Isai H, et al. Study of liver function in a graft suffering from warm ischemia in porcine liver transplantation. Transplant Proc 1996;28(3):1.789-1.791.

37. Millis JM, Melinek J, Csete M, et al. Randomized controlled trial to evaluate flush and reperfusion techniques in liver transplantation. Transplantation 1997;63(3):397-403.

38. Oldhafer KJ, Schuttler W, Wiehe B, et al. Treatment of preservation/ reperfusion liver injury by the protease inhibitor aprotinin after ischemia storage. Transplant Proc 1991;23(5):2.380-2.381.

39. Paulsen AW, Valek TR, Blessing WS, et al. Hemodynamics during liver transplantation with veno-venous bypass. Transplant Proc 1987; 19(1):2.417-2.419.

40. Pirenne J, Gunson B, KhaleefH et al. Influence of ischemia-reperfusion injury on rejection after liver transplantation. Transplant Proc 1997; 29(1/2):366-367.

41. Sasaki H, Matsuno T, Tanaka N, et al. Activation of apoptosis during the reperfusion phase after rat liver ischemia. Transplant Proc 1996; 28(3):1.908-1.909.

42. Wu G, Tomei D, Bathurst IC, et al. Antiapoptotic compound to enhance hypothermic liver preservation. Transplantation 1997;63(6): 803- 809.

43. Colletti LM, Remick DG, Burtch GD, et al. Role of tumor necrosis factor - a in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat. J Clin lnvest 1990;85: 1.936-1.943.

44. Cursio R, Gugenheim J, Tovey M, et al. Protective properties of anti- IFNa/b Antibodies in normothermic hepatic ischaemia in the rat. Transplant Proc 1 996;28( 1):73-74.

45. Ohar OK, Nagasue N, Kimoto T, et al. The salutary effect of FK 506 in ischemia-reperfusion injury of the canine liver. Transplantation 1992; 54(4):583-588.

46. Farhood A, McGuire GM, Manning AM, et al. lntercellular adhesion molecule 1 (ICAM-l) expression and its role in neutrophil-induced ischemia-reperfusion injury in rat liver. J Leuk Biol, New York NY, 1995; 57:368-374.

47. Helling TS, Hacker KA, Kragel PJ, et al. Evidence for cytoprotection by prostaglandin E, with normothermic hepatic ischemia. J Surg Res 1994;56(4):309-313.

48. Swenson O, Grana L, lnouye T, et al. Immediate and long-term effects of acute hepatic ischemia. Arch Surg 1967;95:451-463.

49. Tomizawa N, Ohwada S, Ohya T, et al. Effects of neutrophil elastase inhibitor on reperfusion injury in the canine liver. Transplant Proc 1996;28(3): 1767-1768.

50. Vollmar B, Glasz J, Menger MO, et al. Leukocytes contribute to hepatic ischemia / reperfusion injury via intercellular adhesion molecule - I - mediated venular adherence. Surgery 1995; 117(2): 195-200.

51. VollmarB, GlaszJ, Post S, et al. Role ofmicrocirculatoryderangements in manifestation of portal triad cross-clamping-induced hepatic reperfusion injury. J Surg Res, New York NY, 1996; 60(1):49-54.

52. Mor E, Tillery W, Solomon H, et al. The predictive value of hepatocyte glycogen content on liver allograft biopsy. Transplantation 1995; 59(1):141-143.

53. Jaeschke H, Farhood A, Bautista AP, et al. Complement activates Kupffer cells and neutrophils during reperfusion after hepatic ischemia. Am J Physioll993; 264(4):G 801-809.

54. Jaeschke H, Schini VB, Farhood A. Role of nitric oxide in the oxidant stress during ischemia/reperfusion injury of the liver. Life Sci 1992; 50(23):1797-1804.

55. Suzuki S, Toledo-Pereyra LH, Rodriguez FJ, et al. Neutrophil infiltration as an important factor in liver ischemia and reperfusion injury. Transplantation 1993;55(6):1.265-1.272.

56. Toledo-Pereyra LH, Suzuki S. Neutrophils, cytokines, and adhesion molecules in hepatic ischemia and reperfusion injury. J Am Coll Surg 1994;179(6):758-762.

57. Toledo-Pereyra LH, Suzuki S. Celular and biomolecular mechanisms of liver ischemia and reperfusion injury. Transplant Proc 1994;26(1): 325-327.

Recebido em 12/11/98

Aceito para publicação em 20/5/99

Trabalho realizado no Núcleo de Cirurgia Experimental do Depto. de Cirurgia do Centro de Ciências da Saúde e do Hospital das Clínicas da Universidade Federal de Pernambuco.

  • 1
    Aggarwal S, Kang Y, Freeman JA, et al. Post-reperfusion syndrome: cardiovascular collapse following hepatic reperfusion during liver transplantation. Transplant Proc 1987;19(4) supl 3:54-55.
  • 2
    Aggarwal S, Kang Y, Freeman JA, et al. Post-reperfusion syndrome: hypotension after reperfusion of the transplanted liver. J Crit Care 1993;8(3): 154.
  • 3
    Arll S, Monden K., Adachi Y, et al. Pathogenic role of Kupffer cell activation in the reperfusion injury of cold-preserved liver. Transplantation, 1994;58(10):1072-1077.
  • 4
    Blanot 5, Gillon MC, Lopes I, et al. Circulating endotoxins and postreperfusion syndrome during orthotopic liver transplantation. Transplantation 1 995;60( I): 103-106.
  • 5
    Fukuzawa K., Emre S, Senyuz O, et al. N-acetylcysteine ameliorates reperfusion injury after warm hepatic ischemia. Transplanfation, 1995;59(1):6-9.
  • 6
    Kahn D, Hickman R, Dent DM, et al. For how long can the liver tolerate ischaemia? Eur Surg Res 1986;18:277-282.
  • 7
    Ontell SI, Makowka L, Trager J, et al. Pharmacologic modulation of experimental postischemic hepatic function. Ann Surg 1989; 209 (2): 200-210.
  • 8
    Peng XX, Currin RT, Thunnan RG, et al. Protection by pentoxiflylline against normothermic liver ischemia/reperfusion in rats. Transplantation 1995;59(11):1537-1541.
  • 9
    Piratvisuth T, Dunne JB, Williams R, et al. Amlodipine improves hepatic hemodynamic and metabolic function in the isolated perfused rat liver after sequential cold and warm ischemia. Transplanlalíon 1995; 60(1):23-28.
  • 10
    Suehiro T, Boros P, Emre P, et al. Value of caval effluent in predicting early graft function after orthotopic liver transplantation. Transplanl Proc 1997;29(1/2):469-470.
  • 11
    Harris KA, Wallace C, Wall WJ. Tolerance of the liver to ischemia in the pig. J Surg Res 1982;33:524-530.
  • 12
    Hasselgren P. Prevention and treatment of ischemia of the liver. Surg Gynecol Obstet  1987;164:187-196.
  • 13
    Mays E Truman. Simpósio sobre cirurgia hepática: Oclusão vascular. Clín Cír Am N  1977;57(2):291-323.
  • 14
    Barbieri A, Zonta F, Saracino ML, et al. Evaluation of the reperfusion syndrome after liver ischemia in the rat.  J.  Surg  Res  New York NY , 1996; 62(suppl. 2): 153-158.
  • 15
    DeWeese MS, Lewis Jr. C, Mich AA. Partial hepatectomy in the dog: an experimental study. Surgery 1951;30(4):642-651.
  • 16
    Emond J, Wachs ME, Renz JF, et al. Total vascular exclusion for major hepatectomy in patients with abnormal liver parenchyma. Arch Surg 1995;130:824-831.
  • 17
    Furnival CM, Mackenzie RJ, Blumgart LH. The mechanism of impaired coagulation after partial hepatectomy in in the dogs. Surg Gynecol Obstet  1976;143: 81-86.
  • 18
    Huguet C, Gavelli A, Chieco PA, et al. Liver ischemia for hepatic resection: Where is the limit? Surgery  1992;111:251-259.
  • 19
    Huguet C, Nordlinger B, Bloch P, et al. Tolerance of the human liver to prolonged normothermic ischemia. Arch Surg 1978;113:1448-.1451.
  • 20
    Child III CG - The liver and Shock – cap. 9. In: The hepatic circulation and portal hypertension. Philadelphia PA, W.B. Saunders Company, 1954. p. 122-126.
  • 21
    Fonkalsrud EW. Common mechanisms of hypotension in irreversible shock and liver transplantation. Surg Gynecol Obstet  1969; 128(3): 601-602.
  • 22
    Rappaport AM, MacDonald MH, Borowy ZJ. Hepatic coma following ischemia of the liver. Surg Gynecol Obstet 1953;97:748-762.
  • 23
    Ito Y, Takahashi T, Saro K, et al. Effects of oxigenation during initial perfusion of the liver on hepatic metabolism and morphology following simple hypothermic storage in brain-dead rabbits. Transplant Proc 1997;29(1/2):359-361.
  • 24
    Kootstra G. The asystolic, or non-heartbeating donor. Transplantalíon 1997;63(7):917-921.
  • 25
    Kusano T, Shiraishi M, Miyaguni T, et al. Organ preserving effect of lidocaine administration in the model of orthotopic liver trans- plantation from non-heartbeating donors. Transplant Proc 1996; 28(3):1928-1929.
  • 26
    Lindell SL, Southard JH, Vreugdenhil P, et al. Kupffer cells depress hepatocyte protein synthesis on cold storage of the rat liver. Transplantation 1994;58(8):869-874.
  • 27
    Nauta RJ, Tsimoyiannis E, Uribe M, et al. Oxigen-derived free radicaIs in the hepatic ischemia and reperfusion injury in the rat. Surg Gynecol Obstet 1990;171:120-125.
  • 28
    Schon MR, Hunt CJ, Pegg DE, et al. The possibility of resuscitating livers after warm ischemic injury. Transplantation 1993;56(1): 24-31.
  • 29
    Takada Y, Taniguchi H, Fukunaga K, et al. Hepatic allograft procurement from non-heartbeating donors. Limits of warm ischemia in porcine liver transplantation. Transplantation 1997;63(3):369-373.
  • 30
    Garcia- Valdecasas JC, Rull R, Grande L, et al. Prostacyclin, thromboxane, and oxigen free radicals and postoperative liver function in human liver transplantation. Transplantation 1995; 60(7):662-667.
  • 31
    Ikeda T, Yanaga K, Kishikawa K, et al. Ischemic injury in liver transplantation: Difference in injury sites between warm and cold ischemia in rats. Hepatology 1992;16(2):454-465.
  • 32
    Isai H, Nakajima Y, Kimura J, et al. Calcium mobilization in porcine orthotopic liver transplantation. Transplant Proc 1996;28(3): 1.780- 1.781.
  • 33
    Ishine N, Tanaka N, Yagi T, et al - Postreperfusion syndrome in swine liver transplantation: Comparison between orthotopic liver transplantation and total hepatectomy with portacaval shunt using aortic graft. Transplant Proc 1996;28(3): 1.756-1.758.
  • 34
    Ishine N, Yagi T, Ishikawa T, et al. Hemodynamic analysis of post- reperfusion syndrome and the effect of preventing this syndrome using thromboxane A, synthetase inhibitor (OKY -046) in swine liver transplantation. Transplant Proc 1997;29(1/2):378-381.
  • 35
    Jugan E, Albaladejo P, Jayais p, et al. The failure of venovenous bypass to prevent graft liver postreperfusion syndrome. Transplantation 1992; 54(1):81-84.
  • 36
    Kamachi H, Nakajima Y, Isai H, et al. Study of liver function in a graft suffering from warm ischemia in porcine liver transplantation. Transplant Proc 1996;28(3):1.789-1.791.
  • 37
    Millis JM, Melinek J, Csete M, et al. Randomized controlled trial to evaluate flush and reperfusion techniques in liver transplantation. Transplantation 1997;63(3):397-403.
  • 38
    Oldhafer KJ, Schuttler W, Wiehe B, et al. Treatment of preservation/ reperfusion liver injury by the protease inhibitor aprotinin after ischemia storage. Transplant Proc 1991;23(5):2.380-2.381.
  • 39
    Paulsen AW, Valek TR, Blessing WS, et al. Hemodynamics during liver transplantation with veno-venous bypass. Transplant Proc 1987; 19(1):2.417-2.419.
  • 40
    Pirenne J, Gunson B, KhaleefH et al. Influence of ischemia-reperfusion injury on rejection after liver transplantation. Transplant Proc 1997; 29(1/2):366-367.
  • 41
    Sasaki H, Matsuno T, Tanaka N, et al. Activation of apoptosis during the reperfusion phase after rat liver ischemia. Transplant Proc 1996; 28(3):1.908-1.909.
  • 42
    Wu G, Tomei D, Bathurst IC, et al. Antiapoptotic compound to enhance hypothermic liver preservation. Transplantation 1997;63(6): 803- 809.
  • 43
    Colletti LM, Remick DG, Burtch GD, et al. Role of tumor necrosis factor - a in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat.  J Clin lnvest 1990;85: 1.936-1.943.
  • 45
    Ohar OK, Nagasue N, Kimoto T, et al. The salutary effect of FK 506 in ischemia-reperfusion injury of the canine liver. Transplantation 1992; 54(4):583-588.
  • 46
    Farhood A, McGuire GM, Manning AM, et al. lntercellular adhesion molecule 1 (ICAM-l) expression and its role in neutrophil-induced ischemia-reperfusion injury in rat liver. J Leuk Biol, New York NY, 1995; 57:368-374.
  • 47
    Helling TS, Hacker KA, Kragel PJ, et al. Evidence for cytoprotection by prostaglandin E, with normothermic hepatic ischemia. J Surg Res 1994;56(4):309-313.
  • 48
    Swenson O, Grana L, lnouye T, et al. Immediate and long-term effects of acute hepatic ischemia. Arch Surg 1967;95:451-463.
  • 49
    Tomizawa N, Ohwada S, Ohya T, et al. Effects of neutrophil elastase inhibitor on reperfusion injury in the canine liver. Transplant Proc 1996;28(3): 1767-1768.
  • 50
    Vollmar B, Glasz J, Menger MO, et al. Leukocytes contribute to hepatic ischemia / reperfusion injury via intercellular adhesion molecule - I - mediated venular adherence. Surgery 1995; 117(2): 195-200.
  • 51
    VollmarB, GlaszJ, Post S, et al. Role ofmicrocirculatoryderangements in manifestation of portal triad cross-clamping-induced hepatic reperfusion injury. J Surg Res, New York NY, 1996; 60(1):49-54.
  • 52
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  • Endereço para correspondência:
    Prof. Edmundo Machado Ferraz
    Rua Dom Sebastião Leme, 173/2.501
    52011-160 - Recife-PE
  • Datas de Publicação

    • Publicação nesta coleção
      26 Jan 2010
    • Data do Fascículo
      Jun 1999

    Histórico

    • Aceito
      20 Maio 1999
    • Recebido
      12 Nov 1998
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