Pathogenesis of neonatal asphyxia
Keywords:
Asphyxia, Pathogenesis, Reperfusion Inury
Abstract
Asphyxia results from compromised gas exchange. Pathogenesis of neonatal asphyxia involves energy crisis, lactic acidosis, excitotoxicity& free radical injury. Initial poor oxygenation leads to hypoxemia with intact organ function.Later hypoxia develops with anaerobic metabolism followed by asphyxia with involvement of major organs. The changes during asphyxia depend on organ involvement & its severity. Interference with cerebral blood flow secondary to systemic hypotension leads to failure of cerebral autoregulation thereby leading to ischemia, neuronal &oligodendoglial damage via excitoxicity. Reduced oxygen supply leads to ineffective oxidative phosphorylation, anaerobic metabolism & depletion of ATP reserves, accumulation of lactic acid & hydrogen ions & reduced cellular functions. ATP-dependent sodium-potassium pump fail leading to disruption of ion exchange across cell membrane leading to cell injury. Types of hypoxic brain damage include Haemorrhagic lesions, Destructive lesions involving white matter & grey matter. Neuropathological patterns of injury include Selective neuronal necrosis, White matter lesions, Combined lesions & Advanced lesions including Ulegyria, Multifocal cystic encephalopathy, Status marmaratus&Unifocalpseudocyst. Brain ischemia, inflammation & neuronal cell death are the 3 major steps in the pathogenesis of neural damage during asphyxia. Brain histology helps in timing of asphyxia which depend on aetiology & stage of neurodevelopment.Reperfusion temporarily corrects this energy failure, however it may trigger delayed neuronal death or secondary damage due to brain swelling. Ischemia & reperfusion induce both rapid & delayed changes in gene expression. Asphyxia negatively affects integrity of the genome, triggering activation of sentinel proteins that maintain genome integrity.
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References
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3. Ross MG. Labor and fetal heart rate decelerations: relation to fetal metabolic acidosis. ClinObstet Gynecol. 2011 Mar;54(1):74-82. doi: 10.1097/GRF.0b013e31820a106d.
4. Perlman JM. Summary proceedings from the neurology group on hypoxic-ischeamic encephalopathy. Pediatrics. 2006; 117: S28-S33.
5. Robertson CMT, Perlman M. Follow-up of the term infant after hypoxic-ischemic encephalopathy. Paediatr Child Health.2006; 11: 278-282.
6. Squier W: Pathology of fetal and neonatal brain damage: identifying the timing. Acquired damage to the developing brain, Timing and causation. Edited by: Squier W. 2002, London: Arnold, 110-127.
7. Bennet L, Gunn AJ. The fetal heart rate response to hypoxia: insights from animal models. ClinPerinatol. 2009 Sep;36(3):655-72. doi: 10.1016/j.clp.2009.06.009. [PubMed]
8. Westgate JA, Wibbens B, Bennet L, Wassink G, Parer JT, Gunn AJ. The intrapartum deceleration in center stage: a physiologic approach to the interpretation of fetal heart rate changes in labor. Am J Obstet Gynecol. 2007; 197: 236.e1-236.e11.DOI: http://dx.doi.org/10.1016/j.ajog.2007.03.063.
9. Shah PS, Perlman M. Time courses of intrapartum asphyxia: neonatal characteristics and outcomes. Am J Perinatal. 2009; 26: 39-44. [PubMed]
10. Distefano G, Pratico AD. Actualities on molecular pathogenesis and repairing process of cerebral damage in perinatal hypoxic-ischemic encephalopathy.Ital J Pediatr. 2010 Sep 16;36:63. doi: 10.1186/1824-7288-36-63.
11. Fathali N, Khatibi NH, Ostrowski RP, Zhang JH. The evolving landscape of neuroinflammation after neonatal hypoxia-ischemia.ActaNeurochir Suppl. 2011;111:93-100. doi: 10.1007/978-3-7091-0693-8_15. [PubMed]
12. Giulian D, Vaca K. Inflammatory glia mediate delayed neuronal damage after ischemia in the central nervous system. Stroke. 1993;24:I84–I90. doi: 10.1161/01.STR.24.1.84.
13. Lehnardt S, Lehmann S, Kaul D, Tschimmel K, Hoffmann O, Cho S, et al. Toll-like receptor 2 mediates CNS injury in focal cerebral ischemia. J Neuroimmunol. 2007;190:28–33. doi: 10.1016/j.jneuroim.2007.07.023. [PubMed]
14. Hermoso MA, Cidlowski JA. Putting the brake on inflammatory responses: the role of glucocorticoids.IUBMB Life. 2003;55:497–504. doi: 10.1080/15216540310001642072. [PubMed]
15. Buller KM, Carty ML, Reinebrant HE, Wixey JA. Minocycline: a neuroprotective agent for hypoxic-ischemic brain injury in the neonate? J Neurosci Res. 2009 Feb 15;87(3):599-608. doi: 10.1002/jnr.21890.
16. Girard S, Kadhim H, Roy M, Lavoie K, Brochu ME, Larouche A, et al. Role of perinatal inflammation in cerebral palsy. Pediatr Neurol. 2009 Mar;40(3):168-74. doi: 10.1016/j.pediatrneurol.2008.09.016. [PubMed]
17. Northington FJ, Chavez-Valdez R, Martin LJ.Neuronal cell death in neonatal hypoxia-ischemia.Ann Neurol. 2011 May;69(5):743-58. doi: 10.1002/ana.22419. [PubMed]
18. Morales P, Fiedler JL, Andres S, Berrios C, Huaiquin P, Bustamante D, et al. Plasticity of hippocampus following perinatal asphyxia: effects on postnatal apoptosis and neurogenesis. J Neurosci Res. 2008 Sep;86(12):2650-62. doi: 10.1002/jnr.21715.
19. Ness JM, Harvey CA, Strasser A, Bouillet P, Klocke BJ, Roth KA. Selective involvement of BH3-only Bcl-2 family members Bim and Bad in neonatal hypoxia-ischemia. Brain Res. 2006;1099:150–159. doi: 10.1016/j.brainres.2006.04.132.
20. Graham EM, Sheldon RA, Flock DL, Ferriero DM, Martin LJ, O’Riordan DP, et al. Neonatal mice lacking functional Fas death receptors are resistant to hypoxic-ischemic brain injury. Neurobiol Dis. 2004 Oct;17(1):89-98.doi: 10.1016/j.nbd.2004.05.007.
21. Cheng Y, Black IB, DiCicco-Bloom E. Hippocampal granule neuron production and population size are regulated by levels of bFGF. Eur J Neurosci. 2002;15:3–12. doi: 10.1046/j.0953-816x.2001.01832.x.
22. Golan H, Huleihel M. The effect of prenatal hypoxia on brain development: short- and long-term consequences demonstrated in rodent models. Dev Sci. 2006;9(4):338–349. doi: 10.1111/j.1467-7687.2006.00498.x.
23. Daval JL, Pourie G, Grojean S, Lievre V, Strazielle C, Blaise S, et al. Neonatal hypoxia triggers transient apoptosis followed by neurogenesis in the rat CA1 hippocampus. Pediatric Research (2004) 55, 561–567; doi:10.1203/01.PDR.0000113771.51317.37.
24. Blomgren K, Zhu C, Wang X, Karlsson JO, Leverin AL, Bahr BA, et al. Synergistic activation of caspase-3 by m-calpain after neonatal hypoxia-ischemia: a mechanism of “pathological apoptosis”? J Biol Chem. 2001;276:10191–10198. doi: 10.1074/jbc.M007807200.
25. Johnston MV, Fatemi A, Wilson MA, Northington F. Treatment advances in neonatal neuroprotection and neurointensive care. Lancet Neurol. 2011 Apr;10(4):372-82. doi: 10.1016/S1474-4422(11)70016-3. [PubMed]
26. Ginet V, Puyal J, Clarke PG, Truttmann AC. Enhancement of autophagic flux after neonatal cerebral hypoxia-ischemia and its region-specific relationship to apoptotic mechanisms. Am J Pathol. 2009 Nov; 175(5): 1962–1974.doi: 10.2353/ajpath.2009.090463.
27. Folkerth RD: The neuropathology of acquired pre- and perinatal brain injuries. SeminDiagnPathol. 2007, 24: 48-57.DOI: http://dx.doi.org/10.1053/j.semdp.2007.02.006. [PubMed]
28. Herrera-Marschitz M, Morales P, Leyton L, Bustamante D, Klawitter V, Espina-Marchant P, et al. Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins. Neurotox Res. 2011 May;19(4):603-27. doi: 10.1007/s12640-010-9208-9.
29. Rothman SM, Olney JW. Glutamate and the pathophysiology of hypoxic–ischemic brain damage. Ann Neurol. 1986;19:105–111. doi: 10.1002/ana.410190202. [PubMed]
30. Chen HL, Pistollato F, Hoeppner DJ, Ni HT, McKay RD, Panchision DM. Oxygen tension regulates survival and fate of mouse central nervous system precursors at multiple levels. Stem Cells. 2007 Sep;25(9):2291-301.
31. Kleman NW, Sun D, Cengiz P. Mechanisms underlying neonatal hypoxia ischemia. Open Drug Discovery J2010;2:129–3710.
32. Jantzie LL, Talos DM, Selip DB, et al.. Developmental regulation of group I metabotropic glutamate receptors in the premature brain and their protective role in a rodent model of periventricular leukomalacia. Neuron Glia Biol2010;6:277–88.
33. Ferrari DC, Nesic O, Perez-Polo JR.. Perspectives on neonatal hypoxia/ ischemia-induced edemaformation.Neurochem Res 2010;35:1957–65. [PubMed]
34. Ferrari DC, Nesic OB, Perez-Polo JR.. Oxygen resuscitation does not ameliorate neonatal hypoxia/ischemia-induced cerebral edema. J Neurosci Res 2010;88:2056–65.
35. Squier W, Cowan FM. The value of autopsy in determining the cause of failure to respond to resuscitation at birth. SeminNeonatol 2004;9:331–45. [PubMed]
36. Knapp AG, Dowling JE. Dopamine enhances excitatory amino acid-gated conductances in cultured retinal horizontal cells. Nature. 1987;325:437–439. doi: 10.1038/325437a0.
37. Globus MY, Busto R, Dietrich WD, Martinez E, Valdes I, Ginsberg MD. Effect of ischemia on the in vivo release of striatal dopamine, glutamate, and gamma-aminobutyric acid studied by intracerebralmicrodialysis. J Neurochem. 1988;51:1455–1464. doi: 10.1111/j.1471-4159.1988.tb01111.x.
38. Saugstad OD. Hypoxanthine as an indicator of hypoxia: its role in health and disease through free radical production. Pediatr Res. 1988;23:143–150. doi: 10.1203/00006450-198802000-00001. [PubMed]
39. Goplerud JM, Mishra OP, Delivoria-Papadopoulos M. Brain cell membrane dysfunction following acute asphyxia in newborn piglets. Biol Neonate. 1992;61:33–41. doi: 10.1159/000243528.
40. Connors G, Hunse C, Gagnon R, Richardson B, Han V, Rosenberg H 1992 Perinatal assessment of cerebral blood flow velocity wave forms in the human fetus and neonate. Pediatr Res 31:649–652. [PubMed]
41. Rosenberg AA, Murdaugh E, White CW 1989 The role of oxygen free radicals in post asphyxia cerebral hypoperfusion in newborn lambs. Pediatr Res 26:215–219. Pediatr Res 26:215–219. [PubMed]
42. Siesjö BK 1992 Pathophysiology and treatment of focal cerebral ischemia. Part I. Pathophysiology.J Neurosurg. 1992 Aug;77(2):169-84. [PubMed]
43. Connolly ES, Winfree CJ, Springer TA, Naka Y, Liao H, Yan SD, Stern DM, Solomon RA, Gutierrez-Ramos J-C, Pinsky DJ 1996 Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion. Role of neutrophil adhesion in the pathogenesis of stroke. J Clin Invest. 1996 Jan 1;97(1):209-16. [PubMed]
44. Palmer C 1995 Hypoxic-ischemic encephalopathy. Therapeutic approaches against microvascular injury, and role of neutrophils, PAF, and free radicals.ClinPerinatol 22:481–517.
45. Pluta R, Lossinsky AS, Wisniewski HM, Mossakowski MJ 1994 Early blood-brain barrier changes in the rat following transient complete cerebral ischemia induced by cardiac arrest. Brain Res 633:41–52.
46. Petito CK, Pulsinelli WA, Jacobson G, Plum F 1982 Edema and vascular permeability in cerebral ischemia: Comparison between ischemic neuronal damage and infarction. J NeuropatholExp Neurol. 1982 Jul;41(4):423-36.
47. del Zoppo GJ, Schmid-Schönbein GW, Mori E, Copeland BR, Chang C-M 1991 Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons. Stroke. 1991 Oct;22(10):1276-83.
48. Zhang R-L, Chopp M, Chen H, Garcia JH 1994 Temporal profile of ischemic tissue damage, neutrophil response, and vascular plugging following permanent and transient (2H) middle cerebral artery occlusion in the rat. J Neurol Sci. 1994 Aug;125(1):3-10.
49. Thomas WS, Mori E, Copeland BR, Yu J-Q, Morrissey JH, del Zoppo GJ 1993 Tissue factor contributes to microvascular defects after focal cerebral ischemia. Stroke 24:847–854.
50. An G, Lin T-N, Liu J-S, Xue J-J, He Y-Y, Hsu CY 1993 Expression of c-fos and c-jun family genes after focal cerebral ischemia. Ann Neurol 33:457–464.
51. Brand T, Sharma HS, Fleischmann KE, Duncker DJ, McFalls EO, Verdouw PD, Schaper W 1992 Proto-oncogene expression in porcine myocardium subjected to ischemia and reperfusion. Circ Res 71:1351–1360.doi: 10.1161/01.RES.71.6.1351. [PubMed]
52. Witzgall R, Brown D, Schwarz C, Bonventre JV 1994 Localization of proliferating cell nuclear antigen, vimentin, c-Fos, and clusterin in the postischemic kidney. Evidence for a heterogenous genetic response among nephron segments, and a large pool of mitotically active and dedifferentiating cells.J Clin Invest. 1994 May;93(5):2175-88. [PubMed]
53. Pombo CM, Bonventre JV, Avruch J, Woodgett JR, Kyriakis JM, Force T 1994 The stress-activated protein kinases are major c-jun amino-terminal kinases activated by ischemia and reperfusion. J BiolChem 269(42) :26546–26551.
54. Alano CC, Ying W, Swanson RA. Poly(ADP-ribose) polymerase-1-mediated cell death in astrocytes requires NAD+ depletion and mitochondrial permeability transition. J Biol Chem. 2004;279:18895–18902. doi: 10.1074/jbc.M313329200.
55. Leppard JB, Dong Z, Mackey ZB, Tomkinson AE. Physical and functional interaction between DNA ligase IIIalpha and poly(ADP-Ribose) polymerase 1 in DNA single-strand break repair. Mol Cell Biol.2003; Aug 23( 16):5919–5927. doi: 10.1128/MCB.23.16.5919-5927.2003.
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CITATION
DOI: 10.17511/jopm.2016.i01.05
How to Cite
Dr. Rabindran, & Gedam, D. S. (1). Pathogenesis of neonatal asphyxia. Tropical Journal of Pathology and Microbiology, 2(1), 23-30. https://doi.org/10.17511/jopm.2016.i01.05
Section
Review Article
OAI - Open Archives Initiative
