参考文献/References:
[1] Tirschwell DL. Intracerebral haemorrhage is hard to stop, and must be attacked before, during and after[J]. BMJ Evid Based Med, 2019, 24(5): e4.
[2] Wang YJ, Li ZX, Gu HQ, et al. China stroke statistics 2019: areport from the national center for healthcare quality management in neurological diseases, china national clinical research center for neurological diseases, the chinesestroke association, national center for chronic and non-communicable disease control and prevention, chinesecenter for disease control and prevention and institute for global neuroscience and stroke collaborations [J]. Stroke and Vascular Neurology, 2020, 5(3):211-239.
[3] Sacco S, Marini C, Toni D, et al. Incidence and 10-year survival of intracerebral hemorrhage in a population-based registry[J]. Stroke, 2009, 40(2): 394-399.
[4] Van Asch CJ, Luitse MJ, Rinkel GJ, et al. Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis[J]. Lancet Neurol, 2010, 9(2): 167-176.
[5] Keep RF, Hua Y, Xi GH. Intracerebral haemorrhage: mechanisms of injury and therapeutic targets[J]. Lancet Neurol, 2012, 11(8): 720-731.
[6] Veltkamp R, Purrucker J. Management of spontaneous intracerebral hemorrhage[J]. Curr Neurol Neurosci Rep, 2017, 17(10): 80.
[7] Broderick JP, Brott TG, Duldner JE, et al. Volume of intracerebral hemorrhage. A powerful and easy-to-use predictor of 30-day mortality[J]. Stroke, 1993, 24(7): 987-993.
[8] Chang GY. Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage[J]. Neurology, 2007, 68(6): 471-472; author reply 472.
[9] Mayer SA. Ultra-early hemostatic therapy for intracerebral hemorrhage[J]. Stroke, 2003, 34(1): 224-229.
[10] BrottT, Broderick J, Kothari R, et al. Early hemorrhage growth in patients with intracerebral hemorrhage[J]. Stroke, 1997, 28(1): 1-5.
[11] Mayer SA, Rincon F. Ultra-early hemostatic therapy for acute intracerebral hemorrhage[J]. Semin Hematol, 2006, 43(1, 1): S70-S76.
[12] Anderson CS, Huang Y, Wang JG, et al. Intensive blood pressure reduction in acute cerebral haemorrhage trial(INTERACT): a randomised pilot trial[J]. Lancet Neurol, 2008, 7(5): 391-399.
[13] Qureshi AI, Palesch YY, Martin R, et al. Effect of systolic blood pressure reduction on hematoma expansion, perihematomal edema, and 3-Month outcome among patients with intracerebral hemorrhage results from the antihypertensive treatment of acute cerebral hemorrhage study[J]. Arch Neurol, 2010, 67(5): 570-576.
[14] Anderson CS, Heeley E, Huang Y, et al. Rapid Blood-Pressure lowering in patients with acute intracerebral hemorrhage[J]. N Engl J Med, 2013, 368(25): 2355-2365.
[15] Alrahbi S, Alaraimi R, Alzaabi A, et al. Intensive blood-pressure lowering in patients with acute cerebral hemorrhage[J]. CJEM, 2018, 20(2): 256-259.
[16] Monroe DM, Hoffman M, Oliver JA, et al. Platelet activity of high-dose factor VIIa is Independent of tissue factor[J]. Br J Haematol, 1997, 99(3): 542-547.
[17] HednerU.NovoSeven as a Universal haemostatic agent[Z],2000:S107-S111.
[18] Mayer SA, Brun NC, Begtrup K, et al. Recombinant activated factor VII for acute intracerebral hemorrhage[J]. N Engl J Med, 2005, 352(8): 777-785.
[19] Mayer SA, Brun NC, Begtrup K, et al. Efficacy and safety of recombinant activated factor VII for acute intracerebral hemorrhage[J]. N Engl J Med, 2008, 358(20): 2127-2137.
[20] Gladstone DJ, Aviv RI, Demchuk AM, et al. Effect of recombinant activated coagulation factor VII on hemorrhage expansion among patients with spot Sign-Positive acute intracerebral hemorrhage: the SPOTLIGHT and STOP-IT randomized clinical trials[J]. JAMA Neurol, 2019, 76(12): 1493-1501.
[21] Dunn CJ, Goa KL. Tranexamic acid:a review of its use in surgery and other indications[J]. Drugs, 1999, 57(6): 1005-1032.
[22] Baharoglu MI, Germans MR, Gj R, et al. Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage[J]. Cochrane Database Syst Rev, 2013(8): CD001245.
[23] Sprigg N, Flaherty K, Appleton JP, et al. Tranexamic acid for hyperacute primary IntraCerebralHaemorrhage(TICH-2): an international randomised, placebo-controlled, phase 3 superiority trial[J]. Lancet, 2018, 391(1135): 2107-2115.
[24] Hu W, Xin Y, Chen X, et al. Tranexamic acid in cerebral hemorrhage: a Meta-Analysis and systematic review[J]. CNS Drugs, 2019, 33(4): 327-336.
[25] Collins R, Peto R, Hennekens C, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials[J]. Lancet, 2009, 373(9678): 1849-1860.
[26] Lovelock CE, Molyneux AJ, Rothwell PM, et al. Change in incidence and aetiology of intracerebral haemorrhage in Oxfordshire, UK, between 1981 and 2006: a population-based study[J]. Lancet Neurol, 2007, 6(6): 487-493.
[27] Thompson BB, Béjot Y, Caso V, et al. Prior antiplatelet therapy and outcome following intracerebral hemorrhage: a systematic review[J]. Neurology, 2010, 75(15): 1333-1342.
[28] Naidech AM, Jovanovic B, Liebling S, et al. Reduced platelet activity is associated with early clot growth and worse 3-month outcome after intracerebral hemorrhage[J]. Stroke, 2009, 40(7): 2398-2401.
[29] Baharoglu MI, Cordonnier C, Salman RA, et al. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy(PATCH): a randomised, open-label, phase 3 trial[J]. Lancet, 2016, 387(138): 2605-2613.
[30] Desborough MJ, Oakland KA, Landoni G, et al. Desmopressin for treatment of platelet dysfunction and reversal of antiplatelet agents: a systematic review and meta-analysis of randomized controlled trials[J]. J ThrombHaemost, 2017, 15(2): 263-272.
[31] Leissinger C, Carcao M, Gill JC, et al. Desmopressin(DDAVP)in the management of patients with congenital bleeding disorders[J]. Haemophilia, 2014, 20(2): 158-167.
[32] Naidech AM, Maas MB, Levasseur-Franklin K, et al. Desmopressin improves platelet activity in acute intracerebral hemorrhage[J]. Stroke, 2014, 45(8): 2451-2453.
[33] Aronowski J, Zhao X. Molecular pathophysiology of cerebral hemorrhage: secondary brain injury[J]. Stroke, 2011, 42(6): 1781-1786.
[34] Wang J. Preclinical and clinical research on inflammation after intracerebral hemorrhage[J]. Prog Neurobiol, 2010, 92(4): 463-477.
[35] Lu A, Tang Y, Ran R, et al. Brain genomics of intracerebral hemorrhage[J]. J Cereb Blood Flow Metab, 2006, 26(2): 230-252.
[36] Rosell A, Vilalta A, Garcia-Berrocoso TA, et al. Brain perihematoma genomic profile following spontaneous human intracerebral hemorrhage[J]. PLoS One, 2011, 6(2): e16750.
[37] Hua Y, Xi GH, Keep RF, et al. Complement activation in the brain after experimental intracerebral hemorrhage[J]. J Neurosurg, 2000, 92(6): 1016-1022.
[38] Xi G, Hua Y, Keep RF, et al. Systemic complement depletion diminishes perihematomal brain edema in rats[J]. Stroke, 2001, 32(1): 162-167.
[39] Ducruet AF, Zacharia BE, Hickman ZL, et al. The complement cascade as a therapeutic target in intracerebral hemorrhage[J]. Exp Neurol, 2009, 219(2): 398-403.
[40] Huang FP, Xi G, KeepRF, et al. Nemoianua,Hoff JT[J]. Brain edema after experimental intracerebral hemorrhage:role of hemoglobin degradation products.JNeurosurg, 2002, 96(2): 287-293.
[41] Wu J, Hua Y, Keep RF, et al. Iron and iron-handling proteins in the brain after intracerebral hemorrhage[J]. Stroke, 2003, 34(12): 2964-2969.
[42] Han N, Ding SJ, Wu T, et al. Correlation of free radical level and apoptosis after intracerebral hemorrhage in rats[J]. Neurosci Bull, 2008, 24(6): 351-358.
[43] Nakamura T, Keep RF, Hua Y, et al. Oxidative DNA injury after experimental intracerebral hemorrhage[J]. Brain Res, 2005, 1039(1/2): 30-36.
[44] Ratan RR, Siddiq A, Aminova L, et al. Small molecule activation of adaptive gene expression: tilorone or its analogs are novel potent activators of hypoxia inducible factor-1 that provide prophylaxis against stroke and spinal cord injury[J]. Ann N Y Acad Sci, 2008, 1147(1): 383-394.
[45] Regan RF, Panter SS. Hemoglobin potentiates excitotoxic injury in cortical cell culture[J]. J Neurotrauma, 1996, 13(4): 223-231.
[46] Okauchi M, Hua Y, Keep RF, et al. Effects of deferoxamine on intracerebral hemorrhage-induced brain injury in aged rats[J]. Stroke, 2009, 40(5): 1858-1863.
[47] Gu Y, Hua Y, Keep RF, et al. Deferoxamine reduces intracerebral hematoma-induced Iron accumulation and neuronal death in piglets[J]. Stroke, 2009, 40(6): 2241-2243.
[48] Selim M, Yeatts S, Goldstein JN, et al. Safety and tolerability of deferoxamine mesylate in patients with acute intracerebral hemorrhage[J]. Stroke, 2011, 42(11): 3067-3074.
[49] Selim M, Foster LD, Moy CS, et al. Deferoxamine mesylate in patients with intracerebral haemorrhage(i-DEF): a multicentre, randomised, placebo-controlled, double-blind phase 2 trial[J]. Lancet Neurol, 2019, 18(5): 428-438.
[50] Fitzgerald G, Patrono C. The coxibs,selective inhibitors of cyclooxygenase-2[J]. N Engl J Med, 2001, 345(6): 433-442.
[51] Vane JR, Bakhle YS, Botting RM. Cyclooxygenases 1 and 2[J]. Annu Rev PharmacolToxicol, 1998, 38(1):97-120.
[52] Graham SH, Hickey RW. Cyclooxygenases in central nervous system diseases: a special role for cyclooxygenase 2 in neuronal cell death[J]. Arch Neurol, 2003, 60(4): 628-630.
[53] Gong C, Ennis SR, Hoff JT, et al. Inducible cyclooxygenase-2 expression after experimental intracerebral hemorrhage[J]. Brain Res, 2001, 901(1/2): 38-46.
[54] Chu K, Jeong SW, Jung KH, et al. Celecoxib induces functional recovery after intracerebral hemorrhage with reduction of brain edema and perihematomal cell death[J]. J Cereb Blood Flow Metab, 2004, 24(8): 926-933.
[55] Lee SH, Park HK, Ryu WS, et al. Effects of celecoxib on hematoma and edema volumes in primary intracerebral hemorrhage: a multicenter randomized controlled trial[J]. European Journal of Neurology, 2013, 20(8): 1161-1169.
[56] Simard JM, Tsymbalyuk N, Tsymbalyuk OA, et al. Glibenclamide is superior to decompressive craniectomy in a rat model of malignant stroke[J]. Stroke, 2010, 41(3): 531-537.
[57] Simard JM, Geng Z, Woo SK, et al. Glibenclamide reduces inflammation, vasogenic edema, and caspase-3 activation after subarachnoid hemorrhage[J]. J Cereb Blood Flow Metab, 2009, 29(2): 317-330.
[58] Sheth KN. Novel approaches to the primary prevention of edema after ischemia[J]. Stroke, 2013, 44(6 Suppl 1): S136.
[59] Jiang B, Li L, Chen Q, et al. Role of glibenclamide in brain injury after intracerebral hemorrhage[J]. Transl Stroke Res, 2017, 8(2): 183-193.
[60] Febbraio M, Hajjar DP, Silverstein RL. CD36: a class B scavenger receptor involved in angiogenesis, atherosclerosis, inflammation, and lipid metabolism[J]. J Clin Invest, 2001, 108(6): 785-791.
[61] Zhao X, Grotta J, Gonzales N, et al. Hematoma resolution as a therapeutic target: the role of microglia/macrophages[J]. Stroke, 2009, 40(3 Suppl): S92-S94.
[62] Wasserman JK, Zhu X, Schlichter LC. Evolution of the inflammatory response in the brain following intracerebral hemorrhage and effects of delayed minocycline treatment[J]. Brain Res, 2007, 1180(1180): 140-154.
[63] Wasserman JK, Schlichter LC. Minocycline protects the blood-brain barrier and reduces edema following intracerebral hemorrhage in the rat[J]. Exp Neurol, 2007, 207(2): 227-237.
[64] Fouda AY, Newsome AS, Spellicy S, et al. Minocycline in acute cerebral hemorrhage: an early phase randomized trial[J]. Stroke, 2017, 48(10): 2885-2887.
[65] Wang Z, Kawabori M, HoukinK.FTY720(fingolimod)ameliorates brain injury through multiple mechanisms and is a strong candidate for stroke treatment[Z],2020:2979-2993.
[66] Fu Y, Hao J, Zhang N, et al. Fingolimod for the treatment of intracerebral hemorrhage: a 2-arm proof-of-concept study[J]. JAMA Neurol, 2014, 71(9): 1092-1101.
[67] Racca V, Di Rienzo M, Cavarretta R, et al. Fingolimod effects on left ventricular function in multiple sclerosis[J]. MultScler, 2016, 22(2): 201-211.
[68] Karlsson G, Francis G, Koren G, et al. Pregnancy outcomes in the clinical development program of fingolimod in multiple sclerosis[J]. Neurology, 2014, 82(8): 674-680.