Abstract:Objective To investigate the cerebral protective effects of propofol in patients with intracerebral hemorrhage during intracranial surgery.Methods Sixty patients with intracerebral hemorrhage were randomly divided into two groups (n=30 each): propofol group (P group) and etomidate group (E group). At four time points viz. before narcosis(t0), after induction(t1), 1 h after operation(t2), 2 h after operation(t3), jugular bulb venous oxygen saturation(SjvO2) were recorded, the cerebral oxygen uptake rate(CERO2) were calculated with the Fick formula. Venous blood samples were taken preoperatively(T0), 1 h after surgery(T1), postoperative 1 h(T2)and 24 h(T3) to test the neurological injury marker S100β.The GOS and MMSE tests 30 days after surgery were recorded.Results In two groups, SjvO2 were higher at t1,t2 and t3 when compared with t0. CERO2 (30.9%±5.04%,30.2%±6.17%, 28.7%±3.21%)were lower at t1,t2 and t3 in group P, the same was in group E(24.9%±4.31%) at t1 (P<0.05). Compared with group E, in group P,SjvO2 was significantly higher at t1,t2 and t3 whereas the CERO2 was lower(P<0.05). The level of S100β in group P (1.17±0.26)μg/L was lower than in group E (1.52±0.19)μg/L (P<0.05)at T2. There was no differences in GOS and MMSET between the propofol group and etomidate group.Conclusions Propofol can improve the cerebral oxygen metabolism and reduce S100β level in blood but fails to improve the GOS and MMSET. The cerebral protection of propofol exists but does not reduce major neurological sequelae.
Hofman P A, Stapert S Z, Van Kroonenburgh M J, et al. MR imaging, single-photon emission CT, and neurocognitive performance after mild traumatic brain injury [J].AJNR Am J Neuroradiol, 2001, 22(3): 441-449.
[2]
Kotani Y, Nakajima Y, Hasegawa T, et al. Propofol exerts greater neuroprotection with disodium Edentate (EDTA) than without it [J]. J Cereb Blood Flow Metab, 2008, 28(2): 354-366.
[3]
Adembri C, Venturi L, Tani A, et al. Neuroprotective effects of propofol in models of cerebral ischemia: inhibition of mitochondrial swelling as a possible mechanism [J]. Anesthesiology, 2006, 104(1): 80-89.
[4]
Zhu S M, Xiong X X, Zheng Y Y, et al. Propofol inhibits aquaporin 4 expression through a protein kinase C-dependent pathway in an astrocyte model of cerebral ischemia/reoxygenation[J]. Anesth Analg, 2009, 109(5): 1493-1499.
[5]
Bilotta F, Gelb A W, Stazi E, et al. Pharmacological perioperative brain neuroprotection: a qualitative review of randomized clinical trials [J]. Br J Anaesth, 2013, 110(6):113-120.
[6]
Grogan K, Stearns J, Hogue C W. Brain protection in cardiac surgery [J]. Anesthesiol Clin, 2008, 26(3): 521-538.
[7]
Roach G W, Newman M F, Murkin J M, et al. Multicenter study of perioperative ischemia (MsSPI). In effectiveness of burst suppression therapy in mitigating perioperative cerebrovascular dysfunction[J]. Anesthesiology, 1999, 90(5): 1255-1264.
[8]
Kanbak M, Saricaoglu F, Avci A, et al. Propofol offers no advantage over isoflurane anesthesia for cerebral protection during cardiopulmonary bypass: a preliminary study of S-100b protein levels [J]. Can J Anaesth, 2004, 51(7):712-717.
[9]
Zaidan J R, Klochany A, Martin W M, et al. Effect of thiopental on neurologic outcome following coronary artery bypass grafting [J].Anesthesiology,1991,74(3):406-411.
[10]
Nussmeier N A, Arlund C, Slogoff S. Neuropsychiatric complications after cardiopulmonary bypass: cerebral protection by a barbiturate [J]. Anesthesiology, 1986, 64(2):140-142.
Zhang H Q, Peng H Y, Li S Z, et al. The clinical effct and therapeut ic mechani sm of early correction of acidosis in patient with severe head injury and its therapeutic mechanism [J]. Chin J Emerg Med, 2004, 13 (3):194-196.