Dose dependent neuroprotection of the noble gas argon after cardiac arrest in rats is not mediated by KATP-Channel opening

被引:41
作者
Bruecken, Anne [1 ]
Kurnaz, Pinar [1 ]
Bleilevens, Christian [1 ]
Derwall, Matthias [1 ]
Weis, Joachim [2 ]
Nolte, Kay [2 ]
Rossaint, Rolf [1 ]
Fries, Michael [1 ]
机构
[1] Univ Hosp RWTH Aachen, Dept Anaesthesiol, D-52074 Aachen, Germany
[2] Univ Hosp RWTH Aachen, Inst Neuropathol, D-52074 Aachen, Germany
关键词
Cardiopulmonary resuscitation; Hypoxia-ischaemia; Brain; Reperfusion injury; Argon; Neuroprotective agents; TRAUMATIC BRAIN-INJURY; IN-VITRO MODEL; NEONATAL ASPHYXIA; HYPOTHERMIA COMBINE; CEREBRAL-ISCHEMIA; POTASSIUM CHANNEL; XENON; PIGS; ANESTHESIA; NEURONS;
D O I
10.1016/j.resuscitation.2014.02.014
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Purpose: Argon at a dosage of 70% is neuroprotective when given 1 h after cardiac arrest (CA) in rats. In a rodent model, we investigated if the neuroprotective effects of argon are dose dependent and mediated by adenosine triphosphate dependent potassium (K-ATP) channels. Methods: Forty-seven male Sprague-Dawley rats were subjected to 7 min of CA and 3 min of cardiopulmonary resuscitation (CPR). In protocol I animals were randomized to receive either 70% or 40% argon ventilation 1 h after successful CPR or no argon-treatment. Animals of the second protocol also received 1 h of 70% argon ventilation or no argon treatment but were randomized to a group receiving the KATP channel blocker 5-hydroxydecanoate (5-HD). For all animals a neurological deficit score (NDS) was calculated daily for seven days following the experiment before the animals were killed and the brains harvested for histopathological analyses. Results: All animals survived. Control animals exhibited severe neurologic dysfunction at all points in time as measured with the NDS. Argon treated animals showed significant improvements in the NDS through all postoperative days in a dose dependent fashion. This was paralleled by a significant reduction in the neuronal damage index in the neocortex and the hippocampal CA 3/4 region. Administration of 5-HD neither abolished the positive effects on functional recovery nor on histopathologic changes observed in the argon group. Conclusion: Our study demonstrates a dose dependent neuroprotective effect of argon administration in this rodent model, which is not mediated via ATP dependent potassium channels. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:826 / 832
页数:7
相关论文
共 32 条
[11]   Xenon reduces neurohistopathological damage and improves the early neurological deficit after cardiac arrest in pigs [J].
Fries, Michael ;
Nolte, Kay Wilhelm ;
Coburn, Mark ;
Rex, Steffen ;
Timper, Anne ;
Kottmann, Kai ;
Siepmann, Katharina ;
Haeusler, Martin ;
Weis, Joachim ;
Rossaint, Rolf .
CRITICAL CARE MEDICINE, 2008, 36 (08) :2420-2426
[12]   Combining xenon and mild therapeutic hypothermia preserves neurological function after prolonged cardiac arrest in pigs [J].
Fries, Michael ;
Bruecken, Anne ;
Cizen, Ayseguel ;
Westerkamp, Maren ;
Loewer, Celine ;
Deike-Glindemann, Jan ;
Schnorrenberger, Nora K. ;
Rex, Steffen ;
Coburn, Mark ;
Nolte, Kay W. ;
Weis, Joachim ;
Rossaint, Rolf ;
Derwall, Matthias .
CRITICAL CARE MEDICINE, 2012, 40 (04) :1297-1303
[13]   Two-pore-domain K+ channels are a novel target for the anesthetic gases xenon, nitrous oxide, and cyclopropane [J].
Gruss, M ;
Bushell, TJ ;
Bright, DP ;
Lieb, WR ;
Mathie, A ;
Franks, NP .
MOLECULAR PHARMACOLOGY, 2004, 65 (02) :443-452
[14]   Neuroprotection against Traumatic Brain Injury by Xenon, but Not Argon, Is Mediated by Inhibition at the N-Methyl-D-Aspartate Receptor Glycine Site [J].
Harris, Katie ;
Armstrong, Scott P. ;
Campos-Pires, Rita ;
Kiru, Louise ;
Franks, Nicholas P. ;
Dickinson, Robert .
ANESTHESIOLOGY, 2013, 119 (05) :1137-1148
[15]   Xenon and hypothermia combine additively, offering long-term functional and histopathologic neuroprotection after neonatal hypoxia/ischemia [J].
Hobbs, Catherine ;
Thoresen, Marianne ;
Tucker, Alexander ;
Aquilina, Kristian ;
Chakkarapani, Ela ;
Dingley, John .
STROKE, 2008, 39 (04) :1307-1313
[16]   Utstein-style guidelines for uniform reporting of laboratory CPR research. [J].
Idris, AH ;
Becker, LB ;
Ornato, JP ;
Hedges, JR ;
Bircher, NG ;
Chandra, NC ;
Cummins, RO ;
Dick, W ;
Ebmeyer, U ;
Halperin, HR ;
Hazinski, MF ;
Kerber, RE ;
Kern, KB ;
Safar, P ;
Steen, PA ;
Swindle, MM ;
Tsitlik, JE ;
vonPlanta, I ;
vonPlanta, M ;
Wears, RL ;
Weil, MH .
RESUSCITATION, 1996, 33 (01) :69-84
[17]   Neuroprotection (and lack of neuroprotection) afforded by a series of noble gases in an in vitro model of neuronal injury [J].
Jawad, Noorulhuda ;
Rizvi, Maleeha ;
Gua, Jianteng ;
Adeyi, Olar ;
Tao, Guocai ;
Maze, Mervyn ;
Ma, Daqing .
NEUROSCIENCE LETTERS, 2009, 460 (03) :232-236
[18]   Mode of death after admission to an intensive care unit following cardiac arrest [J].
Laver, S ;
Farrow, C ;
Turner, D ;
Nolan, J .
INTENSIVE CARE MEDICINE, 2004, 30 (11) :2126-2128
[19]   Argon: Neuroprotection in in vitro models of cerebral ischemia and traumatic brain injury [J].
Loetscher, Philip D. ;
Rossaint, Jan ;
Rossaint, Rolf ;
Weis, Joachim ;
Fries, Michael ;
Fahlenkamp, Astrid ;
Ryang, Yu-Mi ;
Grottke, Oliver ;
Coburn, Mark .
CRITICAL CARE, 2009, 13 (06)
[20]   Xenon and Sevoflurane Protect against Brain Injury in a Neonatal Asphyxia Model [J].
Luo, Yan ;
Ma, Daqing ;
leong, Edmund ;
Sanders, Robert D. ;
Yu, Buwei ;
Hossain, Mahmuda ;
Maze, Mervyn .
ANESTHESIOLOGY, 2008, 109 (05) :782-789