Effects of terlipressin as early treatment for protection of brain in a model of haemorrhagic shock.
Effects of terlipressin as early treatment for protection of brain in a model of haemorrhagic shock.
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DOI：
10.1186/s13054-015-0825-9
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发表时间：
2015-03-13
期刊：
影响因子：
--
通讯作者：
Malbouisson LM
中科院分区：
文献类型：
--
作者：
Ida KK;Otsuki DA;Sasaki AT;Borges ES;Castro LU;Sanches TR;Shimizu MH;Andrade LC;Auler JO Jr;Dyson A;Smith KJ;Rocha Filho JA;Malbouisson LM
我们研究了在出血性休克（HS）所致低血压恢复期间使用特利加压素治疗是否能有效恢复脑灌注压（CPP）和脑组织水平衡、氧化应激和细胞凋亡标志物。在这项随机对照研究中，将接受HS（目标平均动脉压（MAP）40 mmHg，持续30分钟）的动物随机分配至接受乳酸林格氏溶液（LR组; n =14;体积等于流血的量的3倍）、特利加压素（TERLI组; n =14; 2 mg推注）、无治疗（HAEMO组; n =12）或假手术（n =6）。在基线、休克和治疗后5、30、60（T60）、90和120分钟（T120）记录CPP、全身血流动力学（热稀释技术）和血气分析。在动物被杀死后，获得脑组织样品以测量水平衡的标志物（水通道蛋白-4（AQP 4））、Na+-K+-2Cl−共转运蛋白（NKCC 1））、氧化应激（硫代巴比妥酸反应物质（TBARS）和锰超氧化物歧化酶（MnSOD））和凋亡损伤（Bcl-x和Bax）。尽管HS诱导的心输出量（CO）和高乳酸血症减少，但与假手术动物相比，特利加压素复苏恢复了MAP，并导致CPP恢复，并在T60和T120通过AQP 4，NKCC 1，TBARS和MnSOD表达和Bcl-x/Bax比值正常化表示脑保护。与假手术组相比，LR组CO和血乳酸水平在T60和T120时恢复，CPP和MAP显著降低，TBARS水平和AQP 4、NKCC 1和MnSOD表达及Bcl-x/Bax比值显著升高。在HS诱导的低血压恢复期间，特利加压素可有效使CPP和水平衡、氧化损伤和细胞凋亡的脑标志物恢复正常。这种升压剂对HS脑灌注的作用需要进一步研究。
We investigated whether treatment with terlipressin during recovery from hypotension due to haemorrhagic shock (HS) is effective in restoring cerebral perfusion pressure (CPP) and brain tissue markers of water balance, oxidative stress and apoptosis. In this randomised controlled study, animals undergoing HS (target mean arterial pressure (MAP) 40 mmHg for 30 minutes) were randomised to receive lactated Ringer’s solution (LR group; n =14; volume equal to three times the volume bled), terlipressin (TERLI group; n =14; 2-mg bolus), no treatment (HAEMO group; n =12) or sham (n =6). CPP, systemic haemodynamics (thermodilution technique) and blood gas analyses were registered at baseline, shock and 5, 30, 60 (T60), 90 and 120 minutes after treatment (T120). After the animals were killed, brain tissue samples were obtained to measure markers of water balance (aquaporin-4 (AQP4)), Na+-K+-2Cl− co-transporter (NKCC1)), oxidative stress (thiobarbituric acid reactive substances (TBARS) and manganese superoxide dismutase (MnSOD)) and apoptotic damage (Bcl-x and Bax). Despite the HS-induced decrease in cardiac output (CO) and hyperlactataemia, resuscitation with terlipressin recovered MAP and resulted in restoration of CPP and in cerebral protection expressed by normalisation of AQP4, NKCC1, TBARS and MnSOD expression and Bcl-x/Bax ratio at T60 and T120 compared with sham animals. In the LR group, CO and blood lactate levels were recovered, but the CPP and MAP were significantly decreased and TBARS levels and AQP4, NKCC1 and MnSOD expression and Bcl-x/Bax ratio were significantly increased at T60 and T120 compared with the sham group. During recovery from HS-induced hypotension, terlipressin was effective in normalising CPP and cerebral markers of water balance, oxidative damage and apoptosis. The role of this pressor agent on brain perfusion in HS requires further investigation.
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影响因子：
82.9
作者：
Manley, GT;Fujimura, M;Verkman, AS
通讯作者：
Verkman, AS
影响因子：
25.7
作者：
Eefsen, Martin;Dethloff, Thomas;Larsen, Fin Stolze
通讯作者：
Larsen, Fin Stolze
影响因子：
168.9
作者：
LEVACHER, S;LETOUMELIN, P;POURRIAT, JL
通讯作者：
POURRIAT, JL
影响因子：
9
作者：
Bulger, Eileen M.;May, Susanne;Hoyt, David B.
通讯作者：
Hoyt, David B.
影响因子：
8.3
作者：
GRUBB, RL;RAICHLE, ME;TERPOGOS.MM
通讯作者：
TERPOGOS.MM