右美托咪定对止血带诱发下肢缺血再灌注损伤的影响

Abstract
Figure/Table
References
Related Citation (15)

Download: PDF (661 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To analyze the effect of dexmedetomidine on the level of serum inflammation cytokines and oxygen free radicals during lower extremity ischemia/refusion.Methods The study was performed on patients undergoing arthroscopic operation under spinal anesthesia. Forty patients were randomly allocated into two groups: Group control (C,n=20) and Group dexmedetomidine (D,n=20). In Group D, patients were sedated with dexmedetomidine at a continuous infusion [1 μg/kg for 10 minutes, followed by 1 μg/(kg·h)] until the end of surgery, whereas the control group received an equivalent volume of saline. Femoral venous blood samples were obtained before spinal anesthesia(T0), at tourniquet inflation 1 h(T1), after tourniquet deflation 20 minutes(T2) ,1 h(T3) and 6 h(T4) .Then the serum concentrations of SOD,MDA,TNF-α and IL-6 were measured.Results Serum SOD activity was significantly higher in the group D after tourniquet deflation 1 h and 6 h compared with those of in the group C (P<0.05) .There was a significant lowering in the serum SOD activity after tourniquet deflation 1 h and 6 h compared with the baseline in the group C(P<0.05). Serum MDA was significantly greater during ischemia and reperfusion period in the control group compared with the baseline (P<0.05) and significantly attenuated in the group D after tourniquet deflation 1 h (P<0.05) and 6 h (P<0.05).Serum TNF-α was highly elevated during ischemia and reperfusion period in the control group and the group D compared with the baseline(P<0.05) and the decrease was significantly observed in the group D compared with the group C after deflation 6 h(P<0.05). Secrum IL-6 was not significantly different in both groups at tourniquet inflation 1 h and deflation 20 min’and 1 h compared with baseline. There was a significantly greater level of IL-6 after tourniquet deflation 6 h compared with the baseline and compared with the group D (P<0.05).Conclusions Dexmedetomidine may offer advantages by inhibiting lipid peroxidation and attenuating the production of inflammatory cytokines during lower extremity ischemia/refusion injury due to tourniquet application .

Key words： Dexmedetomidine tourniquet application ischemia/ reperfusion

Received: 20 January 2016

ZTFLH:

R614.2

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	CHEN Hui
	HAO Nannan
	and LEI Zhili

Cite this article:

CHEN Hui,HAO Nannan,and LEI Zhili. Effect of dexmedetomidine on lower extremity ischemia/refusion injury due to tourniquet application during arthroscopy[J]. Med. J. Chin. Peop. Armed Poli. Forc., 2016, 27(8): 826-829.

URL:

http://journal08.magtechjournal.com/Jwk_wjyx/EN/ OR http://journal08.magtechjournal.com/Jwk_wjyx/EN/Y2016/V27/I8/826

[1]	Seybold E A, Busconi B D. Anterior thigh compartment syndromefollowing prolonged tourniquet application and lateral positioning[J].Am J Orthop ,1996,25:493-496.
[2]	Yassin M M, Harkin D W, Barros A A, et al. Lower limb ischemia-reperfusion injury triggers a systemic inflammatory response and multiple organ dysfunction[J]. World J Surg,2002,26(1):115-121
[3]	Gutteridge J M. Lipid peroxidation and antioxidants as biomarkers oftissue damage[J]. Clin Chem ,1995,41:1819-1828.
[4]	Uysal H Y, Cuzdan S S, Kayíran O, et al. Preventive effect of Dexmedetomidine in ischemia-reperfusion injury[J]. J Craniofac Surg, 2012 ,23(5):1287-1291.
[5]	Yagmurdur H, Ozcan N, Dokumaci F, et al. Dexmedetomidine reduces the ischemia-reperfusion injury markers during upper extremity surgery with tourniquet[J]. J Hand Surg Am, 2008,33(6):941-947.
[6]	Lan W, Harmon D, Wang J H, et al. The effect of lidocaine on in vitro neutrophil and endothelial adhesion molecule expression induced by plasma obtained during tourniquetinducedischaemia and reperfusion[J]. Eur J Anaesthesiol, 2004,21: 892-897.
[7]	McIntyre T M, Patel K D, Zimmerman G A, et al. radical-mediated leukocyte adherence. In: Granger DN, Schinbein GW, editors. Physiology and pathophysiology of leukocyte adhesion[J]. Oxford University Press, 1995,25: 261-277.
[8]	Frangiogiannis N G, Lindsey M L, Michael L H, et al. Resident cardiac mast cells degranulate and release preformed TNF-alpha, initiating the cytokine cascade in experimental canine myocardial / reperfusion[J]. Circulation ,1998;98:699-710.
[9]	Svoboda P, Kantorova I, Ochmann J. Dynamics of interleukin 1, 2, and 6 and tumor necrosis factor alpha in multiple trauma patients[J]. J Trauma,1994,36:336-340.
[10]	Leon L R, White A A, Kluger M J. Role of IL-6 and TNF in thermoregulationand survival during sepsis in mice[J]. Am J Physiol, 1998,275:269-277.
[11]	O’Riordain M G, O’Riordain D S, Molloy R G,et al.Dosage and timing of anti-TNF-alpha antibody treatmentdetermine its effect of resistance to sepsis after injury[J]. J Surg Res. 1996,64:95-101.
[12]	Biffl W L, Moore E E, Moore F A, et al. Interleukin-6 in the injured patient, Marker of injury or mediator of inflammation? [J]. Ann Surg,1996,224:647-664.