Effect of Hydrogen Sulfide on Arterial Baroreflex in Rat with Sepsis_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

QIAO Wei ¹ , CHAI Chen ¹ , YANG Lei ¹ , LI Xiaoyun ² , LU Yan ² , CAO Nong ¹

1.The First Department of General Surgery, The First Hospital of Lanzhou University, Lanzhou 730000, Gansu Province, China;;
2.Department of Clinical Laboratory, The First Hospital of Chinese PLA, Lanzhou 730030, Gansu Province, China;

Corresponding author：

Keywords：

Hydrogen sulfide; Sepsis; Arterial baroreflex

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ObjectiveTo investigate the potential role and mechanism of hydrogen sulfide (H2S) in regulating arterial baroreflex (ABR) in septic rats. MethodsThe rat model of cecal ligation and puncture (CLP) induced sepsis was established. Fortyseven male SpargueDawley rats were randomly divided into 9 groups: ① Sham operation (SO)+0.9% NaCl (NS) intravenous injection (i.v.) group; ② SO+NaHS i.v. group; ③ CLP+NaHS i.v. group; ④ SO+artificial cerebrospinal fluid (aCSF) bilater nucleus tractus solitarii (NTS) microinjection group; ⑤ SO+NaHS bilater NTS microinjection group; ⑥ SO+vehicle (DMSO)+NaHS group; ⑦ SO+Gli+NaHS group; ⑧ CLP+vehicle (DMSO) group; ⑨ CLP+Gli group. The ABR function was measured before administration and 5 min and 30 min after administration. Results① The ABR value of rats at different time in the same group: Compared with the ABR value before administration in the SO+NaHS i.v. group, CLP+NaHS i.v. group, SO+NaHS bilater NTS microinjection group, and SO+vehicle+NaHS group, the ABR values of rats significantly decreased at 5 min and 30 min after administration (P lt;0.05, P lt;0.01), which significantly increased in the CLP+Gli group at 5 min and 30 min after administration (P lt;0.05). ② The ABR value of rats at the same time in the different groups: Before administration, the ABR value of rat in the CLP+NaHS i.v. group was significantly lower than that in the SO+NS i.v. group or SO+NaHS i.v.group (P lt;0.05). At 5 min and 30 min after adminis tration, the ABR value of rat in the CLP+NaHS i.v. group was significantly lower than that in the SO+NS i.v. group or SO+NaHS i.v. group (P lt;0.05), which in the SO+NaHS i.v. group or SO+NaHS bilater NTS microinjection group was significantly lower than that in the SO+NS i.v. group or SO+aCSF bilater NTS microinjection group, respectively (P lt;0.05, P lt;0.01), in the SO+Gli+NaHS group or CLP+Gli group was significantly higher than that in the SO+vehicle+NaHS group or CLP+vehicle group, respectively (P lt;0.05). ConclusionsH2S plays an adverse role in septic ABR function, and opening KATP channel located at the pathway of ABR, may be the mechanism involved in the downregulation of ABR function in septic rat. Notably, the NTS may be also responsible for reduction of ABR value.

Citation： QIAO Wei ,CHAI Chen,YANG Lei,LI Xiaoyun,LU Yan,CAO Nong. Effect of Hydrogen Sulfide on Arterial Baroreflex in Rat with Sepsis. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2011, 18(4): 374-379. doi: Copy

1.	李德馨. Sepsis的定义和治疗进展-在隧道尽头的亮点? [J]. 国外医学麻醉学与复苏分册, 2003, 24(4): 193195.
2.	Shen FM, Guan YF, Xie HH, et al. Arterial baroreflex function determines the survival time in lipopolysaccharideinduced shock in rats [J]. Shock, 2004, 21(6): 556560.
3.	Shi KY, Shen FM, Liu AJ, et al. The survival time postcecal ligation and puncture in sinoaortic denervated rats [J]. J Cardiovasc Pharmacol, 2007, 50(2): 162167.
4.	Schmidt HB, Werdan K, MüllerWerdan U. Autonomic dysfunction in the ICU patient [J]. Curr Opin Crit Care, 2001, 7(5): 314322.
5.	Pancoto JA, Corrêa PB, OliveiraPelegrin GR, et al. Autonomic dysfunction in experimental sepsis induced by cecal ligation and puncture [J]. Auton Neurosci, 2008, 138(12): 5763.
6.	Li L, Bhatia M, Zhu YZ, et al. Hydrogen sulfide is a novel mediator of lipopolysaccharideinduced inflammation in the mouse [J]. FASEB J, 2005, 19(9): 11961198.
7.	康凯, 姜洪池. 气体信号分子硫化氢与疾病 [J]. 中国普外基础与临床杂志, 2009, 16(2): 170173.
8.	Zhang H, Zhi L, Moore PK, et al. Role of hydrogen sulfide in cecal ligation and punctureinduced sepsis in the mouse [J]. Am J Physiol Lung Cell Mol Physiol, 2006, 290(6): L1193L1201.
9.	Seagard JL, Dean C, Hopp FA. Neurochemical transmission of baroreceptor input in the nucleus tractus solitarius [J]. Brain Res Bull, 2000, 51(2): 111118.
10.	Frigero M, Bonagamba LG, Machado BH. The gain of the baroreflex bradycardia is reduced by microinjection of NMDA receptor antagonists into the nucleus tractus solitarii of awake rats [J]. J Auton Nerv Syst, 2000, 79(1): 2833.
11.	Xiao L, Wu YM, Zhang H, et al. Hydrogen sulfide facilitates carotid sinus baroreflex in anesthetized rats [J]. Acta Pharmacol Sin, 2006, 27(3): 294298.
12.	Zhang H, Moochhala SM, Bhatia M. Endogenous hydrogen sulfide regulates inflammatory response by activating the ERK pathway in polymicrobial sepsis [J]. J Immunol, 2008, 181(6): 43204331.
13.	Dawe GS, Han SP, Bian JS, et al. Hydrogen sulphide in the hypothalamus causes an ATPsensitive K+ channeldependent decrease in blood pressure in freely moving rats [J]. Neuroscience, 2008, 152(1): 169177.
14.	Wang WZ, Gao L, Wang HJ, et al. Interaction between cardiac sympathetic afferent reflex and chemoreflex is mediated by the NTS AT1 receptors in heart failure [J]. Am J Physiol Heart Circ Physiol, 2008, 295(3): H1216H1226.
15.	Chen CQ, Xin H, Zhu YZ. Hydrogen sulfide: third gaseous transmitter, but with great pharmacological potential [J]. Acta Pharmacol Sin, 2007, 28(11): 17091716.
16.	Zhang H, Zhi L, Moochhala S, et al. Hydrogen sulfide acts as an inflammatory mediator in cecal ligation and punctureinduced sepsis in mice by upregulating the production of cytokines and chemokines via NFkappaB [J]. Am J Physiol Lung Cell Mol Physiol, 2007, 292(4): L960L971.
17.	Collin M, Anuar FB, Murch O, et al. Inhibition of endogenous hydrogen sulfide formation reduces the organ injury caused by endotoxemia [J]. Br J Pharmacol, 2005, 146(4): 498505.
18.	Sivarajah A, McDonald MC, Thiemermann C. The production of hydrogen sulfide limits myocardial ischemia and reperfusion injury and contributes to the cardioprotective effects of preconditioning with endotoxin, but not ischemia in the rat [J]. Shock, 2006, 26(2): 154161.
19.	Hui Y, Du J, Tang C, et al. Changes in arterial hydrogen sulfide (H2S) content during septic shock and endotoxin shock in rats [J]. J Infect, 2003, 47(2): 155160.
20.	肖琳, 武宇明, 何瑞荣. 新型气体信号分子－硫化氢心血管作用的研究进展 [J]. 河北医科大学学报, 2006, 27(2): 142145.
21.	顾俊, 卢竞前, 李易. 硫化氢与心血管疾病研究进展 [J]. 实用医药杂志, 2009, 26(9): 8486.
22.	Yokoshiki H, Sunagawa M, Seki T, et al. ATPsensitive K+ channels in pancreatic, cardiac, and vascular smooth muscle cells [J]. Am J Physiol, 1998, 274(1 Pt 1): C25C37.
23.	Quast U. ATPsensitive K+ channels in the kidney [J]. Naunyn Schmiedebergs Arch Pharmacol, 1996, 354(3): 213225.
24.	Kimura Y, Dargusch R, Schubert D, et al. Hydrogen sulfide protects HT22 neuronal cells from oxidative stress [J]. Antioxid Redox Signal, 2006, 8(34): 661670.
25.	VayssettesCourchay C, Bouysset F, Verbeuren TJ. Sympathetic activation and tachycardia in lipopolysaccharide treated rats are temporally correlated and unrelated to the baroreflex [J]. Auton Neurosci, 2005, 120(12): 3545.
26.	Matias CM, Saggau P, QuintaFerreira ME. Blockade of presynaptic K ATP channels reduces the zincmediated posttetanic depression at hippocampal mossy fiber synapses [J]. Brain Res, 2010, 1320: 2227.

1. 李德馨. Sepsis的定义和治疗进展-在隧道尽头的亮点? [J]. 国外医学麻醉学与复苏分册, 2003, 24(4): 193195.
2. Shen FM, Guan YF, Xie HH, et al. Arterial baroreflex function determines the survival time in lipopolysaccharideinduced shock in rats [J]. Shock, 2004, 21(6): 556560.
3. Shi KY, Shen FM, Liu AJ, et al. The survival time postcecal ligation and puncture in sinoaortic denervated rats [J]. J Cardiovasc Pharmacol, 2007, 50(2): 162167.
4. Schmidt HB, Werdan K, MüllerWerdan U. Autonomic dysfunction in the ICU patient [J]. Curr Opin Crit Care, 2001, 7(5): 314322.
5. Pancoto JA, Corrêa PB, OliveiraPelegrin GR, et al. Autonomic dysfunction in experimental sepsis induced by cecal ligation and puncture [J]. Auton Neurosci, 2008, 138(12): 5763.
6. Li L, Bhatia M, Zhu YZ, et al. Hydrogen sulfide is a novel mediator of lipopolysaccharideinduced inflammation in the mouse [J]. FASEB J, 2005, 19(9): 11961198.
7. 康凯, 姜洪池. 气体信号分子硫化氢与疾病 [J]. 中国普外基础与临床杂志, 2009, 16(2): 170173.
8. Zhang H, Zhi L, Moore PK, et al. Role of hydrogen sulfide in cecal ligation and punctureinduced sepsis in the mouse [J]. Am J Physiol Lung Cell Mol Physiol, 2006, 290(6): L1193L1201.
9. Seagard JL, Dean C, Hopp FA. Neurochemical transmission of baroreceptor input in the nucleus tractus solitarius [J]. Brain Res Bull, 2000, 51(2): 111118.
10. Frigero M, Bonagamba LG, Machado BH. The gain of the baroreflex bradycardia is reduced by microinjection of NMDA receptor antagonists into the nucleus tractus solitarii of awake rats [J]. J Auton Nerv Syst, 2000, 79(1): 2833.
11. Xiao L, Wu YM, Zhang H, et al. Hydrogen sulfide facilitates carotid sinus baroreflex in anesthetized rats [J]. Acta Pharmacol Sin, 2006, 27(3): 294298.
12. Zhang H, Moochhala SM, Bhatia M. Endogenous hydrogen sulfide regulates inflammatory response by activating the ERK pathway in polymicrobial sepsis [J]. J Immunol, 2008, 181(6): 43204331.
13. Dawe GS, Han SP, Bian JS, et al. Hydrogen sulphide in the hypothalamus causes an ATPsensitive K+ channeldependent decrease in blood pressure in freely moving rats [J]. Neuroscience, 2008, 152(1): 169177.
14. Wang WZ, Gao L, Wang HJ, et al. Interaction between cardiac sympathetic afferent reflex and chemoreflex is mediated by the NTS AT1 receptors in heart failure [J]. Am J Physiol Heart Circ Physiol, 2008, 295(3): H1216H1226.
15. Chen CQ, Xin H, Zhu YZ. Hydrogen sulfide: third gaseous transmitter, but with great pharmacological potential [J]. Acta Pharmacol Sin, 2007, 28(11): 17091716.
16. Zhang H, Zhi L, Moochhala S, et al. Hydrogen sulfide acts as an inflammatory mediator in cecal ligation and punctureinduced sepsis in mice by upregulating the production of cytokines and chemokines via NFkappaB [J]. Am J Physiol Lung Cell Mol Physiol, 2007, 292(4): L960L971.
17. Collin M, Anuar FB, Murch O, et al. Inhibition of endogenous hydrogen sulfide formation reduces the organ injury caused by endotoxemia [J]. Br J Pharmacol, 2005, 146(4): 498505.
18. Sivarajah A, McDonald MC, Thiemermann C. The production of hydrogen sulfide limits myocardial ischemia and reperfusion injury and contributes to the cardioprotective effects of preconditioning with endotoxin, but not ischemia in the rat [J]. Shock, 2006, 26(2): 154161.
19. Hui Y, Du J, Tang C, et al. Changes in arterial hydrogen sulfide (H2S) content during septic shock and endotoxin shock in rats [J]. J Infect, 2003, 47(2): 155160.
20. 肖琳, 武宇明, 何瑞荣. 新型气体信号分子－硫化氢心血管作用的研究进展 [J]. 河北医科大学学报, 2006, 27(2): 142145.
21. 顾俊, 卢竞前, 李易. 硫化氢与心血管疾病研究进展 [J]. 实用医药杂志, 2009, 26(9): 8486.
22. Yokoshiki H, Sunagawa M, Seki T, et al. ATPsensitive K+ channels in pancreatic, cardiac, and vascular smooth muscle cells [J]. Am J Physiol, 1998, 274(1 Pt 1): C25C37.
23. Quast U. ATPsensitive K+ channels in the kidney [J]. Naunyn Schmiedebergs Arch Pharmacol, 1996, 354(3): 213225.
24. Kimura Y, Dargusch R, Schubert D, et al. Hydrogen sulfide protects HT22 neuronal cells from oxidative stress [J]. Antioxid Redox Signal, 2006, 8(34): 661670.
25. VayssettesCourchay C, Bouysset F, Verbeuren TJ. Sympathetic activation and tachycardia in lipopolysaccharide treated rats are temporally correlated and unrelated to the baroreflex [J]. Auton Neurosci, 2005, 120(12): 3545.
26. Matias CM, Saggau P, QuintaFerreira ME. Blockade of presynaptic K ATP channels reduces the zincmediated posttetanic depression at hippocampal mossy fiber synapses [J]. Brain Res, 2010, 1320: 2227.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Effect of Hydrogen Sulfide on Arterial Baroreflex in Rat with Sepsis

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