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[The role of hydrogen sulfide in acute lung injury during endotoxic shock and its relationship with nitric oxide and carbon monoxide].
Zhonghua Yi Xue Za Zhi. 2008 Aug 19; 88(32):2240-5.ZY

Abstract

OBJECTIVE

To explore the role of hydrogen sulfide (H2S) in acute lung injury (ALI) during endotoxic shock (ES) and its relationship with nitric oxide (NO) and carbon monoxide (CO).

METHODS

Sixty-four adult male SD rats were randomly divided into 4 equal groups: control group injected with normal saline via the caudal vein, lipopolysaccharide (LPS)-treated group injected with LPS to establish ES model, LPS + NaHS group injected with LPS and sodium hydrosulfide (NaHS, an exogenous H2S donor], and LPS + PPG group injected with LPS and polypropylene glycol (PPG, a H2S synthase inhibitor). The mean artery pressure (MAP) was measured via a polyethylene catheter in the right common carotid artery for 6 h. Then the rats were sacrificed with their lungs taken out to determine the lung water content, lung tissue malonyldialdehyde (MDA), NO, and CO contents, as well as lung tissue cystathionine-gamma-lyase (CSE), myeloperoxidase (MPO), nitric oxide synthase (NOS), and heme oxygenase (HO) activities. The H2S content in blood plasma was detected also. Morphological changes of the lung tissues were observed under light microscope and the index of quantitative assessment (IQA) of lung injury was calculated. Immunohistochemistry and Western blotting were used to detect the lung tissue inducible NOS (iNOS) and HO-1 protein expression.

RESULTS

Compared with the control group, the MAP of the LPS group was significantly lower, the pathological changes in lung tissue was more obvious, and the IQA, lung water content, lung MDA content, lung MPO and CSE activities as well as plasma H2S content were all significantly higher (P < 0.05 or P < 0.01). Compared to the LPS group, the plasma H2S and lung CSE activity of the LPS + NaHS group were higher, the lung injury was more severe, and the MAP was lower. And compared to the LPS group, the MAP of the LPS + PPG group was higher, and the lung injury was milder (both P < 0.05). The eNOS activity in the lung tissue of the LPS group was (5.26 +/- 0.25) Uxmg(-1)xprot(-1), significantly lower than that of the control group [(6.45 +/- 0.42) Uxmg(-1)xprot(-1)]; and the iNOS activity and NO content of the LPS group were (12.6 +/- 0.6) Uxmg(-1)xprot(-1) and (144 +/- 25) micromol/L respectively, both higher than those of the control group [(10.5 +/- 0.7) Uxmg(-1)xprot(-1) and (68 +/- 5) micromol/L respectively] (P < 0.05 or P < 0.01). Compared with the LPS group, the lung tissue eNOS activity of the LPS + PPG group was significantly higher, and the iNOS activity [(10.2 +/- 0.4) Uxmg(-1)xprot(-1)], iNOS protein expression, and NO content [(74 +/- 5) micromol/L]were all significantly lower (P < 0.05 or P < 0.01). Compared with the LPS group, the lung tissue eNOS activity of the LPS + NaHS group [(4.81 +/- 0.23) Uxmg(-1)xprot(-1)] was significantly lower, and the iNOS activity [(14.6 +/- 0.4) Uxmg(-1)xprot(-1)], iNOS protein expression, and NO content [(217 +/- 18) micromol/L] were significantly higher (P < 0.05 or P < 0.01). The lung tissue HO activity [(173 +/- 31) pkat/g], HO protein expression, and CO content [(3.63 +/- 0.24)%] of the LPS group were all significantly higher than those of the control group [(125 +/- 22) pkat/g, (2.48 +/- 0.33)%, both P < 0.05], and the LPS + PPG group [(88 +/- 17) pkat/g, (2.98 +/- 0.23)%, both P < 0.05]. Compared to the LPS group, the lung tissue HO activity [(263 +/- 37) pkat/g], HO protein expression, and CO content [(4.35 +/- 0.32)%] of the LPS + NaHS group were all significantly higher (all P < 0.05).

CONCLUSION

The increase of H(2)S generation participates in the lung tissue injury during ES and this event is related to eNOS activity decrease, iNOS activity increase that causes the production of large amount of NO. H2S up-regulates the HO-1/CO system in the lung tissues during ES, which may be the endogenous compensatory response against the injury.

Links

Publisher Full Text

Authors+Show Affiliations

Huang XL
Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.
Zhou XH
No affiliation info available
Wei P
No affiliation info available
Xian XH
No affiliation info available
Ling YL
No affiliation info available

MeSH

Acute Lung InjuryAnimalsBlood PressureCarbon MonoxideCystathionine gamma-LyaseHeme Oxygenase (Decyclizing)Hydrogen SulfideLipopolysaccharidesLungMaleMalondialdehydeNitric OxideNitric Oxide SynthasePeroxidaseRatsRats, Sprague-DawleyShock, SepticSulfides

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

19087669

Citation

Huang, Xin-li, et al. "[The Role of Hydrogen Sulfide in Acute Lung Injury During Endotoxic Shock and Its Relationship With Nitric Oxide and Carbon Monoxide]." Zhonghua Yi Xue Za Zhi, vol. 88, no. 32, 2008, pp. 2240-5.
Huang XL, Zhou XH, Wei P, et al. [The role of hydrogen sulfide in acute lung injury during endotoxic shock and its relationship with nitric oxide and carbon monoxide]. Zhonghua Yi Xue Za Zhi. 2008;88(32):2240-5.
Huang, X. L., Zhou, X. H., Wei, P., Xian, X. H., & Ling, Y. L. (2008). [The role of hydrogen sulfide in acute lung injury during endotoxic shock and its relationship with nitric oxide and carbon monoxide]. Zhonghua Yi Xue Za Zhi, 88(32), 2240-5.
Huang XL, et al. [The Role of Hydrogen Sulfide in Acute Lung Injury During Endotoxic Shock and Its Relationship With Nitric Oxide and Carbon Monoxide]. Zhonghua Yi Xue Za Zhi. 2008 Aug 19;88(32):2240-5. PubMed PMID: 19087669.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [The role of hydrogen sulfide in acute lung injury during endotoxic shock and its relationship with nitric oxide and carbon monoxide]. AU - Huang,Xin-li, AU - Zhou,Xiao-hong, AU - Wei,Peng, AU - Xian,Xiao-hui, AU - Ling,Yi-ling, PY - 2008/12/18/entrez PY - 2008/12/18/pubmed PY - 2009/4/10/medline SP - 2240 EP - 5 JF - Zhonghua yi xue za zhi JO - Zhonghua Yi Xue Za Zhi VL - 88 IS - 32 N2 - OBJECTIVE: To explore the role of hydrogen sulfide (H2S) in acute lung injury (ALI) during endotoxic shock (ES) and its relationship with nitric oxide (NO) and carbon monoxide (CO). METHODS: Sixty-four adult male SD rats were randomly divided into 4 equal groups: control group injected with normal saline via the caudal vein, lipopolysaccharide (LPS)-treated group injected with LPS to establish ES model, LPS + NaHS group injected with LPS and sodium hydrosulfide (NaHS, an exogenous H2S donor], and LPS + PPG group injected with LPS and polypropylene glycol (PPG, a H2S synthase inhibitor). The mean artery pressure (MAP) was measured via a polyethylene catheter in the right common carotid artery for 6 h. Then the rats were sacrificed with their lungs taken out to determine the lung water content, lung tissue malonyldialdehyde (MDA), NO, and CO contents, as well as lung tissue cystathionine-gamma-lyase (CSE), myeloperoxidase (MPO), nitric oxide synthase (NOS), and heme oxygenase (HO) activities. The H2S content in blood plasma was detected also. Morphological changes of the lung tissues were observed under light microscope and the index of quantitative assessment (IQA) of lung injury was calculated. Immunohistochemistry and Western blotting were used to detect the lung tissue inducible NOS (iNOS) and HO-1 protein expression. RESULTS: Compared with the control group, the MAP of the LPS group was significantly lower, the pathological changes in lung tissue was more obvious, and the IQA, lung water content, lung MDA content, lung MPO and CSE activities as well as plasma H2S content were all significantly higher (P < 0.05 or P < 0.01). Compared to the LPS group, the plasma H2S and lung CSE activity of the LPS + NaHS group were higher, the lung injury was more severe, and the MAP was lower. And compared to the LPS group, the MAP of the LPS + PPG group was higher, and the lung injury was milder (both P < 0.05). The eNOS activity in the lung tissue of the LPS group was (5.26 +/- 0.25) Uxmg(-1)xprot(-1), significantly lower than that of the control group [(6.45 +/- 0.42) Uxmg(-1)xprot(-1)]; and the iNOS activity and NO content of the LPS group were (12.6 +/- 0.6) Uxmg(-1)xprot(-1) and (144 +/- 25) micromol/L respectively, both higher than those of the control group [(10.5 +/- 0.7) Uxmg(-1)xprot(-1) and (68 +/- 5) micromol/L respectively] (P < 0.05 or P < 0.01). Compared with the LPS group, the lung tissue eNOS activity of the LPS + PPG group was significantly higher, and the iNOS activity [(10.2 +/- 0.4) Uxmg(-1)xprot(-1)], iNOS protein expression, and NO content [(74 +/- 5) micromol/L]were all significantly lower (P < 0.05 or P < 0.01). Compared with the LPS group, the lung tissue eNOS activity of the LPS + NaHS group [(4.81 +/- 0.23) Uxmg(-1)xprot(-1)] was significantly lower, and the iNOS activity [(14.6 +/- 0.4) Uxmg(-1)xprot(-1)], iNOS protein expression, and NO content [(217 +/- 18) micromol/L] were significantly higher (P < 0.05 or P < 0.01). The lung tissue HO activity [(173 +/- 31) pkat/g], HO protein expression, and CO content [(3.63 +/- 0.24)%] of the LPS group were all significantly higher than those of the control group [(125 +/- 22) pkat/g, (2.48 +/- 0.33)%, both P < 0.05], and the LPS + PPG group [(88 +/- 17) pkat/g, (2.98 +/- 0.23)%, both P < 0.05]. Compared to the LPS group, the lung tissue HO activity [(263 +/- 37) pkat/g], HO protein expression, and CO content [(4.35 +/- 0.32)%] of the LPS + NaHS group were all significantly higher (all P < 0.05). CONCLUSION: The increase of H(2)S generation participates in the lung tissue injury during ES and this event is related to eNOS activity decrease, iNOS activity increase that causes the production of large amount of NO. H2S up-regulates the HO-1/CO system in the lung tissues during ES, which may be the endogenous compensatory response against the injury. SN - 0376-2491 UR - https://www.unboundmedicine.com/medline/citation/19087669/[The_role_of_hydrogen_sulfide_in_acute_lung_injury_during_endotoxic_shock_and_its_relationship_with_nitric_oxide_and_carbon_monoxide]_ L2 - http://journal.yiigle.com/LinkIn.do?linkin_type=pubmed&amp;issn=0376-2491&amp;year=2008&amp;vol=88&amp;issue=32&amp;fpage=2240 DB - PRIME DP - Unbound Medicine ER -