[Relationship between hydrogen sulfide and myocardial damage in endotoxemic rats].
To investigate the changes and role of hydrogen sulfide (H2S) in myocardial damage in endotoxemic rats, a rat model of endotoxemia induced by injection of lipopolysaccharide (LPS) was developed. Male Wistar rats were divided into four groups: control group, LPS group, LPS + propargylglycine (PPG, a metabolic enzyme inhibitor of H2S) group and LPS + NaHS (H2S donor) group. The mean arterial pressure (MAP) of rats within 4 h was observed, TNF-alpha and H2S contents in plasma, TNF-alpha and H2S contents, lactate dehydrogenase (LDH) and myeloperoxidase (MPO) activity in cardiac muscles were determined. The morphological structure of cardiac muscle was observed. Administration of LPS caused a sustained fall in MAP within 4 h, and significant increases in TNF-alpha and H2S contents in plasma (P<0.05). Plasmic H2S content was negatively correlated with MAP (r = -0.936, -0.913 and -0.908 at 1, 2 and 4 h, respectively, P<0.05). LPS also induced increases in TNF-alpha and H2S contents, LDH and MPO activity in cardiac muscles and myocardial damage. Treatment with PPG reduced the increases in TNF-alpha and H2S contents in plasma, TNF-alpha and H2S contents, LDH and MPO activity in cardiac muscles, ameliorated the hypotensive effect and myocardial damage caused by LPS administration (P<0.05). However, treatment with NaHS increased TNF-alpha and H2S contents in plasma, TNF-alpha and H2S contents, LDH and MPO activity in cardiac muscles, and aggravated the hypotensive action and tissue injuries caused by LPS administration (P<0.05). It is suggested that hypotension and myocardial damage in endotoxemic rats are partly induced by increase in H2S content.
Xian
Xiao-Hui
XH
Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.
Huang
Xin-Li
XL
Zhou
Xiao-Hong
XH
Zhang
Jing-Kun
JK
Ling
Yi-Ling
YL
D000818:Animals; D001794:Blood Pressure; D019446:Endotoxemia / Q000378:metabolism / Q000473:pathology*; D006862:Hydrogen Sulfide / Q000097:blood*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D009206:Myocardium / Q000737:chemistry / Q000473:pathology*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D006862:Hydrogen Sulfide