[Effect of hydrogen sulfide on rat pulmonary artery reactivity and injury induced by lipopolysaccharide].Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2010 Aug; 22(8):465-8.ZW
To explore the effects of hydrogen sulfide (H2S) on abnormal pulmonary artery reactivity and injury induced by lipopolysaccharide (LPS).
Seventy-two rats were divided into four groups randomly according to table of random number: control group, LPS group, sodium hydrosulfide (NaHS) as a donor of H2S+LPS group and NaHS+normal saline (NS) group (n=18 in each group). Rats were challenged with 0.8 ml/kg LPS (200 microg/200 microl) by intratracheal instillation. NaHS (28 micromol/kg, 0.5 ml) was injected intraperitoneally 10 minutes before LPS instillation and 2 hours after LPS instillation. Twelve hours later, 6 rats from each group were sacrificed. Blood from carotid artery was collected to detect H2S content in serum. After that, pulmonary artery rings (PARs) were prepared carefully, then the contraction response of PARs to phenylephrine (PE, 10(-6) mol/L) and the endothelium-dependent relaxation response to acetylcholine (ACh, 10(-6) mol/L) were measured using isolated vascular ring tension detecting technique. Six rats from each group were sacrificed for determination of malondialdehyde (MDA) content of pulmonary artery, and the remaining 6 rats from each group were sacrificed for observation of morphological changes in pulmonary artery tissue.
Compared with control group, after LPS instillation, the contraction response (g/mg) of PARs to PE increased greatly (0.86+/-0.20 vs. 0.56+/-0.13), the relaxation response to ACh significantly decreased [(65.18+/-7.05)% vs. (84.13+/-8.84)%]. MDA content (mmol/L) in pulmonary artery tissues increased (32.03+/-7.81 vs. 5.82+/-0.92), and H2S (micromol/L) content in serum decreased (175.23+/-27.36 vs. 238.12+/-16.38). Changes of all results were significant (P<0.05 or P<0.01). The pulmonary artery tissue and endothelium were injured. However, these changes were reversed by administration of NaHS intraperitoneally, the contraction response of PARs to PE decreased [(0.61+/-0.17) g/mg], the relaxation response to ACh increased [(82.92+/-9.71)%], MDA content in pulmonary artery tissue decreased [(16.88+/-3.54) mmol/L] and H2S content in serum increased [(242.70+/-38.80) micromol/L]. There was significant difference in all results (P<0.05 or P<0.01). The injury to the tissue induced by LPS were alleviated significantly. There was no statistical difference in above indexes between NaHS+NS group and control group, except for the level of H2S.
Exogenous H2S could not only reverse abnormal vascular reactivity of PARs induced by LPS but also alleviate the injury to pulmonary artery tissue induced by LPS.