The interventional effects of saturated hydrogen saline on lung injury in rats with cecal ligation and puncture operation / 中国应用生理学杂志

OBJECTIVE@#To investigate the hypothesis that hydrogen could ameliorate cecal ligation and puncture (CLP)-induced lung injury of rats by inhibiting cystathionine-gamma-lyase/hydrogen sulfide (CSE/HS) system.@*METHODS@#A total number of 24 healthy male SD rats weighting 250～300 g were randomly divided into four groups (n=6 in each group): sham operation group(sham group), hydrogen-rich saline control group(H group), CLP group and hydrogen-rich saline treatment group(CLP+H group). The rats were treated with hydrogen-rich saline or saline 10 min before CLP or sham operation. At 8 h of sham or CLP operation, lung samples were obtained to detect the changes of the CSE/HS system using biochemical and RT-PCR methods. In order to further confirm the role of HS during hydrogen improve the lung injury of CLP rats, we also observed the effect of hydrogen-rich saline on the lung injury induced by HS donor-sodium sodium hydrosulfide (NaHS). Thirty-two healthy male SD rats (250~300 g) were randomly divided into four groups (n=8 in each group): control group, HS group, HS+H group and H group. Saline(10 mg/kg) or NaHS(HS donor, 56 μmol/kg) was injected intraperitoneally (10 mg/kg) respectively into rats in the control rats or HS group. For rats in the HS+H and H group, hydrogen-rich saline (10 mg/kg) was injected 10 min before saline or NaHS administration. Eight hours after the LPS saline or NaHS administration, lung coefficient, MDA content, and MPO activity were detected. The contents of TNF-α, IL-6 and IL-10 in lung tissue were measured, and the morphological changes of lung tissue were also observed.@*RESULTS@#CSE/HS system up-regulating were observed in animals exposed to CLP. Hydrogen-rich saline treatment significantly inhibited CSE/HS system as indicated by significantly reduced HS production in lung, along with a decreased CSE activity and CSE mRNA expression (all P＜0.05). Importantly, the results showed that lung injury and lung tissue inflammation were observed in animals exposed to NaHS. Hydrogen-rich saline treatment significantly attenuated lung injury as indicated by significantly improved histological changes in lung, significantly reduced index of quantitative assessment (IQA), MDA content and lung coefficient (all P＜0.05). MPO activity in lung tissue was significantly reduced along with decreased productions of TNF-α and IL-6, and an increased production of IL-10 in the presence of hydrogen (all P＜0.05), demonstrating antioxidant and anti-inflammatory effect of hydrogen in NaHS-induced ALI.@*CONCLUSION@#These results indicate that hydrogen-rich saline peritoneal injection improves the lung injury induced by CLP operation. The therapeutic effects of hydrogen-rich saline may be related to suppressing the production of HS.

Association between doctor selection habit and precision search on Internet medical platform / 中华医学图书情报杂志

The difference between doctor selection needs of the public and medical service at present was analyzed according to the questionnaire investigation of doctor selection habit of the public. The association between the focus on doctor personal information and the importance of different factors influencing doctor selection was analyzed ac-cording to the information searching methods used by the public when they selected their doctor. The effective pre-cision search approaches and methods on the Internet medical platform were proposed, including information searching methods on innovation platform, standardizing the weight of different kinds of information, and perfecting the pushing and recommending mechanisms for doctor selection searching results.

Hydrogen sulfide reduces lipopolysaccharide-induced acute lung injury and inhibits expression of phosphorylated p38 MAPK in rats / 生理学报

To investigate the influence of hydrogen sulfide (H₂S) on p38 MAPK signaling pathway during acute lung injury (ALI) caused by lipopolysaccharide (LPS), the rats were randomly divided into six groups: control group, LPS group, LPS + NaHS group, LPS + PPG (cystathionine-γ-lyase inhibitor) group, NaHS group and PPG group. The rats were sacrificed 6 h after injection and lung tissues were obtained. The structure of lung tissues and the number of polymorphonuclear leucocyte (PMN) was observed under optical microscope; the lung myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were tested; intercellular adhesion molecule-1 (ICAM-1) protein expression changes were detected by immunohistochemical staining; phosphorylated p38 MAPK (p-p38 MAPK) protein expression was detected by Western blotting. The results showed that the lung injury in LPS group was observed, at the same time the MPO activity, the content of MDA, ICAM-1 and p-p38 MAPK protein expressions, the number of PMN were all higher than those in control group (all P < 0.05). Pre-injection of NaHS alleviated the changes induced by LPS, while pre-injection of PPG aggravated those alterations (all P < 0.05). ICAM-1 and p-p38 MAPK protein expressions in lung tissue were positively correlated (r = 0.923, P < 0.01). The results suggest that H2S may reduce LPS-induced ALI through inhibiting the conjugation of p38 MAPK and reducing the expression of ICAM-1.

Effect of exogenous hydrogen sulfide on polymorphonuclear neutrophil accumulation in acute lung injury rat induced by lipopolysaccharides and its mechanism / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced polymorphonuclear neutrophil (PMN) accumulation and its mechanism.</p><p><b>METHODS</b>The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS). Adult male Spraguce-Dawley (SD) rats were randomly divided into four groups (n = 8 - 12 per group): Control group (0.5 ml/kg normal saline i.v.), LPS-treated group (1 mg/kg, i.v.), LPS plus NaHS (1 mg/kg i.v. and 28 micromol/kg i.p., respectively) and NaHS group (28 micromol/kg i.p.). Animals were sacrificed at 6 h after agent administration. Morphological changes of lung tissues were observed and polymorphonuclear neutrophil (PMN) number in alveolar septum was tested. The apoptosis of PMN in the bronchoalveolar lavage fluid (BALF) was examined with in situ TdT-mediated dUTP end labeling (TUNEL). Intercellular adhesion factor-1 (ICAM-1) and nuclear factor-kappaB (NF-kappaB) expressions in the lung tissue were analyzed by Western Blot.</p><p><b>RESULTS</b>The results showed that bleeding, edema, PMN accumulation and other pathological signs in the lung tissue emerged after LPS injection. Compared to control rats, the LPS-treated rats had increased PMN number, decreased PMN apoptotic percentages, and increased expressions of ICAM-1 and NF-kappaB. Administration of NaHS into LPS-treated rats reduced the PMN number and expressions of ICAM-1 and NF-kappaB but increased PMN apoptotic percentages. In addition, NaHS alleviated the degree of ALI. There were no significant differences of the above indicators between NaHS-treated rats and control rats.</p><p><b>CONCLUSION</b>NaHS can reduce the PMN accumulation in the lung, and its mechanism is related to down-regulation expression of ICAM-1 and promotion of PMN apoptosis induced by inhibition of NF-kappaB pathway.</p>

Protection of carbon monoxide-releasing molecule against lung injury induced by limb ischemia-reperfusion / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To observe the role and mechanism of CO-releasing molecule (CORM)-2 in lung injury induced by ischemia-reperfusion (IR) of hind limbs in rats.</p><p><b>METHODS</b>A rat model of lung injury induced by IR of hind limbs was established. A total of 40 Sprague Dawley (SD) rats were randomly divided into 5 groups (n equal to 8): sham, sham + CORM-2, IR, IR + CORM-2 and IR + dimethyl sulfoxide (DMSO). Rats in the IR group received hind limb ischemia for 2 hours and reperfusion for 2 hours, rats in the sham group underwent sham surgery without infrarenal aorta occlusion, rats in the IR+CORM-2 group and in the sham + CORM-2 group were given CORM-2 (10 micromol/kg intravenous bolus) 5 minutes before reperfusion or at the corresponding time points, while rats in the IR + DMSO group was treated with the same dose of vehicle (DMSO) at the same time. The lung tissue structure, polymorphonuclear neutrophil (PMN) count, wet-to-dry weight ratio (W/D), malondialdehyde (MDA) content, myeloperoxidase (MPO) activity, intercellular adhesion molecule-1 (ICAM-1) expression,IkBa degradation and nuclear factor (NF)-kB activity in the lungs were assessed.</p><p><b>RESULTS</b>As compared with the sham group, lung PMNs number, W/D, MDA content, MPO activity, ICAM-1 expression and NF-kB activity significantly increased in the IR group, but the level of IkBa decresed (P less than 0.01). Compared with the IR group, lung PMNs number, W/D, MDA content, MPO activity and ICAM-1 expression significantly decreased in the IR+COMR-2 group (P less than 0.01), while the level of IkBa increased.</p><p><b>CONCLUSIONS</b>These data demonstrate that CORM-2 attenuates limb IR-induced lung injury through inhibiting ICAM-1 protein expression, NF-kB pathway and the leukocytes sequestration in the lungs following limb IR in rats, suggesting that CORM-2 may be used as a therapeutic agent against lung injury induced by limb IR.</p>

Application of fluorescence in situ hybridization in prenatal diagnosis of complex chromosomal abnormalities / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the application of fluorescence in situ hybridization (FISH) technique in prenatal diagnosis of complex chromosomal abnormalities.</p><p><b>METHODS</b>Eleven prenatal diagnosis cases (8 from amniocentesis and 3 from cord blood) with complex chromosomal abnormalities detected by routine G-banding, were further analyzed by FISH.</p><p><b>RESULTS</b>The FISH technique confirmed the results of balanced chromosome rearrangements detected by G-banding, and clarified the structure of the derivative chromosomes in the 3 amniocentesis samples and the origin of the mark chromosomes in the 2 cord blood samples.</p><p><b>CONCLUSION</b>FISH can be used to diagnose the complex chromosomal abnormalities accurately in prenatal diagnosis, and can provide very useful genetic information for clinical diagnosis and treatment.</p>

Role of endogenous and exogenous hydrogen sulfide in acute lung injury induced by LPS in rats / 中国应用生理学杂志

<p><b>AIM</b>To explore the role of endogenous and exogenous hydrogen sulfide (H2S) in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats and the underlying mechanisms.</p><p><b>METHODS</b>120 Sprague-Dawley rats were randomly divided into four groups: control, LPS (instilled intratracheally to induce ALI), NaHS (H2S donor) + LPS, and propargylglycin (PPG) + LPS. Animals were sacrificed at 4 h or 8 h after agent administration. Lung weight/body weight ratio (LW/BW) was measured and calculated. Morphological changes of lung tissues were observed. H2S concentration, NO concentration (NO) and carbon monoxide (CO) level in plasma were tested. Malondialdehyde (MDA) content, CSE activity, inducible nitric oxide synthase (iNOS) activity and hemeoxygenase (HO) activity of the lung were determined. PMN and protein content in BALF were also tested. Immunohistochemisty technique was performed to examine the expression of iNOS and HO-1 protein in lung tissues. The correlation of H2S content with the above indices was analyzed.</p><p><b>RESULTS</b>Compared with control conditions, severe injuries of lung tissues and a raised LW/BW, MDA content, PMN and protein content in BALF were observed in rats treated with LPS. LPS also lead to a drop in plasma H2S concentration and lung CSE activity. The enzyme activity of iNOS and HO, the protein expression of them and plasma NO, CO level increased after LPS instillation. Administration of NaHS before LPS could attenuated the changes induced by LPS. Pre-administration of PPG exacerbated the injuries induced by LPS, increased PMN and protein content in BALF, the plasma NO level, lung iNOS activity and its protein expression, but there was no prominent variation in CO level, HO activity and HO-1 protein expression compared with those of LPS group. The H2S content was positively correlated with CSE activity, CO content and HO-1activity (r = 0.945-0.987, P < 0.01), and negatively correlated with the other indices (r = -0.994 - -0.943, P < 0.01).</p><p><b>CONCLUSION</b>Downregulation of H2S/CSE was involved in the pathogenesis of acute lung injury induced by LPS. Endogenous and exogenous H2S provided protection against the lung injuries, which might be explained by its anti-oxidative effects, attenuating inflammatory over-reaction in lung induced by PMN,the downregulation NO/iNOS system and the upregulation of CO/HO-1 system.</p>

Role of polymorphonuclear neutrophil in exogenous hydrogen sulfide attenuating endotoxin-induced acute lung injury / 生理学报

The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS) and cultured human peripheral blood polymorphonuclear neutrophil (PMN) were used to study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. Control group, NaHS group, LPS group and LPS + NaHS group were established both in in vivo and in vitro studies. Microvascular permeability, PMN accumulation in lung and apoptosis of PMN were detected. The results showed that: (1) In in vivo study, PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS + NaHS group (P<0.05, P<0.01); (2) In in vitro study, the apoptotic rates of PMN in LPS group and NaHS group were significantly higher than that in control group (P<0.01), while compared with LPS group, LPS + NaHS group showed significantly higher apoptotic rate (P<0.01). These results suggest that NaHS attenuates LPS-induced microvascular permeability and alleviates ALI. PMN apoptosis induced by NaHS is possibly one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.

Ameliorative effects of exogenous sulfur dioxide on lipopolysaccharide-induced acute lung injury in rats / 生理学报

To investigate the influence of sulfur dioxide (SO₂) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), we examined the influence of exogenous SO₂ on pulmonary tissue inflammatory response. A rat model of ALI induced by intravenous (IV) injection of LPS was developed. Male Sprague-Dawley (SD) rats were divided into four groups randomly: control group, LPS group, LPS plus SO₂ group (IV injection of 0.5 mL Na₂SO₃/NaHSO₃ 10 min before LPS administration) and SO₂ group (only given Na₂SO₃/NaHSO₃). Animals were sacrificed 6 h after agent administration. Lung weight/body weight ratio (LW/BW) was measured and calculated. Morphological changes of lung tissues were observed. The number of polymorphonuclear neutrophil (PMN) in the bronchoalveolar lavage fluid (BALF), intercellular adhesion factor-1 (ICAM-1) expression in the lung tissue and IL-1, IL-6 and IL-10 levels in the serum were tested. The results showed that, compared to control rats, the LPS-treated rats had severe injuries of lung tissues and an increased LW/BW, increased index of quantitative assessment (IQA) score, increased PMN number in the BALF, increased ICAM-1 expression in the lung tissue and increased IL-1, IL-6 and IL-10 levels in the serum 6 h after LPS injection. Administration of the SO₂ donor, Na₂SO/₃NaHSO₃, into LPS-treated rats reduced the LW/BW, PMN number and ICAM-1 expression, and alleviated the degree of ALI (measured by the IQA score). In addition, Na₂SO₃/NaHSO₃ decreased IL-1 and IL-6 levels, but increased IL-10 level in the serum. There were no significant differences in the above indexes between SO₂-treated rats and control rats. These results suggest that exogenous SO₂ could inhibit the pulmonary tissue inflammatory response in rats with LPS-induced ALI.

Role of endogenous hydrogen sulfide in pulmonary hypertension induced by lipopolysaccharide / 生理学报

The purpose of the present study was to explore the role of endogenous hydrogen sulfide (H2S) in pulmonary arterial hypertension induced by endotoxin. Adult male Sprague-Dawley (SD) rats were randomly divided into four groups: Control group (0.5 mL/kg body weight of normal saline, i.v.), lipopolysaccharide (LPS)-treated group (5 mg/kg body weight of LPS, i.v.), LPS + NaHS (5 mg/kg body weight of LPS, i.v., and 28 μmol/kg body weight of NaHS, i.p.) and LPS + PPG group (5 mg/kg body weight of LPS, i.v., and 30 μmol/kg body weight of PPG, i.p.). Rats were anesthetized with 20% urethane (1 g/kg body weight, i.p.). A polyethylene catheter was inserted into the pulmonary artery through the right external jugular vein to measure the mean pulmonary arterial pressure (mPAP) for 7 h, and then the pulmonary artery was isolated rapidly by the method described previously. Pulmonary arterial activity was detected. H2S concentration and cystathionine γ-lyase (CSE) activity in pulmonary artery tissues were determined by biochemical method. CSE mRNA expression was detected by competitive reverse transcriptase-polymerase chain reaction (RT-PCR). Compared with control, LPS significantly increased mPAP [(1.82±0.29) kPa vs (1.43±0.26) kPa, P<0.01], decreased H2S production [(26.33±7.84) vs (42.92±8.73) pmol/g wet tissue per minute, P<0.01), and reduced endothelium-dependent relaxation response [(75.72±7.22)% vs (86.40±4.40) %, P<0.01) induced by ACh (1×10(-6) mol/L). These effects were partly reversed by co-administration of NaHS and enhanced by co-administration of PPG. Both CSE activity and CSE mRNA expression were consistent with H2S production. It is suggested that the inhibitory effect of LPS on endothelium-dependent relaxation results in pulmonary hypertension, which might be mediated through H(2)S.

Molecular and cytogenetic study on 18 cases of amenorrhea: the use of fluorescence in situ hybridization and high resolution-comparative genomic hybridization / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To explore the use of fluorescence in situ hybridization (FISH) and high resolution-comparative genomic hybridization (HR-CGH) techniques in amenorrhea study.</p><p><b>METHODS</b>After routine gynecologic examination, ultrasonography and endocrine examination, 17 cases of primary amenorrhea and 1 case of secondary amenorrhea were analysed by using chromosomal diagnoses including multiplex FISH and HR-CGH analyses.</p><p><b>RESULTS</b>Among 17 cases of primary amenorrhea, 7 revealed a 46,XX karyotype; 10 cases (58.8%) had abnormal karyotype, including 3 cases of 46,XY females, 2 cases of Turner's syndrome with 45,X and 45,X/46,XX, and other 5 cases with abnormal structure of X chromosome (including partial monosomy of X,X isochromosome and X/Y mosaic). The karyotype of the patient with secondary amenorrhea was translocation between X chromosome and euchromosome.</p><p><b>CONCLUSION</b>The using of FISH and HR-CGH can correctly diagnose the patients' karyotypes, and provide absolutely necessarily medical genetic data for clinical diagnosis and therapy.</p>

Relationship between hydrogen sulfide and myocardial damage in endotoxemic rats / 生理学报

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.

Multiple factors contributing to lipopolysaccharide-induced reactivity changes in rabbit pulmonary artery / 生理学报

To explore the underlying mechanism(s) of pulmonary arterial hypertension in endotoxic shock, the roles of N-acetylcysteine (NAC), nitric oxide (NO) and carbon monoxide (CO) were investigated. Pulmonary arterial rings (3-mm width) were prepared from 24 rabbits. Lipopolysaccharide (LPS), after 7-hour incubation, decreased the endothelium-dependent relaxation response of the arterial ring (pre-contracted with phenylephrine) to acetylcholine (1 mumol/L), but did not affect the endothelium-independent relaxation response to sodium nitroprusside. The LPS effects were reduced by a concomitant incubation with the free radical scavenger (NAC), NO donor (L-arginine), and CO donor (hemin), respectively. On the other hand, the LPS effects were enhanced by applying heme oxygenase-1 (HO-1) inhibitor (zinc protoporphyrin) to block CO production. The response to acetylcholine changed from relaxation to contraction, however, the contractile response to phenylephrine increased significantly after pre-incubation with nitric oxide synthase (NOS) inhibitor (L-NAME) to block NO production, confirming the importance of CO and NO. These results show that LPS impairs endothelium-dependent relaxation of the pulmonary artery, which can be greatly reduced by the antioxidant, or by supplying with NO and CO. Thus, multiple factors are involved in this model of endotoxin-induced pulmonary hypertension.

Melatonin improves vascular reactivity of endotoxemia rats / 生理学报

The purpose of the present study was to investigate the effect of melatonin (MT) on the abnormal reactivity of thoracic aorta and pulmonary artery induced by lipopolysaccharide (LPS) in rats. Sprague-Dawley rats were divided into four groups randomly: (1) Vehicle group; (2) LPS group: LPS (4 mg/kg, i.p.); (3) LPS+MT group: MT (5 mg/ml, i.p.) was given 30 min before LPS and 60 min after LPS (4 mg/kg ,i.p); (4) MT group: received two doses of MT, 90 min after the first injection of MT another dose of MT was given. Six hours after LPS injection,the rats were killed and both thoracic aortic rings (TARs) and pulmonary artery rings (PARs)were prepared. The reactivity of TARs and PARs in the four subgroups was tested separately. The contraction response to phenylephrine (PE) and the endothelium-dependent relaxation response (EDRR) to ACh were observed with the isolated artery ring technique. Concentration-response curves were generated with ACh or PE (1 x 10(-8) - 1 x 10(-5) mol/L). Superoxide dismutes (SOD) activity and the content of malondialhyde (MDA) in artery tissues were detected. For TARs, LPS significantly reduced the contraction response to PE compared with the vehicle group (P<0.01) and the curve of cumulative dose responses to PE in the LPS group shifted downward. Although EDRR to ACh in the LPS group had the tendency to decrease but still showed no significant difference compared with the vehicle group (P>0.05). For PARs, EDRR to ACh was depressed significantly in the LPS group (P<0.01), while no effect on contraction response to PE in the LPS group was observed, compared with the vehicle group (P> 0.05). Compared with the LPS group, TARs in the LPS+MT group exhibited an increased contraction response to PE, but were still lower than that in the vehicle group. Similarly, EDRR to ACh of PARs in the LPS+MT group was improved significantly and there was no difference between the LPS+MT group and the vehicle group. The vascular reactivity was unaffected in MT group compared with the vehicle group in both TARs and PARs. SOD activity in the LPS +MT group increased significantly and the content of MDA decreased markedly compared with the LPS group. These results suggest that MT may improve the vascular reactivity in endotoxemia rats due to its antioxidant properties.

Endogenous carbon monoxide attenuates lung injury following ischemia-reperfusion in the hind limbs of rats / 生理学报

To investigate the role of endogenous heme oxygenase (HO)/carbon monoxide (CO) system in the lung injury as assessed by lung histology, polymorphonuclear count, malondialdehyde content and wet-to-dry weight ratio following ischemia-reperfusion (I/R) of hind limbs, zinc protoporphyrin (ZnPP), an inhibitor of HO activity, was used, and the lung HO activity and blood carboxyhemoglobin (COHb) level were measured. The results showed that HO activity and COHb level were increased significantly and lung injury occurred after limb I/R. After administration of ZnPP, the lung injury was further aggravated while the HO activity and COHb level were significantly decreased. These findings suggest that upregulation of HO activity followed by subsequent CO production attenuates the lung injury induced by limb I/R in rats.

The role of N-acetylcysteine against the injury of pulmonary artery induced by LPS / 中国应用生理学杂志

<p><b>AIM</b>To investigate the alleviating effect of N-acetylcysteine (NAC) on lung injury induced by lipopolysaccharides (LPS) and its mechanism.</p><p><b>METHODS</b>The effects of NAC on changes of the pulmonary arterial reactivity and the ultrastructure of pulmonary arterial endothelium induced by LPS were observed with the isolated artery ring technique and scanning electron microscope (SEM). Malondialdehyde (MDA), nitric oxide (NO) contents and superoxide dismutase (SOD) activity of pulmonary artery tissues were detected.</p><p><b>RESULTS</b>The exposure of pulmonary artery to LPS (4 microg/ml, 7 h) led to reduction of endothelium-dependent relaxation response to acetylcholine (ACh), which was reversed by the concomitant exposure to NAC (0.5 mmol/L, 7 h), whereas NAC itself had no effect on the response. Significant structural injury were observed under SEM in LPS group and alleviated the changes in LPS + NAC group. The MDA, NO contents increased but SOD activity decreased in LPS group, which were reversed by the concomitant exposure to NAC.</p><p><b>CONCLUSION</b>NAC protects pulmonary artery endothelium and enhances endothelium-dependent relaxation response of pulmonary artery by antioxidation effect, which may be one of the mechanisms of its reversing pulmonary artery hypertension and following lung injury induced by LPS.</p>