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1.
AIM: To study the protective effect of A2a adenosine receptor (A2aAR) on hypoxic pulmonary hypertension in the rats treated with salidroside. METHODS: Sprague-Dawley rats were randomly divided into 6 groups: normal control group, hypoxia group, hypoxia+salidroside (low dose) group, hypoxia+salidroside (median dose) group, hypoxia+salidroside (high dose) group, and hypoxia+CGS-21680 (a selective agonist of A2aAR) group. Pulmonary hypertension in the rats was produced for 4 weeks. Mean pulmonary artery pressure (mPAP), mean carotid arterial pressure (mCAP) and the weight ratio of right ventricle/(left ventricle+septum)［RV/(LV+S)］ were measured. The expression of A2aAR in the pulmonary arterioles was determined by immunohistochemistry and in situ hybridization. The mRNA expression of A2aAR in the lung tissues was detected by real-time RT-PCR. The protein level of A2aAR in the lung tissues was analyzed by Western blotting. RESULTS: The mPAP in hypoxia group was significantly higher than that in normal control group. The mPAP in hypoxia+salidroside (high dose) group and CGS-21680 group was significantly lower than that in hypoxia group. RV/(LV+S) in hypoxia group were significantly higher than that in normal control group. RV/(LV+S) in hypoxia+salidroside (median dose) group, hypoxia+salidroside (high dose) group and CGS-21680 group were lower than that in hypoxia group. The ratio of vessel wall area/vessel total area (WA/TA) in hypoxia group was significantly higher than that in normal control group. WA/TA in hypoxia+salidroside (low dose) group, hypoxia+salidroside (median dose) group, hypoxia+salidroside (high dose) group and CGS21680 group were obviously lower than that in hypoxia group. The expression of A2aAR was significantly higher in hypoxia group than that in normal control group. The expression of A2aAR in hypoxia+salidroside (high dose) group and CGS-21680 group was obviously higher than that in hypoxia group. CONCLUSION: The A2aAR attenuates pulmonary vessel remodeling and pulmonary hypertension induced by hypoxia. Salidroside protects the pulmonary vessel from remodeling and inhibits the development of hypoxia-induced pulmonary hypertension by up-regulation of A2aAR expression.  相似文献   

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3.
AIM: To investigate the effect of hypercapnia on hypoxia-induced pulmonary hypertension and the changes of lysyl oxidase (LOX) and extracellular matrix collagen cross-links in the rat. METHODS: Sprague-Dawley rats were randomly divided into 4 groups:normoxia group, hypoxia group, hypercapnia group and hypoxia+hypercapnia group. LOX activity was detected by fluorescence spectrophotometry. LOX protein expression was detected by immunohistochemistry and Western blot. The mRNA expression of LOX in the pulmonary artery was detected by real-time PCR. RESULTS: The levels of mean pulmonary artery pressure (mPAP), RV/(LV+S) and WA/TA in hypoxia group were significantly higher than those in normoxia group (P<0.01). Moreover, the levels of mPAP and RV/(LV+S) in hypoxia+hypercapnia group were significantly lower than those in hypoxia group (P<0.01). However, no significant difference of mPAP and RV/(LV+S) between hypercapnia group and normoxia group was observed. In hypoxia group, the collagen cross-links in the lung tissue was significantly higher than that in normoxia group and hypercapnia group (P<0.01). Importantly, collagen cross-links in the lung tissue of hypoxia+hypercapnia group was significantly lower than that in hypoxia group (P<0.01). There was no significant difference in collagen cross-links between hypercapnia group and normoxia group. The expression of LOX at mRNA and protein levels and its activity in the pulmonary arteries of hypoxia group were significantly increased as compared with normoxia group (P<0.01). Furthermore, the expression of LOX at mRNA and protein levels and its activity in the pulmonary arteries in hypoxia+hypercapnia group were lower than those in hypoxia group (P<0.01). CONCLUSION: Hypoxia not only up-regulates LOX but also promotes collagen cross-linking in the rat lung, which contributes to the development of pulmonary hypertension. Hypercapnia inhibits hypoxia-induced LOX expression and collagen cross-linking, therefore impairing the progress in hypoxia-induced pulmonary hypertension.  相似文献   

4.
AIM:To investigate the expression of matrix metalloproteinases(MMPs) in pulmonary arterioles of rats with chronic hypoxia and hypercapnia-induced pulmonary hypertension.METHODS:MMP-2, MMP-9 and MMP-2 mRNA, MMP-9 mRNA were observed in pulmonary arterioles by the techniques of immunohistochemistry and in situ hybridization.RESULTS:①The mean pulmonary artery pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum (RV/LV+S) of hypoxia-hypercapnia groups were higher than those of normal control group (P＜0.01). ②Light microscopy showed that vessel wall and media of pulmonary arterioles were thicker in rats of hypoxia-hypercapnia groups than normal control group. There were vessel smooth muscle cell hypertrophy, vessel cavity straitness in hypoxia-hypercapnia group, but no same performance was found in normal control group. ③The expression of MMP-2, MMP-9 and MMP-2 mRNA, MMP-9 mRNA in pulmonary arterioles were significantly higher in rats of hypoxia-hypercapnia groups than control group (P＜0.01).CONCLUSION:Expression of matrix metalloproteinases in pulmonary arterioles is enhanced by hypoxia hypercapnia. This may be involved in pulmonary vascular remodeling in rats with pulmonary hypertension.  相似文献   

5.
AIM: To investigate whether asiaticoside attenuates hypoxic pulmonary hypertension by inhibiting p38/NF-κB signaling pathway. METHODS: BALB/c mice (n=30) were randomly divided into normoxia (N) group, hypoxia (H) group, and hypoxia+asiaticoside group. Right ventricular systolic pressure (RVSP), mean carotid artery pressure (mCAP), the weight ratio of right ventricle/(left ventricle+ventricular septum)[RV/(LV+S)], the ratio of right ventricle/body weight (RV/BW), vessel wall area/vessel total area (WA/TA) and vessel wall diameter/vessel wall total diameter (WT/TT) were determined after the model was established. The protein levels of p38, p-p38, NF-κB and p-NF-κB in the lung tissues were detected by Western blot. The fluorescence intensity of p-p38 and p-NF-κB were measured by immunofluorescence method. The serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by ELISA. RESULTS: Compared with N group, the levels of RVSP, RV/(LV+S), RV/BW, WA/TA and WT/TT were significantly increased in H group, while administration of asiaticoside decreased the levels of RVSP, RV/(LV+S), RV/BW, WA/TA and WT/TT (P<0.05). Compared with N group, the relative protein levels of p-p38 and p-NF-κB in H group were significantly increased (P<0.05), and the concentrations of IL-6 and TNF-α were significantly increased, which were apparently attenuated by asiaticoside injection. CONCLUSION: Inhibition of p38/NF-κB signaling pathway and reduction of inflammatory responses may be the important mechanisms of asiaticoside in the prevention and treatment of hypoxic pulmonary hypertension.  相似文献   

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7.
AIM: To explore the effects of hydroxylamine on the pulmonary arterial pressure in chronic hypoxic hypercapnic rats. METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into 3 groups (8 rats in each group): the normal control group (NC), hypoxic hypercapnia+normal saline group (NS), hypoxic hypercapnia+hydroxylamine group (HA). The animals in NS and HA groups were kept in the O2 (9%-11%) and CO2 (5%-6%) cabin, 8 h a day and 6 days a week for 4 weeks. Before entering the cabin, the rats in HA group were administered with 1 mL hydroxylamine (12.5 mg/kg) by intraperitoneal injection, while the rats in NS group were given intraperitoneal injection of 1 mL saline solution. The mean pulmonary arterial pressure (mPAP) was measured by external jugular vein cannulation. The heart was removed, and the right ventricle (RV) and the left ventricle plus the septum (LV+S) were dissected. The ratio of the wet weight of the RV to that of the LV+S was calculated. The changes of the pulmonary vascular construction were observed under optical microscope. The concentration of H2S in the plasma was measured with a spectrometer. The expression of cystathionine-γ-lyase (CSE) in the pulmonary arterioles and bronchi was measured by immunohistochemistry and RT-PCR. RESULTS: The values of mPAP, RV/(LV+S),vessel wall area/total area (WA/TA) and media thickness of pulmonary arterioles (PAMT) in NS group and HA group were significantly higher than those in NC group (P<0.05). The level of H2S in the plasma, the content of CSE protein and the expression of CSE mRNA in NC group were significantly lower than those in NS group (P<0.05). The values of mPAP, RV/(LV+S), WA/TA and PAMT in HA group were significantly lower than those in NS group (P<0.05). The level of H2S in the plasma, the content of CSE protein and the expression of CSE mRNA in HA group were significantly higher than those in NS group (P<0.05). CONCLUSION: Hydroxylamine may decrease the pulmonary arterial hypertension induced by chronic hypoxic hypercapnia in rats by increasing the level of H2S in the plasma, the content of CSE protein and the mRNA expression of CSE, thus improving the pulmonary vascular structural remodeling.  相似文献   

8.
AIM: To observe the change of CX3CL1/fractalkine (FKN) in the rats with monocrotaline-induced pulmonary hypertension, and to study the intervention of puerarin. METHODS: The pulmonary hypertension model was established in vivo by intraperitoneal injection of monocrotaline. Thirty male Sprague-Dawley rats (270-310 g) were randomly divided into 3 groups: control group (C), monocrotaline model group (M)and puerarin treatment group (M+P). The mean pulmonary arterial pressure (mPAP), mean right ventricular pressure (mRVP), mean carotid arterial pressure (mCAP) and the weight ratio of right ventricle (RV) to left ventricle plus septum (LV+S) were also detected. The structural changes of pulmonary arterioles were observed under optical microscope. Remodeling of lung blood vessels was determined by measuring the ratio of vessel wall area to total area (WA/TA) and the medium thickness of pulmonary artery (PAMT). The concentration of soluble fractalkine(sFKN) in plasma was measured by ELISA. The expression of FKN in the pulmonary artery wall was measured by immunohistochemistry. The mRNA level of FKN in the lung tissues was detected by RT-PCR.RESULTS: mPAP, mRVP, RV/(LV+S), WA/TA and PAMT in M group were higher than those in C group (P<0.01). RV/(LV+S), WA/TA and PAMT in M+P group were significantly lower than those in M group (P<0.01). No significant difference of mCAP among the 3 groups was observed. The levels of sFKN, FKN mRNA and FKN protein in M group were higher than those in C group (P<0.01), and the above data in M+P group were lower than those in M group(P<0.05). The serum level of sFKN had a positive correlation with PAMT and RV/(LV+S) (r＝0.719, r=0.685,respectively, P<0.01).CONCLUSION: Puerarin down-regulates the expression of FKN and suppresses the development of pulmonary hypertension and pulmonary vessel remodeling.  相似文献   

9.
AIM: To investigate the changes of 5-hydroxytryptamine(5-HT)levels and to observe the expression and distribution of 5-HT1B receptors in the lung tissues of hypoxic pulmonary hypertension(HPH) rats for exploring the mechanisms of hypoxic pulmonary hypertension.METHODS: Forty male Sprague-Dawley rats were randomly divided into 4 groups: normoxia control(control group), 3 weeks hypoxia group, 4 weeks hypoxia group and 5 weeks hypoxia group. The rats in normoxia control group stayed in normal environment. The rats in 3 weeks hypoxia group, 4 weeks hypoxia group and 5 weeks hypoxia group were kept respectively in hypoxia chamber for 3 weeks, 4 weeks and 5 weeks respectively to establish the HPH animal model. After HPH was established, the mean pulmonary pressure(mPAP) and the right ventricular systolic pressure(RVSP) were recorded by a micro-catheter. RV/(LV+S) ratio was calculated to assess the right ventricular hypertrophy. 5-HT levels in plasma and lung tissues of HPH rats were measured by ELISA. The expression and distribution of 5-HT1B receptors in the lung tissues were measured by the methods of immunohistochemistry and Western blotting. RESULTS: Compared to the normoxia controls, mPAP, RVSP and RV/(LV+S)% in 3 weeks hypoxic rats increased significantly(P<0.05), and continued to increase following prolonged hypoxia. The results of ELISA showed that 5-HT levels in plasma and lung tissues of HPH rats continued to increase following prolonged hypoxic exposure(P<0.05). The 5-HT1B receptors were localized mainly in the intima of the pulmonary arteries in normal rats. Exposed to hypoxia, the immuno-reactivity for 5-HT1B receptors increased in the media of pulmonary arteries in 3 weeks hypoxic rats, particularly those bordering the adventitia. The increase in the expression of 5-HT1B receptor was observed following prolonged hypoxic exposure. The results of Western blotting showed the same changes of 5-HT1B receptor expression in the lung tissues as that of 5-HT1B immuno-reactivity in pulmonary arteries.CONCLUSION: Hypoxia induces the high 5-HT levels and the over-expression of 5-HT1B receptors in the pulmonary arteries of HPH rats, indicating the underlying mechanism of 5-HT in the development of HPH.  相似文献   

10.
中国园艺学会第九届第8次常务理事扩大会决定，“中国园艺学会第七届青年学术讨论会”由山东农业大学园艺科学与工程学院和山东省园艺学会承办，将于2006年7月或8月在山东泰安举行。  相似文献   

11.
AIM: To study the effect of chronic hypoxic hypercapnia on gene expression of thromboxane synthase and prostacyclin synthase in pulmonary arterioles. METHODS: Sprague-Dawley rats were randomly divided into two groups: control group and hypoxic hypercapnic group. TXS mRNA and PGI2-SmRNA were observed in pulmonary arterioles by in situ hybridization. RESULTS: mPAP, weight ratio of right ventricle (RV) to left ventricle plus septum(LV+S), contents of TXB2 and 6-keto-PGF1α in plasma and lung and TXS mRNAin pulmonary arterioles were much higher in rats of hypoxic hypercapnic group than those of control group. Differences of PGI2-SmRNA in pulmonary arterioles were not significant in two groups. Light microscopy showed hypertrophy of vessel smooth muscle cells and vessel cavity straitness were found in hypoxic hypercapnic group. CONCLUSION: Changes of gene expressions of thromboxane synthase and prostacyclin synthase and imbalance of TXA2/PGI2 may play an important role in hypoxic hypercapnic pulmonary hypertension.  相似文献   

12.
AIM: To investigate the roles of nitric oxide/L-arginine (NO/L-Arg) pathway and urotensin-Ⅱ (UⅡ) in the development of pulmonary hypertension induced by chronic hypoxia-hypercapnia in rats.METHODS: Forty male Sprague-Dawley rats were randomly divided into four groups (n=10): normal control group (A), hypoxia-hypercapnia+saline group (B), hypoxia-hypercapnia+L-Arg liposome group (C) and hypoxia-hypercapnia+N-nitro-L-arginine methyl ester (L-NAME) group (D).Contents of UⅡ, UⅡ mRNA and receptor of UⅡ (UT) mRNA in pulmonary arterioles were measured with immunohistochemistry analysis and in situ hybridization, respectively.Change of small pulmonary vascular microstructure was also investigated.RESULTS: (1) The mean pulmonary artery pressure (mPAP) and the weight ratio of right ventricle to left ventricle plus septum ［RV/(LV+S)］ in B and D groups were all higher than those in A group (respectively, P<0.05), with C group significantly lower than those in B group (respectively, P<0.01).(2) Light microscopy showed that the ratio of vessel wall area to total area (WA/TA) and the media thickness of pulmonary arterioles (PAMT) in B group were higher than those in A group (P<0.05), with C group significantly lower than those in B group.(3) The contents of UⅡ, UⅡ mRNA and UT mRNA in pulmonary arterioles in B and D groups were all higher than those in A group (respectively, P<0.01), while the expression of UⅡ and UⅡ mRNA in C group were lower than those in B group (P<0.01).CONCLUSION: The pathological process of pulmonary hypertension induced by chronic hypoxia-hypercapnia might be related to upregulation of UⅡ located in pulmonary arterioles, which might be partially inhibited by exogenous NO in rats.  相似文献   

13.
AIM:We used an animal model of chronic hypoxia to mimic right ventricular hypertrophy and try to study the potential mechanism of myocardium apoptosis of right heart in rat under chronic hypoxia. METHODS: Rat hypoxia models were established by exposing the rats to normobaric chronic hypoxia (oxygen levels were maintained at 9.5%-10.5%). Sixty rats were separated into two groups: one exposed to hypoxia and the other serving as control. Ten rats, randomly selected from each group were killed at 14, 21, 28 d after hypoxia. The apoptosis was determined. The changes of RV weight to left ventricle and interventricular septum weight ratio［RV/(LV+S)］, the RV weight to body weight ratio (RV/BW) were also observed. The β-MHC, bcl-2 and bad mRNA levels in right ventricle were detected by semi-quantitative RT-PCR assays and expression of β-MHC, Bcl-2 and Bad protein levels were detected by Western blotting.RESULTS: The RV/(LV+S), RV/BW and apoptosis index in chronic hypoxia group were higher than those in normal control group (P<0.01). The results of RT-PCR and Western blotting showed that β-MHC mRNA levels and protein levels in chronic hypoxia group were higher than those in normal control group (P<0.01). The rate of apoptosis, the RV/(LV+S), RV/BW and the expression of β-MHC in hypoxia group all increased with time. The bcl-2 mRNA and Bcl-2 protein expressions in chronic hypoxia group were lower compared with control group at 14, 21 and 28 d (P<0.05). In contrast, no significant change of bad mRNA and Bad protein expressions in chronic hypoxia group were observed compared with control group (P>0.05). Finally, a decreased bcl-2/bad〖STBZ〗 ratio in chronic hypoxia group was found compared with control group (P<0.05). Both the expression of bcl-2 and the bcl-2/bad ratio decreased with time (P<0.05).CONCLUSION:These data demonstrate that chronic hypoxia may induce right ventricular hypertrophy, as well as cardiomyocytes apoptosis. Furthermore, apoptosis in hypertrophic cardiomyocytes induced by hypoxia is mainly due to the inhibition of bcl-2 expression and decrease of bcl-2/bad ratio.  相似文献   

14.
AIM: To study the expression and distribution of osteopontin (OPN) in lungs and pulmonary arteries in pulmonary hypertensive rats induced by hypoxia-hypercapnia, and to explore the role of OPN in pathogenesis of pulmonary hypertension. METHODS: Forty-eight male Sprague-Dawley rats (Weight 180 g-220 g) were randomly divided into four groups: normal control group (NC), hypoxic hypercapnia 1-week，2-week and 4-week group (1HH, 2HH and 4HH). The expressions of OPN mRNA and protein in lungs and pulmonary arteries were detected by RT-PCR and immunohistochemistry. ELISA was used to detect the concentration of OPN in lung homogenates. The content of OPN in pulmonary arteries was detected by Western blotting. RESULTS: ① The mean pulmonary artery pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum ［RV/(LV+S)］ in all hypoxic hypercapniac groups were higher than those in normal control group (P<0.01), respectively. Differences of mean carotid artery pressure (mCAP) among these four groups were not significant (P>0.05). ② The expression of OPN mRNA was significantly increased in pulmonary arteries and lung tissues in hypoxic hypercapnic groups compared with normal control group (P<0.01). ③ The result of immunohistochemistry showed that OPN was only detected in bronchus and alveolar epithelium, but not detected in pulmonary arterioles of normal control group. In contrast，OPN expression was evident in pulmonary arterioles of 1HH rats，especially in media. Moreover, the expression of OPN was markedly increased in group 2HH and 4HH. ④ OPN levels in lung homogenates in 1HH, 2HH and 4HH were increased by 69%, 128% and 187% (P<0.01), respectively, compared with control rats. ⑤ Western blotting analysis showed that the contents of OPN were significantly higher in all hypoxic hypercapnic groups than those in NC group (P<0.01).CONCLUSION: The expressions of OPN in pulmonary arteioles and lung are increased in rats with pulmonary hypertension. OPN might play an important role in the pathogenesis of pulmonary hypertension induced by chronic hypoxia and hypercapnia.  相似文献   

15.
AIM: To study the role of adrenomedullin(AM) in the pathogenesis of hypoxic pulmonary hypertension. METHODS: Rats were exposed to chronic hypoxia for 14 days. After the measurement of the right ventricular systolic pressure (RVSP), the rats were executed. The weight of the right ventricle (RV), the left ventricle(LV) and the ventricular septum(SP) were determined. The ration RV/(LV+SP) was used to express the thickness of RV. In situ hybridization was used for the detection of the expression of AM mRNA in the lung and RV. RESULTS: The RVSP in the hypoxic group was (63.63±3.42) mmHg,which was significantly higher than that in control group [(34.13±3.40) mmHg]. The RV/(LV+SP) in hypoxic group was 0.439±0.039,which was increased obviously when compared with that of control (0.230±0.025). The level of AM mRNA expressed in the RV in the hypoxia group was significantly higher than that in the control group. CONCLUSION: The expression of AM mRNA in RV increased in the hypoxic condition, which suggests that AM may attenuate the inappropriate increase in pulmonary artery pressure.  相似文献   

16.
AIM:To study the effect of safflower injection on expression of COX-2 mRNA in chronic hypoxic hypercapnic rat pulmonary arterioles.METHODS: Sprague-Dawley rats were randomly divided into normal control group, hypoxic hypercapnic group (B), hypoxic hypercapnia+ safflower injection group (C). The concentration of TXB2 and 6-Keto-PGF1α in plasma and in lung were detected by the technique of radioimmunoassay. COX-2 mRNA was observed in arterioles from rats by the technique of in situ hybridization. RESULTS: ① Mean pulmonary arterial pressure(mPAP), weight ratio of right ventricle (RV) to left ventricle plus septum (LV+S) were much higher in B group than those in control group. No significant difference of mean carotid arterial pressure(mCAP) was observed in three groups. ② The concentration of TXB2 and the ratio of TXB2/6-keto-PGF1α were significantly higher in B group than those in control group. ③ Light microscopy showed that vessel wall area/total area, the density of medial smooth muscle cells and the thickness of medial smooth cell layer were significantly higher in B group than those in control group. Electron microscopy showed proliferation of medial smooth muscle cells and collagenous fibers in pulmonary arterioles in B group. Safflower injection reversed the changes mentioned above. ④ Expression of COX-2 mRNA in pulmonary arterioles was much higher in C group than those in B group. Differences of COX-1 mRNA in pulmonary arterioles were not significant between these two groups.CONCLUSION:Safflower injection increases the expression of COX-2 mRNA in chronic hypoxic hypercapnic rat pulmonary arterioles, indicating an important mechanism that safflower injection inhibits the formation of hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling.  相似文献   

17.
AIM: To study whether salidroside plays a protective role in hypoxia-induced pulmonary hypertension by suppressing oxidative stress. METHODS: Sprague-Dawley rats were randomly divided into 4 groups:normoxia (N) group, hypoxia for 4 weeks (H4) group, low-dose salidroside (hypoxia for 4 weeks and treatment with salidroside at 16 mg/kg, H4S16) group and high-dose salidroside (hypoxia for 4 weeks and treatment with salidroside at 32 mg/kg, H4S32) group. The mean pulmonary arterial pressure (mPAP), the weight ratio of right ventricle/(left ventricle+septum)[RV/(LV+S)] and vessel wall area/vessel total area (WA/TA) were evaluated. The levels of malondialdehyde (MDA) in the serum and lung tissues were detected by colorimetric method. The levels of 8-iso-prostaglandin F2α (8-iso-PGF2α) in the serum and lung tissues were measured by ELISA. The activity of superoxide dismutase (SOD) in the serum was analyzed by hydroxylamine method. The expression of NAPDH oxidase 4 (NOX4) and SOD1 in the lung tissues was determined by Western blot. RESULTS: Compared with N group, the levels of mPAP, RV/(LV+S) and WA/TA in H4 group were significantly increased, which were apparently attenuated by salidroside injection in a dose-dependent manner. Meanwhile, salidroside administration apparently decreased the levels of MDA and 8-iso-PGF2α in the serum and lung tissues, as well as the expression of NOX4 in the lung tissues. Besides, compared with N group, the activity of SOD in the serum and the expression of SOD1 in the lung tissues in H4 group were significantly decreased, while administration of salidroside increased the activity of SOD in the serum and the expression of SOD1 in the lung tissues in a dose-dependent manner. CONCLUSION: Salidroside protects the pulmonary vessels from remodeling and attenuates hypoxia-induced pulmonary hypertension by inhibiting oxidative stress.  相似文献   

18.
AIM: To study the effect of chronic hypoxic hypercapnia on expression of heme oxygenase-1 (HO-1). METHODS: Sprague-Dawley rats were randomly divided into three groups: control group(A),hypoxic hypercapnic group(B), hypoxic hypercapnia+hemin group(C). HO-1 and HO-1 mRNA were observed in pulmonary arterioles by the technique of immunohistochemistry and in situ hybridization. RESULTS: ① mPAP and weight ratio of right ventricle (RV) to left ventricle plus septum (LV+S) were significantly higher in rats of B group than those of A and C group (P<0.01). Differences of mCAP were not significant in three groups(P>0.05). ② Blood CO concentration was significantly higher in rats of B group than that of A group (P<0.01), it was much higher in C group than that of B group(P<0.01). ③ Light microscopy showed that vessel well area/total area (WA/TA), density of medial smooth muscle cell (SMC) and media thickness of pulmonary arterioles were much higher in rats of B group than those of A and C group (P<0.01). ④ The observation by electron microscopy showed proliferation of medial smooth muscle cells and collageous fibers of pulmonary arterioles in rats of B group, hemin could reverse the changes mentioned above. ⑤ HO-1 and HO-1 mRNA in pulmonary arterioles was significantly higher in rats of B group than those of A group(P<0.01), and they were significantly higher in rats of C group than those of B group (P<0.01). CONCLUSION: Expression of HO-1 mRNA and HO-1 in pulmonary arterioles was enhanced by hypoxic hypercapnia. Hemin partly inhibited pulmonary hypertension and pulmonary vessel remodeling by enhancing the expression of HO-1 mRNA and HO-1.  相似文献   

19.
AIM: To study the effect of chronic hypoxia on L-Arginine/NO pathway in rat pulmonary artery. METHODS: Changes in pulmonary artery L-Arginine(L-Arg) transport, nitric oxide synthase (NOS) activity, plasma nitrite level and L-Arg level in HPH rats were investigated. RESULTS: (1) The mean pulmonary arterial pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum (RV/LV+S) of HPH group were higher than those in control group (P＜0.01). (2) Plasma L-Arg level in HPH group was not significantly changed. (3) At low (0.2 mmol/L)or high(5.0 mmol/L)concentration of L-Arg, the velocity of L-Arg transport in HPH group was lower than that in control group (P＜0.05 or P＜0.01). (4) The activity of pulmonary artery tNOS, iNOS and cNOS in HPH group were increased by 38.0%, 32.8% and 53.0%, respectively (P＜0.01), compared with control group. (5) Plasma NO level of HPH group was decreased, which was negative correlation to mPAP and RV/LV+S (P＜0.01). CONCLUSION: The decrease of nitric oxide generation might result from L-Arg transport injury, while pulmonary artery tNOS, iNOS and cNOS activity were enhanced during chronic hypoxia.  相似文献   

20.
AIM: To explore the mechanism of notoginsenoside monomer R1 (R1) against hypoxic hypercapnia-induced pulmonary vasoconstriction (HHPV) by investigating the effect of R1 on p38 mitogen-activated protein kinase (p38MAPK) signaling pathway in pulmonary arterial smooth muscle cells (PASMCs) under the condition of hypoxia and hypercapnia. METHODS: Primary cultured PASMCs, which were isolated from Sprague-Dawley rats, were incubated in logarithmic growth phase from the 2nd to 5th generation with different concentrations (8, 40 and 100 mg/L) of R1 under the condition of 6% CO2 plus 1% O2 for 24 h. The expression of p38 at mRNA and protein levels was detected by RT-PCR and Western blotting,respectively. RESULTS: The results of Western blotting and RT-PCR analysis indicated that the protein and mRNA expression levels of p-p38 MAPK were significantly higher in hypoxic hypercapnia group with DMSO control than those in normoxia control group (P<0.01). In R1 treatment groups, the levels of p-p38 MAPK protein and p38 MAPK mRNA were markedly decreased (P<0.01) in a dose-dependent manner. CONCLUSION: p38 MAPK signaling pathway may mediate hypoxic hypercapnia pulmonary vasoconstriction in rats. Notoginsenoside monomer R1 attenuates HHPV, which may be related to blockage of p38 MAPK signal pathway.  相似文献   

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