Protective effect of salidroside on rats with hypoxic pulmonary hyperten-sion by suppressing oxidative stress / 中国病理生理杂志

AIM:To study whether salidroside plays a protective role in hypoxia-induced pulmonary hyperten-sion 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+sep-tum)[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-PGF2αin the serum and lung tis-sues,as well as the expression of NOX 4 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 H4group were significantly decreased,while administration of sali-droside increased the activity of SOD in the serum and the expression of SOD 1 in the lung tissues in a dose-dependent man-ner.CONCLUSION:Salidroside protects the pulmonary vessels from remodeling and attenuates hypoxia -induced pulmo-nary hypertension by inhibiting oxidative stress.

Effects of resveratrol on TNF-α-induced injury and expression of MCP-1 in isolated rat pulmonary artery endothelial cells / 中国病理生理杂志

AIM:To investigate the possible mechanism of resveratrol(Res)on tumor necrosis factor-α (TNF-α)-induced monocyte chemoattractant protein-1(MCP-1)expression in primary rat pulmonary artery endothelial cells(RPAECs).METHODS: RPAECs were randomly divided into 4 groups: control group, solvent(1% DMSO) group,TNF-αgroup and Res group.Each group was divided into 1 h,4 h and 8 h subgroups(n=6 per time point).The TNF-α+C1142(a rodent chimeric mAb that neutralizes rat MCP-1)group was set up at the 8 h time point.At each time point,the protein and mRNA expression of MCP-1 was measured by Western blot and real-time PCR.RESULTS: Pre-treatment of the RPAECs with C1142 significantly down-regulated the expression of MCP-1(P<0.05).The protein and mRNA expression of MCP-1 was markedly increased in TNF-αgroup(P<0.05).Notably,incubation with Res down-re-gulated the protein and mRNA expression of MCP-1,which was significantly lower than that in TNF-αgroup(P<0.05). CONCLUSION:MCP-1 was involved in the process of TNF-α-induced injury of RPAECs.Res down-regulates the expres-sion of MCP-1 in RPAECs,thus attenuating cell injury.

The study of catheterization to measure ventricular pressure in mice through venous cannula in external jugular vein / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To study a feasible method of measuring right ventricular pressure by catheterization in mice.</p><p><b>METHODS</b>Measuring the right ventricular pressure and the pulmonary artery pressure by homemade PE pipe through venous cannula in external jugular vein, using catheterization in mice with powerlab multimodal biometric signal recording system.</p><p><b>RESULTS</b>Forty-six out of 51 mice were experimented with this method smoothly and got a total success rate of 90.2%. Thirty of 33 normal mice and 16 of 18 mice with pulmonary arterial hypertension (PAH) were catheterized successfully. The right ventricular pressure were as follow: systolic blood pressure: (23.4 +/- 5.7) mmHg in normal group vs (32.2 +/- 2.8) mmHg in mice with PAH, diastolic blood pressure: (3.7 +/- 2.6) mmHg vs (3.8 +/- 2.0) mmHg, mean pressure: (12.0 +/- 3.7) mmHg vs (14.9 +/- 2.3) mmHg. After autopsy for those 5 failed cases, we found that 2 cases were into the inferior vena cava, another 2 cases pierced the right auricle and the last one punctured the axillary vein into the chest wall.</p><p><b>CONCLUSION</b>Measuring the right ventricular pressure through venous cannula in external jugular vein with homemade PE pipe in mice gets not only a high success rate but also help to save time. Moreover, this method can be popularized easily. It is a good and feasible method for measuring right ventricular pressure in mice.</p>

Effect of celecoxib on pulmonary hypertension of chronic hypoxia and hypercapnic rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To study the effect of celecoxib on chronic hypoxia and hypercapnic pulmonary hypertension.</p><p><b>METHODS</b>SD rats were randomly divided into normal control group (A), hypoxic hypercapnic group (B), hypoxic hypercapnia+ celecoxib group (C). The content of TXB2 and 6-keto-PGF1alpha in plasma and lung were detected by the technique of radioimmunology.</p><p><b>RESULTS</b>(1) Mean pulmonary arteria pressure(mPAP) was significantly higher in rats of B group than those of A group. mPAP was significantly higher in rats of C group than those of B group. Differences of mPAP were not significant in three groups. (2) The content of TXB2 in plasma and lung and the ratio of TXB2/6-keto-PGF1alpha were significantly higher in rats of B group than those of A group. The ratio of TXB2/6-keto-PGF1alpha was significantly higher and the content of 6-keto-PGF1alpha in plasma and lung was significantly lower in rats of C group than those of B group. (3) Light microscopy showed that WA/TA (vessel wall area/total area) and PAMT (the thickness of medial smooth cell layer) were significantly higher in rats of B group than those of A group. WA/TA and PAMT were significantly higher in rats of C group than those of B group. (4) Electron microscopy showed the thickening of vessel wall and the proliferation of collagen fiber in B group and augmentation of smooth muscle cell and abundance of myofilament in pulmonary arterioles in C group.</p><p><b>CONCLUSION</b>Celecoxib can aggravate hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling by increasing the ratio of TXA2/PGI2.</p>

Cyclooxygenase-2 overexpression and vascular endothelial growth factor expression in pharyngeal tissue of patients with OSAHS correlates with angiogenesis / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To reseach the correlations between cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) expressions and angiogenesis in pharyngeal tissue of patients with obstructive sleep apnea hypopnea syndrome (OSAHS).</p><p><b>METHODS</b>Biopsies were obtained by uvulopalatopharyngoplasty from 40 patients with mild to severe OSAHS. Control specimens of palatopharyngeal and palatoglossal arch mucosa were retreved from 6 patients with chronic tonsillitis and proved have no related disorders. HE was used to observe the changes of pharyngeal tissue, immunohistochemical staining with antibodies against COX-2, VEGF, microvessel density (MVD) (marked with CD34).</p><p><b>RESULTS</b>COX-2 and VEGF mainly expressed at pavement-epithelium and glandular epithelium of pharyngeal tissue, and stronger COX-2 and VEGF expression was found in midrange and severe OSAHS than mild and control group (P < 0.01), so as MVD. COX-2 expression was correlated positively with VEGF expression, and had significant correlation with MVD. VEGF expression had the same correlation with MVD. These three targets had considerable relation with apnea hypopnea index (AHI) and lowest O2 saturation at night.</p><p><b>CONCLUSION</b>There was angiogenesis which had important relationship with hypoxia degree in patients of OSAHS, and COX-2 and VEGF play a crucial role in its development.</p>

Effects of puerarin on proliferation, apoptosis and Kv1.5 gene expression of pulmonary artery smooth muscle cells induced by hypoxia / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effects of puerarin on proliferation, apoptosis and Kv1.5 gene expression of rat pulmonary artery smooth muscle cells (PASMCs) induced by hypoxia.</p><p><b>METHODS</b>The rat PASMCs were divided into 5 groups: control group, hypoxia group, hypoxia plus puerarin (1 × 10(-5) mol/L) group, hypoxia plus puerarin (1 × 10(-4) mol/L) group and hypoxia plus puerarin (1 × 10(-3) mol/L) group, and cultured at 37°C for 24 h. The proliferation of rat PASMCs was detected by CCK-8 assay and flow cytometry, the activity of caspase-3 was measured with spectrophotometric method, Kv1.5 protein was detected by western blot, Kv1.5 mRNA was detected by real-time PCR.</p><p><b>RESULTS</b>The cell viability and proportion of synthesis phase in control group were 0.940 ± 0.045 and 9.67% ± 1.28%, which were significantly lower than those (1.296 ± 0.034 and 18.19% ± 1.19%) in hypoxia group (P < 0.05). The Caspase-3 activity, Kv 1.5 protein and Kv 1.5 mRNA in control group were 0.1073 ± 0.0113, 0.886 ± 0.038 and 0.0377 ± 0.0031, which were significantly higher than those (0.0664 ± 0.0049, 0.602 ± 0.064 and 0.0108 ± 0.0014) in hypoxia group (P < 0.05). As compared with hypoxia group, the cell viability and proportion of synthesis phase in 3 hypoxia plus puerarin groups significantly decreased, and the Caspase-3 activity, Kv 1.5 protein and Kv 1.5 mRNA in 3 hypoxia plus puerarin groups significantly enhanced (P < 0.05).</p><p><b>CONCLUSION</b>Puerarin could decrease the proliferation and increase the apoptosis induced by hypoxia in rat PASMCs, and the up-regulated expression of Kv1.5 gene may be the mechanism of puerarin effects.</p>

The role of angelica injection on P-selectin and anti-cardiolipin antibodies in acute pulmonary embolism rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To study the effect of Chinese medicine, Angelica, injection on the expression of P-, E-selectin and anti-cardiolipin antibody in acute pulmonary embolism rats.</p><p><b>METHODS</b>SD rats were randomly divided into 3 groups: normal control group(Group N), thromboembolism group (Group T), and treatment group of thromboembolism with angelica injection (Group TA). There were three time points in every group: 1 h, 4 h and 8 h. Plasma was detected by P-, with 4% paraformaldehyde, and paraffin embedded sections were detected by immunohistochemistry for P-, E-selectin and anti-cardiolipin antibodies.</p><p><b>RESULTS</b>With HE stain, the inflammatory cells in the lung of rats were relatively rare in every time point in normal control group. In group T and group TA, the inflammatory cells were increasing in every time point in comparison to group N (P < 0.05) and the inflammatory cells were increasing with time in group T. The data revealed that the plasmic level of P-, E-selectin was significantly higher than that in group T1, group T4, group T8 in comparison to the corresponding sub groups of group N (P < 0.05), while it was significantly lower than that in group TA1, group TA4, group TA8 in comparison to the corresponding sub groups of group T (P < 0.05); For the OD value of plasmic anti-cardiolipin antibodies (ACA), no significant difference was observed during was lower expressed by immunohistochemistry.</p><p><b>CONCLUSION</b>Acute pulmonary embolism can lead to infiltration of inflammatory cell in rat lungs. The lung inflammation of acute pulmonary embolism rats can be enhanced probably by the increased release of P-, E-selectin and anti-cardiolipin antibodies, and the enhanced inflammation promotes the release of a series of inflammatory mediators, which exacerbate the injury of lung. Angelica injection relieves the lung inflammation of acute pulmonary embolism rats possibly by inhibiting the expression of P-, E-selectin and anti-cardiolipin antibody, thus playing a role in reducing thrombogenesis.</p>

Primary cell culture and identification methods of rat pulmonary arterial smooth muscle cells / 中国应用生理学杂志

<p><b>OBJECTIVE</b>Set up a method to isolate and identify the small pulmonary arterial smooth muscle cells (PASMCs) in vitro.</p><p><b>METHODS</b>In sterile conditions, separated the male SD rat pulmonary artery, digested by collagenase I and cultured primary PASMCs. Measured cell viability; observed by phase contrast microscope; identified by immunocytochemistry and immunofluorescence staining as a label for smooth muscle alpha-actin.</p><p><b>RESULTS</b>PASMCs were identified by morphology and immunocytochemistry, immunofluorescence staining, with the cell viability is over 96.5%. The primary culture could be subcultured after 4-7 days and successfully passaged without change in morphology and growth characteristic.</p><p><b>CONCLUSION</b>This technique has advantage of the method is simple, short cultivate, good reproducibility, the primary cultured PASMCs quantity and the rapid growth.</p>

The effect of chimonin on collagen metabolism of pulmonary arterioles in chronic hypoxic rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To study the effect and mechanism of chimonin on pulmonary arterioles I and III type collagen metabolism in pulmonary hypertension rats induced by chronic hypoxic hypercapnia.</p><p><b>METHODS</b>Thirty-six Sprague-Dawley rats were randomly divided into three groups: normal control group(A), hypoxic hypercapnic group(B), hypoxic hypercapnia + chimonin group(C). Collagen I, III and their mRNA, Blood CO concentration (COHb%), activity of HO-1 in blood serum and lung homogenate, content of hydroxyproline in lung homogenate, pulmonary arteriole micromorphometric index were observed.</p><p><b>RESULTS</b>Hypoxic hypercapnic rats's mPAP, Hyr of lung homogenate, content of I type collagen and I type collagen mRNA in pulmonary arterioles, were significantly higher than those in control group, pulmonary vessel remodeling of hypoxic hypercapnic rats was significant, those changes in hypercapnia + chimonin group were significantly lower than those in hypoxic hypercapnic group. Blood CO concentration, activity of HO-1 in blood serum and lung homogenate in rats of hypoxic hypercapnic rats were significantly higher than those of control group, and those of hypercapnia + chimonin group were even higher than hypoxic hypercapnic group (P < 0.01). There was no significant difference in mCAP, content of III type collagen and their mRNA in three groups (P > 0.05).</p><p><b>CONCLUSION</b>Chimonin can reduce pulmonary hypertension and pulmonary vessel remodeling induced by hypoxic hypercapnia through inhibiting proliferation of collagen I, the mechanism maybe is up regulating endogenous carbon monoxide system.</p>

Effects of tetramethylpyrazine on fractalkine and tumor necrosis factor-alpha expression in patients with chronic pulmonary heart disease / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To reveal the relationship of chronic pulmonary heart disease (CPHD) with the chemotactic factor Fractalkine (FKN) and tumor necrosis factor-alpha (TNF-alpha), and to explore the action mechanism of tetramethylpyrazine (TMP) for suppressing pulmonary hypertension.</p><p><b>METHODS</b>Patients with CPHD were randomly assigned to two groups, 19 in Group A and 16 in Group B, and a control group (group C) consisting of 18 healthy adults was setup. Conventional treatment were given to all patients, which consisted of Piperacillin 3. 375 g iv dripping twice a day, Levofloxacin 0.6 g + Ambroxol 60 mg + Doxofylline 0.2 g iv dripping once a day, all for 10-14 days, and acid-base and electrolytes balance in patients were monitored and corrected. At the same time, TMP (trade name: Chuanqing, containing 120 mg of TMP in a 2 mL ampoule) was given additionally to patients in Group B at the dosage of 240 mg/d by adding in 250 mL of normal saline via iv dripping. Serum levels of FKN and TNF-alpha were detected before and after treatment by enzyme-linked immunoassay, and the change of mean pulmonary arterial pressure (mPAP) was measured as well.</p><p><b>RESULTS</b>Before treatment, difference of FKN and TNF-alpha levels between the two patients' groups were insignificant (P > 0.05), but all higher than those in Group C respectively (P < 0.01). While after treatment, the two indices and mPAP levels in Group B were statistically lower than those before treatment, also than those in Group A. Regression analysis showed a positive correlation between TNF-alpha and FKN (r = 0.662, P < 0.001).</p><p><b>CONCLUSIONS</b>A high blood FKN and TNF-alpha expression state exists in CPHD patients, which could be suppressed by TMP, and these suppressive effects may be one of the important mechanisms responsible for the pulmonary arterial pressure lowering action of TMP.</p>

Effects and mechanism of oridonin on pulmonary hypertension induced by chronic hypoxia-hypercapnia in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Pulmonary arterial hypertension (PAH) is characterized by suppressing apoptosis and enhancing cell proliferation in the vascular wall. Inducing pulmonary artery smooth muscle cells (PASMC) apoptosis had been regarded as a therapeutic approach for PAH. Oridonin can cause apoptosis in many cell lines, while little has been done to evaluate its effect on PASMC.</p><p><b>METHODS</b>Thirty male Sprague-Dawley rats were randomly assigned to three groups: normal control (NC); hypoxia-hypercapnia (HH); Hypoxia-hypercapnia + oridonin (HHO). Rats were exposed to hypoxia-hypercapnia for four weeks. Cultured human PASMC (HPASMC) were assigned to three groups: normoxia (NO); hypoxia (HY); hypoxia + oridonin (HO). The mean pulmonary artery pressure, mass ratio of right ventricle over left ventricle plus septum (RV/(LV + S)), the ratio of thickness of the pulmonary arteriole wall to vascular external diameter (WT%) and the ratio of the vessel wall area to the total area (WA%) were measured. Morphologic changes of pulmonary arteries were observed under light and electron microscopes. The apoptotic characteristics in vitro and in vivo were detected.</p><p><b>RESULTS</b>The mPAP, RV/(LV + S), WT%, and WA% in the HH group were significantly greater than those in the NC (P < 0.01) and HHO groups (P < 0.01); the activities of caspase-3 and caspase-9, and the expressions of Bax, cyt-C and apoptotic index (AI) in the group HH were less than those in the NC and HHO groups; and the expression of Bcl-2 in group HH was greater than that in the NC and HHO groups. HPASMC mitochondrial membrane potentials in group HO was lower than in group HY (P < 0.01), and cyt-C in the cytoplasm, AI, and caspase-9 in the HO group were greater than that in the HY group (P < 0.01), but the expression of Bcl-2 in the HO group was less than that in the HY group (P < 0.05).</p><p><b>CONCLUSIONS</b>The results suggest that oridonin can lower pulmonary artery pressure effectively, and inhibit pulmonary artery structural remodeling by inducing smooth cell apoptosis via a mitochondria-dependent pathway.</p>

The effects of safflower injection on lipid peroxidation level and expression of heme oxygenase-1 of the rat liver with hypoxia and hypercapnia / 中国应用生理学杂志

<p><b>AIM</b>To investigate the changes of lipid peroxidation level and expression of heme oxygenase-1 of the rat liver with chronic hypoxia and hypercapnia, and the effects of Safflower injection (a compond of Chinese Traditional medicine).</p><p><b>METHODS</b>Thirty male SD rats weighing 180 approximately 220 g were divided into three groups (n=10): control group (N group), chronic hypoxia and hypercapnia for four weeks group(F group), and Safflower injection group (H group). SOD and MDA in liver tissue were measured by spectrophotometric method. And methods Immunohistochemical assay was used to detect the distribution of HO-1 protein. Pathological changes in liver tissues were observed in HE staining section. The mRNA expressions of HO-1 in liver were detected by semi-quantitative RT-PCR.</p><p><b>RESULTS</b>The activity of SOD of the liver in F group were significantly lower than those in N group, and the content of MDA were significantly higher. The activity of SOD of the liver in H group were significantly higher than those in F group, and the content of MDA were significantly lower. In F group there were multiple dispersed immunoreactivity cells in liver. And compared to those in F group, the immunoreactivity cells were significantly decreased in H group. HE staining revealed that there were many hepatocytes with obvious adipose degeneration. Hepatic pathological damage in H group was slighter than that in F group. The expression of HO-1 mRNA of the liver in F group were significantly higher than those in N group (P < 0.01), and those in H group were significantly lower than those in F group (P < 0.01) .</p><p><b>CONCLUSION</b>Chronic hypoxia and hypercapnia increases the level of oxidative stress. Safflower injection have a protective effect, maybe because of the accommodation of the expression of HO-1 of the liver and the elimination of free radicals.</p>

Effect of safflower injection on pulmonary hypertension in rat during chronic hypoxia and hypercapnia / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of Safflower injection (a compound of Chinese Traditional medicine) on pulmonary hypertension in rat during chronic hypoxia and hypercapnia.</p><p><b>METHODS</b>Sprague-Dawley rats were randomly divided into normal control group (A), hypoxic hypercapnic group (B), hypoxic hypercapnia + Safflower injection group (C). The concentration of TXB2 and 6-keto-PGF18 in plasma and in lung homogenate were detected by the radioimmunoassay.</p><p><b>RESULTS</b>(1) mPAP, weight ratio of right ventricle (RV) to left ventricle plus septum (LV + S) were much higher in rats of hypoxic hypercapnic group than those of control group. Differences of mCAP among the three groups were not significant. (2) The concentration of TXB2 and the ratio of TXB2/6-keto-PGF1a were significantly higher in rats of B group than those of A and C group. (3) The results examined by light microscopy showed that WA/TA (vessel wall area/total area), SMC (the density of medial smooth muscle cell) and PAMT (the thickness of medial smooth cell layer) were significantly higher in rats of B group than those of A and C group. (4) The results examined by electron microscopy showed proliferation of medial smooth muscle cells and collagen fibers of pulmonary arterioles in rats of B group, and Safflower injection could reverse the changes mentioned above.</p><p><b>CONCLUSION</b>Safflower injection may inhibit hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling by decreasing the ratio of TXB2/6-keto-PGF1a.</p>

The expression of the early growth responsive gene-1 in acute pulmonary embolism of rats / 中国应用生理学杂志

<p><b>AIM</b>To investigate the dynamic changes of Egr-1 expression in the lungs of acute pulmonary embolism of rats by infusion of autoblood thrombs.</p><p><b>METHODS</b>The model of pulmonary embolism by infusion of autoblood thrombs in the pulmonary artery of rats was established and the mean pulmonary arterial pressure was continuously monitored by computer, and the results were evaluated by lung perfusion scan and pathological changes. Expression of Egr-1 proteinum and mRNA were measured by immunohistochemistry and reverse transcription polymerase chain reaction.</p><p><b>RESULTS</b>The mPAP of rats was increased significantly after infusion of autoblood thrombs at the half hour, and reached high level at the second hour, then remained the high level to four hours compared with group control at the same time point (P < 0.01). ECT image was showed significantly filling defect after infusion of autoblood thrombs at the first hour. The infused thromb was witnessed by hematoxylin and eosin stain. In the tracheal epithelium cells, alveolar epithelium cells and vascular smooth muscle cells of embolism rats, Egr-1 protein expression was increased significantly after embolization at the second hour compared with group control at the same time point (P<0.01), and was decreased slowly at the fourth hour. Egr-1 mRNA expression was showed the similar changes.</p><p><b>CONCLUSION</b>Expression of Egr-1 was low level in group control, but increased significantly after infusion of autoblood thromb at the second hour in the specificity of cells, suggesting that Egr-1 expression might be an important link of pathological changes in the acute pulmonary embolism.</p>

Effect of curcumin on pulmonary hypertension and wall collagen of pulmonary arterioles of chronic hypoxic hypercapnic rats / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of curcumin on pulmonary arterial pressure and type I collagen of pulmonary arterioles in pulmonary hypertensive rats induced by chronic hypoxia and hypercapnia.</p><p><b>METHODS</b>Thirty six rats were randomly divided into three groups: normal control group (NC), hypoxic hypercapnic group (HH) and hypoxic hypercapnia + curcumin group (HC). Collagen I in pulmonary arterioles was observed by the technique of immunohistochemistry.</p><p><b>RESULTS</b>(1) The findings from hemodynamics showed that the mPAP in group HH was significantly higher than that in group NC and HC. Differences of mCAP among groups were not significant (P > 0.05). (2) Light microscopy showed the value of WA/TA (vessel wall area/total area), SMC (the density of medial smooth muscle cells) and thickness of pulmonary arterial media smooth cell layer(PAMT) were significantly higher in group HH than group NC (P < 0.01) and group HC (P < 0.01). (3) Electron microscopy showed that structure of the endothelial cells in pulmonary arterioles in group HC was near to normal, and the proliferation of medial smooth muscle cells and collagen fibers in adventitia was much lighter than those of group HH. (4) Expression of collagen I in pulmonary arterioles was significantly higher in group HH than group NC (P < 0.01) and group HC (P < 0.01).</p><p><b>CONCLUSION</b>Curcumin can decrease pulmonary arterial pressure, improve pulmonary vessel remodeling and inhibit the deposition of collagen I in pulmonary arterioles.</p>

Effect of hypoxic hypercapnia on expression of COX-2 mRNA in pulmonary arterioles / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of chronic hypoxic hypercapnia on expression of COX-2 mRNA in pulmonary arterioles.</p><p><b>METHODS</b>SD rats were randomly divided into two groups: control group and hypoxic hypercapnic group. COX-2 mRNA was observed in pulmonary arterioles by the technique of in situ hybridization.</p><p><b>RESULTS</b>mPAP, weight ratio of right ventricle (RV) to left ventricle plus septum (LV + S) and COX-2 mRNA in pulmonary arterioles were much higher in rats of hypoxic hypercapnic group than those of control group. Light microscopy showed that vessel smooth muscle cell hypertrophy and vessel cavity straightness were found in hypoxic hypercapnic group.</p><p><b>CONCLUSION</b>Changes of expressions of COX-2 mRNA may regulate hypoxic hypercapnic pulmonary hypertension.</p>

Effect of aspirin on pulmonary hypertension in rat during chronic hypoxia and hypercapnia / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of aspirin on chronic hypoxia and hypercapnic pulmonary hypertension.</p><p><b>METHODS</b>SD rats were randomly divided into normal control group (A), hypoxic hypercapnic group (B), hypoxic hypercapnia + aspirin group (C). The concentration of TXB2 and 6-keto-PGF1alpha in plasma and in lung were detected by the technique of radioimmunology.</p><p><b>RESULTS</b>(1) mPAP was significantly higher in B group than those of A and C group. Differences of mCAP were not significant in three groups. (2) Light microscopy showed that WA/TA (vessel wall area/total area) and PAMT (the thickness of medial smooth cell layer) were significantly higher in B group than those of A and C group. (3) The concentration of TXB2 and 6-keto-PGF1alpha in plasma and lung as well as the ratio of TXB2/6-keto-PGF1alpha were significantly higher in rats of B group than those of A and C group.</p><p><b>CONCLUSION</b>Aspirin may inhibit hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling.</p>

An experimental study on the regulation of pulmonary arterial remodeling by protein kinase C in chronic hypoxic rats / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effect of protein kinase C regulating pulmonary arterial remodeling in chronic hypoxic rats.</p><p><b>METHODS</b>Electron microscope, radioactivity, immunohistochemistry and image analyser were used.</p><p><b>RESULTS</b>(1) Mean pulmonary arterial pressure (mPAP) and weight ratio of RV to LV + S were significantly higher than that of control group (P < 0.01). (2) WA/TA and SMC were significantly higher than that of control group (P < 0.01). Electron microscopy showed the proliferation of smooth muscle cells and the disposition of collagenous fiber in pulmonary arterioles induced by hypoxia. (3) The total, cytosolic, particulate fraction PKC activity and the ratio of particulate fraction to total PKC activity were significantly higher than that of control group (P < 0.01). (4) Expression of PKC, collagen I were significantly higher than that of control group (P < 0.01), the difference of collagen III was not significant between two groups (P > 0.05). (5) There were good correlation between the total, particulate fraction PKC activity, the ratio of particulate fraction to total PKC activity, expression of PKC and SMC, collagen I in pulmonary arterioles.</p><p><b>CONCLUSION</b>The PKC regulates the proliferation of pulmonary artery smooth muscle cells and expression of pulmonary arterial collagen in chronic hypoxic rats, which may play an important role in the pathogenesis of pulmonary hypertension and structural remodeling of pulmonary arteries.</p>

Effect and mechanism of chimonin on pulmonary hypertention of chronic hypoxia and hypercapnic rats / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of chimonin on chronic hypoxia and hypercapnic pulmonary hypertension and to explore its mechanism.</p><p><b>METHODS</b>SD rats were randomly divided into normal control group (A), hypoxic hypercapnic group(B), hypoxic hypercapnia + chimonin group (C). HO-1 and HO-1 mRNA was observed in pulmonary arterioles of rats by the technique of immunohistochemistry and in situ hybridization.</p><p><b>RESULTS</b>(1) mPAP was significantly higher in rats of B group than that of A and C group. Differences of mCAP were not significant in three groups. (2) Blood CO concentration was significantly higher in rats of B group than that of A group, it was significantly higher in rats of C group than that of B group. (3) Light microscopy showed that WA/TA (vessel wall area/total area), SMC (the density of medial smooth muscle cell) and PAMT (the thickness of medial smooth cell layer) were significantly higher in rats of B group than those of A and C group. (4) Electron microscopy showed proliferation of medial smooth muscle cells and collagenous fibers of pulmonary arterioles in rats of B group, and chimonin 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 that of A group, they were significantly higher in rats of C group than that of B group.</p><p><b>CONCLUSION</b>Chimonin can inhibit hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling by further increasing the expression of HO-1 mRNA.</p>

Changes of the brain NSE, S100 and effect of ligustrazine in rats of chronic hypoxia and hypercapnia / 中国应用生理学杂志

<p><b>AIM</b>To investigate the changes of the brain NSE, S100 and ultrastructure and effect of ligustrazine in rats of chronic hypoxia and hypercapnia.</p><p><b>METHODS</b>Thirty rats were randomly divided into three groups: control group (A), hypoxia hypercapnia group (B), hypoxia hypercapnia added ligustrazine group (C). The brain NSE, S100 and ultrastructure were observed in rats using the technique of immunohistochemistry and electronic microscope.</p><p><b>RESULTS</b>(1) The mPAP was significantly higher in rats of group B than that of group A and it was much lower in rats of group C than that of group B. Differences of mCAP were not significant in three groups. (2) Serum NO of group B was significantly lower than that of group A, Serum NO of group C was higher than that of group B. (3) Immunohistochemistry showed the average value of integral light density (LD) of NSE and S100 was significantly much lower in rats of group B than that of group A and it was higher in rats of group C than that of group B. (4) The neuron and astrocyte of group B showed vacuolar degeneration and the myelin sheath showed separate. Damage of neuron is alleviated in rats of group C.</p><p><b>CONCLUSION</b>The hypoxia hypercapnia could induce damage of neuron and astrocyte in rats. The ligustrazine may be useful in protecting against hypoxia hypercapnia brain damage.</p>