Objective To explore the therapeutic effect of angiotensin-converting enzyme 2( ACE2) on pulmonary edema after sea-water drowning.Methods Twenty-four Wistar rats were randomly divided into 3 groups, ie. a control group, a seawater drowning group, and an ACE2 treatment group. The rats in the seawater drowning group and the ACE2 treatment group were infused sea-water into their lungs. Then the rats in the ACE2 treatment group were intraperitoneally injected with recombinant rat ACE2. All rats were killed at the time point of 3 hours. Rat arterial blood gas was analyzed and wet /dry weight ratio of lung tissue was measured. The IL-8 content in lung tissue was measured with enzyme linked immunosorbent assay. Pathological changes of lung tissue were observed under light microscope. Results Acute lung injury induced by seawater drowning was successfully reproduced in the rats. The PaO2 in the seawater drowning group was significantly lower than that in the control group and the ACE2 treatment group [ ( 52. 34 ±2. 69) mmHg vs. ( 96. 40 ±3. 47) mm Hg and ( 64. 58 ±3. 42) mm Hg, P lt;0. 05] . The lung W/D ratio and IL-8 level in the seawater drowning group were significantly higher than those in the control group and the ACE2 treatment group ( 8. 30 ±0. 24 vs. 4. 49 ±0. 19 and 5. 65 ±0. 25, P lt; 0. 05; 1112. 2 ±40. 02 vs. 440. 39 ± 4. 06 and 858. 56 ±9. 92, P lt;0. 05) . Lung pathological examination revealed hemorrhage and hyaline membrane formation, alveolar and interstitial edema in the seawater drowning group while those changes significantly relieved in the ACE2 treatment group. Conclusion ACE2 treatment has therapeutic effects on acute lung injury induced by seawater drowning.
ObjectiveTo discuss the effect ofβ2 adrenoceptor on the alveolar fluid clearance (AFC) of the rats with severe acute pancreatitis (SAP). MethodsSD rats was made to SAP model by injecting taurocholate into biliary-pancreatic duct.These rats were randomly divided into sham operation group and SAP group, the SAP group was divided into subgroups of SAP-4 h and SAP-24 h according to the sampling time after making model.The wet-to-dry ratio, AFC, and AFC affected byβ2 adrenoceptor agonist-terbutaline or inhibitor-propranolol were measured in the bilateral lungs.β2 adrenoceptor mRNA expression in the lungs tissues was measured by real-time-PCR. ResultsCompared with the sham operation group, the wet-to-dry ratio was significantly decreased (P < 0.05) and the AFC was significantly increased in the subgroup of SAP-4 h or SAP-24 h (P < 0.05), β2 adrenoceptor agonist-terbutaline couldn't increase the AFC of the subgroup of SAP-4 h or SAP-24 h (P > 0.05), inhibitor-propranolol could decrease AFC of subgroup of SAP-4 h or SAP-24 h (P < 0.05).β2 adrenoceptor mRNA was decreased in the subgroup of SAP-4 h or SAP-24 h as compared with the sham operation group (P < 0.05). ConclusionsBilateral lung liquid volome induced by SAP is less than the normal lung, AFC is increased in the early period of SAP but decreased in the late period.when the lung injury happens, β2 adrenoceptor might modulate AFC in rats of SAP model.The mechanism of lung injury of SAP is so complex that we need more experiments to be done.
ObjectiveTo explore effect of α-adrenoceptor on modulating water of lung in severe acute pancrea-titis (SAP) rat. MethodsThe SD rats were randomly divided into sham operation group (n=5) and SAP group,the SAP group was divided into subgroups of SAP-4 h (n=5) and SAP-24 h (n=5).SAP model was made by injecting taurocholate into bilopancreatic duct.The wet-to-dry ratio,alveolar fluid clearance (AFC),and AFC affected by α1-adrenoceptor inhibitor-prazosin and α2-adrenoceptor inhibitor-yohimbine separately or together were measured in the lungs.The α1-adrenoceptor and α2-adrenoceptor mRNA expressions in the lungs tissues were measured by real-time PCR. Results① The wet-to-dry ratios in the SAP-4 h group and SAP-24 h group were obviously decreased as compared with the sham operation group (P<0.05),which in the SAP-24 h group was significantly lower than that in the SAP-4 h group (P<0.05).② The AFCs in the SAP-4 h group and SAP-24 h group were obviously increased as compared with the sham operation group (P<0.05).The AFCs in the SAP with α1-adrenoceptor inhibitor-prazosin or α2-adrenocpetor inhibitor-yohimbine or prazosin combined with yohimbine were all obviously decreased as compared with the SAP group (P<0.05).③ The α1 adrenoceptor and α2 adrenoceptor mRNAs in the SAP-4 h group and SAP-24 h group were obviously increased as compared with the sham operation group (P<0.05). ConclusionAFC might be modulated by α-adrenoceptor in SAP rat.
ObjectiveTo discuss the change of expression of Na-K-ATPase mRNA in the rats with severe acute pancreatitis (SAP). MethodsTwenty four SPF SD rats were randomly divided into sham group (n=6) and SAP group (n=18), the experiment concluded 3 sub-experiments, and each sub-experiments enrolled 24 rats. After establishment of SAP model successfully, rats of SAP group were randomly divided into SAP-4 h group (n=6), SAP-24 h group (n=6), and SAP-48 h group (n=6). Rats of sham group were only conducted the abdominal exploration. Rats of 4 groups were sacrificed (sham group:4 hours after surgery; SAP-4 h group:4 hours after surgery; SAP-24 h group:24 hours after surgery; SAP-48 h group:48 hours after surgery) to determine the dry/wet ratio, alveolar fluid clearance (AFC), and expressions of Na-K-ATPase mRNA at 2 sides of lung tissues. Results① Dry/wet ratio. Compared with sham group, the dry/wet ratios of SAP-4 h group, SAP-24 h group, and SAP-48 h group were all lower (P < 0.01); compared with SAP-4 h group, the dry/wet ratio of SAP-24 h group was lower (P < 0.01), but dry/wet ratio of SAP-48 h group was higher (P < 0.01); compared with SAP-24 h group, dry/wet ratio of SAP-48 h group was higher (P < 0.01). ② AFC. Compared with sham group, the AFC value of SAP-4 h group and SAP-24 h group were both higher (P < 0.01), but there was no significant difference between sham group and SAP-48 h group (P > 0.05); compared with SAP-4 h group, the AFC value of SAP-24 h group and SAP-48 h group were both lower (P < 0.01); compared with SAP-24 h group, the AFC value of SAP-48 h group was lower (P < 0.01). ③ α1 Na-K-ATPase mRNA. Compared with corresponding side of lung tissue in sham group, the expression level of α1 Na-K-ATPase mRNA at both 2 sides of lung tissues in SAP-4 h group, SAP-24 h group, and SAP-48 h group were higher (P < 0.01); compared with corresponding side of lung tissue in SAP-4 h group, the expression level of α1 Na-K-ATPase mRNA was lower at left lung tissue (P < 0.05) and was higher at right lung tissue (P < 0.01) in SAP-24 h group, and expression level of α1 Na-K-ATPase mRNA at both sides of lung tissues was lower in SAP-48 h group (P < 0.01); compared with corresponding side of lung tissue in SAP-24 h group, the expression level of α1 Na-K-ATPase mRNA at both 2 sides of lung tissues was lower in SAP-48 h group (P < 0.01). There was no significant difference in the expression level of α1 Na-K-ATPase mRNA between left lung tissue and right lung tissue in sham group, SAP-4 h group, and SAP-48 h group (P > 0.05), but the expression level of α1 Na-K-ATPase mRNA at right lung tissue was higher than that of left lung tissue in SAP-24 h group (P < 0.01). ④ β1 Na-K-ATPase. Compared with corresponding side of lung tissue in sham group, the expression level of β1 Na-K-ATPase mRNA at both 2 sides of lung tissues in SAP-4 h group, SAP-24 h group, and SAP-48 h group was higher (P < 0.01); compared with corresponding side of lung tissue in SAP-4 h group, the expres-sion level of β1 Na-K-ATPase mRNA at both 2 sides of lung tissues in SAP-24 h group was higher (P < 0.01), and lower in right lung tissue of SAP-48 h group (P < 0.01); compared with corresponding side of lung tissue in SAP-24 h group, the expression level of β1 Na-K-ATPase mRNA at both 2 sides of lung tissues was lower in SAP-48 h group (P < 0.01). There was no significant difference in the expression level of β1 Na-K-ATPase mRNA between left lung tissue and right lung tissue in sham group and SAP-48 h group (P > 0.05), but the expression level of β1 Na-K-ATPase mRNA at right lung tissue was higher than that of left lung tissue in SAP-4 h and SAP-24 h group (P < 0.05). Conclusionα1 Na-K-ATPase mRNA may be the key factor for AFC, and may involved in the water transformation in lung tissue of SD rat with SAP.
ObjectiveTo improve the seawater-drowning-induced lung injury model in rats, and investigate the protective effect of resveratrol against seawater-drowning-induced lung injury and its mechanism.MethodsA total of 112 SD healthy rats were randomly assigned into 5 groups: a control group (Group C, n=8), a seawater drowning group (Group S, n=32), a resveratrol prophylactic treatment group (Group S+R, n=32), a resveratrol group (Group R, n=8), and an endotracheal intubation group (Group E, n=32). A modified endotracheal intubation model was developed, and endotracheal intubation was used instead of tracheotomy. Blood gas analysis was performed on the abdominal aorta at each time point, then the rats were sacrificed to obtain their lungs. Lung wet-to-dry ratio (W/D), malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO) and cysteinyl aspartate specific proteinase (Caspase-3) were measured by enzyme linked immunosorbent assay. The histological sections of rat lungs were stained with haematoxylin-eosin. Groups S+R and R were pretreated with resveratrol (50 mg/kg) through intragastric administration for 3 days; then models were established and the rats were sacrificed 24 hours after the last intragastric administration.ResultsAfter seawater perfusion, arterial oxygen pressure decreased and arterial carbon dioxide pressure increased in blood gas analysis of rats, MDA content increased, MPO and SOD activity decreased, caspase-3 content and W/D ratio increased, as well as lung tissue pathological damage. The resveratrol pretreatment group showed the same change trend, but the damage degree was relatively light.ConclusionsSeawater perfusion can induce respiratory failure, pulmonary edema and hemorrhage in rats. Lung tissue apoptosis may occur when seawater submergence causes lung injury. Resveratrol pretreatment can ameliorate hypoxia and pulmonary edema in rats.