【摘要】 目的 探讨西地兰联合小剂量酒石酸美托洛尔静脉注射治疗二尖瓣狭窄合并急性肺水肿与快速型心房颤动的疗效与安全性。 方法 将2005年1月-2010年2月收治的60例二尖瓣狭窄合并急性肺水肿与快速型心房颤动患者，随机分配至西地兰组与联合用药组，西地兰组以多次静脉注射西地兰控制心率，联合用药组则予以多次静脉注射西地兰与小剂量酒石酸美托洛尔，分别在用药开始时、用药开始后监测收缩压、心率、呼吸频率与手指脉搏血氧饱和度（SpO2），同时观察肺部啰音、呼吸困难，记录肺水肿改善时间。 结果 两组患者在治疗开始时心异率、呼吸频率、收缩压与SpO2均无差异；在治疗整个过程中，两组患者收缩压无差异；治疗开始后60、90及120 min时联合用药组心率均显著低于西地兰组。联合用药组从在治疗开始到肺水肿改善的时间短于西地兰组[(71.37±13.37)、(78.77±14.74) min，P=0.046]。治疗期间无患者出现病情恶化或死亡。联合用药组患者的酒石酸美托洛尔平均总量为4.22 mg/例。 结论 在排除美托洛尔禁忌症的前提下，静脉注射西地兰与小剂量酒石酸美托洛尔可快速、安全、有效地控制二尖瓣狭窄合并急性肺水肿与心房颤动患者的心率，缓解肺水肿。【Abstract】 Objective To observe the effect of intravenous injection with cedilanid and small does of metoprolol tartrate on mitral stenosis complicating with acute pulmonary edema and atrial fibrillation. Methods Sixty patients with mitral stenosis complicating with acute pulmonary edema and atrial fibrillation from January 2005 to February 2010 were randomly divided into cedilanid group and drug combination group, which was administered with cedilanid, or cedilanid and small does metoprolol tartrate by intravenous injection, respectively. Systolic blood pressure, heart rate, respiratory rate, pulse oxygen saturation (SpO2), dypnea, rales over lung field and the time from beginning of treatment to pulmonary edema improved were monitored as soon as the treatment began. Results There was no significant difference in basic data such as systolic blood pressure, heart rate, respiratory rate and SpO2 at the beginning of treatment between the two groups, and no obvious difference was seen in systolic blood pressure at all the time of treatment between the two groups; while a obvious decrease took place in heart rate between cedilanid group and drug combination group after the treatment began; the time from beginning of treatment to pulmonary edema in drug combination group was much shorter than that in cedilanid group [(71.37±13.37), (78.77±14.74) minutes, P=0.046]. Conclusion Without contraindication of metoprolol, intravenous injection with cedilanid combined with small dose of metoprolol can effectively, quickly and safely treat the patients with mitral stenosis complicating with acute pulmonary edema and atrial fibrillation by controlling the heart rate.
Objective To analyze risk factors and therapy strategies of critically ill patients with acute pulmonary edema(APE)after the 2008 Wenchuan earthquake．Methods Data including the level of hemoglobin，mean arterial pressure(MAP)，central venous pressure(CVP)，serum albumin as well as complications and liquid balance 1 week，3 days，1 day before onset of APE was collected an d an alyzed retrospectively．Resets Among 142 patients during two months after May 12 earthquake APE was detected in 17 cases for 25 times．The hemoglobin Was (86．04 ±16．31)s／L，MAP was(99．40±17．38)mm Hg，CVP Was (13．64 ±4．09)mm Hg and serum albumin was(27．80±8．10)g／L．Acute renal failure，severe infection，cardiovascular disease and extremity lost were more common in APE patients．Theliquid net intake Was (1 725．05±4 624．84)mL for one week，(1 574．70±2 857．13)mL for 3 days and (368．56±1 589．89)mL for 1 day before the onset of APE．The liquid intake Was significantly higher in young group．APE Was alleviated promptly after integrated therapy in all cases．Conclusions Traumapatients with ARF or extremity lost are prone to be compromised with APE．Severe infection and overburden of liquid may be other predisposing factors．
【摘要】 目的 探讨腹水引起的腹内高压对肝硬化小鼠肺组织水通道蛋白1（AQP1）和水通道蛋白5（AQP5）表达的影响。 方法 雄性美国癌症研究所（Institudo of Cancer Reseach，ICR）小鼠50只，随机取10只作正常对照组（腹压0 cm H2O，1 cm H2O=0.098 kPa），其余40只用四氯化碳建立肝硬化小鼠模型，并随机分为4组:肝硬化（腹压0 cm H2O）组、肝硬化（腹压5 cm H2O）组、肝硬化（腹压10 cm H2O）组、肝硬化（腹压20 cm H2O）组，通过腹腔注射不同量的白蛋白生理盐水形成不同的腹压，并维持腹压24 h后取肺组织行病理、免疫组织化学、肺湿/干比值及实时荧光定量PCR检测AQP1和AQP5 mRNA表达量。 结果 与正常对照小鼠相比，肝硬化小鼠肺AQP5、AQP1表达明显下降（Plt;0.05）；肝硬化小鼠随着腹内压的升高，肺湿/干比值升高，AQP5、AQP1表达相应增加（Plt;0.05）。 结论 肝硬化可以影响肺AQP1、AQP5的表达；肝硬化小鼠随着腹内压的升高，AQP1、AQP5表达相应增加，并与肺水肿的严重程度密切相关。【Abstract】 Objective To investigate the role of intra-abdominal hypertension caused by ascites on the expression of Aquaporin (AQP) 1 and AQP 5 in the lung of cirrhotic mice. Methods We randomly chose 10 from 50 male Institude of Cancer Research (ICR) mice to form the control group [intra-abdominal pressure (IAP)=0 cm H2O, 1 cm H2O=0.098 kPa]. The model of cirrhosis were prepared by subcutaneous injection of carbon tetrachloride for the rest 40 mice which were then randomly divided into 4 groups: cirrhosis (IAP=0 cm H2O) group, cirrhosis (IAP=5 cm H2O) group, cirrhosis (IAP=10 cm H2O) group, and cirrhosis (IAP=20 cm H2O) group. Saline with different volume of albumin was injected into the peritoneum of each mouse in order to form different IAP. After 24 hours, analysis of pathology, immunochemistry and wet/dry ratio was done for the lungs of these mice; and the expression of AQP1 and AQP5 at the protein and mRNA levels were analyzed by IHC and qRT-PCR. Results Compared with the normal mice, the expression of AQP1 and AQP5 in lungs of cirrhotic mice were significantly lower (Plt;0.05). Both the lung wet/dry ratio and the expression of AQP1 and AQP5 raised with the increase of IAP. Conclusion Cirrhosis can affect the expression of AQP1 and AQP5 in lungs. The expression of AQP5 and AQP1 in lungs of cirrhotic mice increases with the increase of IAP, which is also closely correlated with the severity of pulmonary edema.
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.
【Abstract】 Objective To analyze the correlations between the mt5351G and mt6680C genotypes in mitochondrial DNA ( mtDNA) haplogroup M and susceptibility to high altitude pulmonary edema ( HAPE)among the Hans. Methods Specimens from206 Hans cases of HAPE and 144 matched Hans controls were collected. Then PCR-RFLP method was used to determine haplogroup M and N of mtDNA, and PCR-LDR was used to genotype mt5351G and mt6680C in the haplogroup M in these samples. Results The frequencies of haplogroup Mand N were 49. 0% and 51.0% in the HAPE patients, and 47. 2% and 52. 8% in the controls, respectively, with no significant difference between the HAPE patients and the controls. In the haplogroup M, the genotype of mt6680C and mt5351G frequencies in the HAPE patients were both significantly higher than the controls ( both 12. 0% vs. 1. 5% , P = 0. 016) . Conclusion The existence of mt5351G and mt6680C genotypes in the haplogroup Mis a risk factor for HAPE among the Hans.