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．
Objective To investigate the influence of hypoxic preconditioning on pulmonary structure of rats exposed to simulated high altitude hypoxia and to explore the role of hypoxia inducible factor-1α（HIF-1α）.Methods Fifty-six Wistar rats were randomly divided into 7 groups(n=8 in each group),ie,a normal control group(N group)，an acute hypoxic control group(H0 group)，an acute hypoxic group(H1 group)，a 3 000 m hypoxic preconditioning group(C3.0 group)，a 3 000 m hypoxic preconditioning + acute hypoxic group (C3.1 group)，a 5 000 m hypoxic preconditioning group(C5.0 group)，and a 5 000 m hypoxic preconditioning + acute hypoxic group(C5.1 group).After treated with hypoxic preconditioning，the animals were exposed to simulated altitude of 6 000 m for 24 hours.Then the protein and mRNA expression of HIF-1α in lung of N，H0，C3.0 and C5.0 groups were assessed by Western blot and RT-PCR，respectively.The lung structure in N，H1，C3.1 and C5.1 groups was observed by light microscope and electron microscope.Results Pulmonary interstitial edema was apparently observed in H1 group，while significantly relieved in two hypoxic preconditioning groups.HIF-1α protein was not detected in rat lungs by Western blot analysis.Compared to N group，the levels of HIF-1α mRNA significantly increased in C3.0 group and C5.0 group(both Plt;0.01).Conclusions Hypoxic preconditioning can relieve hypoxic pulmonary interstitial edema and increase HIF-1α mRNA expression in rat lungs.HIF-1 may be involved in the process of hypoxic preconditioning in rat lungs.
高原性肺水肿(HAPE)是人们由低海拔快速进入高海拔地区（一般3 000 m以上）后2～5 d内发生的非心源性肺水肿，是一种重型急性高原病，起病急、进展快、危害大，若不及时救治，可能危及生命。经过多年努力，对其发病机制及治疗进行了大量研究，取得了一些结果，但仍有许多未明之处，本文综述近年在此领域的研究进展，以期对HAPE的研究具有一定推动作用。
Objective To evaluate the feasibility and efficacy of emergency percutaneous coronary intervention( PCI) under mechanical ventilation for the treatment of patients with acute myocardial infarction complicated with acute pulmonary edema. Methods The clinical data of 15 patients admitted to the emergency ward for acute pulmonary edema caused by acute myocardial infarction from 2007 to 2009 were retrospectively analyzed. These patients received emergency PCI under mechanical ventilatory support.Parameters involved changes of symptoms, arterial blood gas, left ventricular ejection fraction( LVEF) , plasma concentrations of B-type natriuretic peptide( BNP) , and high sensitivity reactive protein( hs-CRP) . Results All patients showed significant improvements in dyspnea, artery blood gas parameters after PCI( P lt;0. 01) .LVEF increased significantly after PCI compared with before weaning [ ( 37. 36 ±0. 02) % vs ( 47. 41 ±0. 02) % , F =461. 47, P lt; 0. 05] . The concentrations of BNP and hs-CRP returned to lower level 4 weeks after PCI [ ( 99. 34 ±5. 15) fmol /mL vs ( 430. 50 ±96. 08) fmol /mL, ( 8. 35 ±2. 49) ng/mL vs ( 89. 50 ±9. 30) ng/mL, both P lt;0. 01] . Conclusion Emergency PCI under mechanical ventilatory support is a feasible and effective approach for patients with acute myocardial infarction complicated with acute pulmonary edema.
【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.
Objective To investigate whether sodium tanshinone ⅡA sulphonate ( STS) treatment attenuates pulmonary edema of seawater drowning ( PE-SWD) , and examine the effects of STS on Na-KATPase(NKA) in PE-SWD. Methods Thirty-six rats were randomly divided into there groups, ie. a normal group ( NG) , a seawater group ( SG) , and a STS treatment group ( TG) . The rat model of PE-SWD was established by seawater instillation. PaO2 , histological changes of lungs, lung wet /dry weight ratio ( W/D) ,pulmonary microvascular permeability ( PMVP) , and NKA activity were detected. Western blot were used to test the effects of STS on NKA-α1 expression. Results Seawater instillation decreased PaO2 and the expression of NKA, while increased W/D ratio and PMVP. At 2 h after seawater instillation, the PaO2 in the TG group were significantly higher than those in the SG group, and peaked at 4 h after seawater instillation.Histological examination showed that there were hemorrhage, edema, markedly thickened alveolar wall, and infiltration of inflammatory cells in alveolar spaces in the SG group, but lung injury was significantly alleviated in the TG group. W/D ratio and PMVP in the TG group were significantly lower than those in the SG group. Additionally, NKA activity and NKA-α1 expression were significantly higher in the TG group than those in the SG group. Conclusion STS treatment can attenuate pulmonary edema of seawater drowning which may be related with up-regulating Na-K-ATPase activity and expression.
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.
The high incidence and mortality rates existed in chronic pulmonary thromboembolism(PTE), with considerable misdiagnosis and missed diagnosis rate. The prognosis for patients with chronic thromboembolic pulmonary hypertension was poor with medical therapy. But the pulmonary thromboendarterectomy was well established.The postoperative pulmonary hypertension and reperfusion pulmonary edema are main complications and death causes. The key management after pulmonary thromboendarterectomy is important which decreases pulmonary hypertension , and prevents reperfusion pulmonary edema and re thromboembolism.