Endothelial Nitric Oxide Synthase Gene Polymorphisms Associated with Susceptibility to High Altitude Pulmonary Edema in Chinese Railway Construction Workers at Qinghai-Tibet over 4500 Meters above Sea Level

Objective To examine whether the polymorphisms of endothelial nitric oxide synthase (eNOS) gene are associated with the susceptibility to high altitude pulmonary edema (HAPE) in Chinese railway construction workers at Qinghai-Tibet where the altitude is over 4 500 m above sea level. Methods A case-control study was conducted including 149 HAPE patients in the construction workers and 160 healthy controls randomly recruited from their co-workers, matching the patients in ethnicity, age, sex, lifestyle, and working conditions. Three polymorphisms of eNOS gene, T-786C in promoter, 894G/T in exon 7, and 27bp variable number tandem repeat (VNTR) in intron 4, were genotyped using polymerase chain reaction (PCR) and confirmed with DNA sequencing. Results The frequencies of 894T allele and heterozygous G/T of the 894G/T variant were significantly higher in HAPE patients group than in the control group (P=0.0028 and P=0.0047, respectively). However, the frequencies of the T-786C in promoter and the 27bp VNTR in intron 4 were not significantly different between the two groups. Haplotypic analysis revealed that the frequencies of two haplotypes (H3,T-T-b, b indicates 5 repeats of 27 bp VNTR; H6, C-G-a, a indicates 4 repeats of 27 bp VNTR) were significantly higher in HAPE patients (both P<0.0001). On the contrary, the frequencies of H1 (T-G-b) and H2 (T-G-a) were lower in HAPE patients than in healthy controls (both P<0.001). Conclusions Two haplotypes (T-T-b and C-G-a) may be strongly associated with susceptibility to HAPE. Compared with the individual alleles of eNOS gene, the interaction of multiple genetic markers within a haplotype may be a major determinant for the susceptibility to HAPE.

Studies on monitoring hemodynamics and oxygen dynamics of adult respiratory distress syndrome secondary to high altitude pulmonary edema

To study monitoring hemodynamics and oxygen dynamics of adult respiratory distress syndrome (ARDS) secondary to high altitude pulmonary edema (HAPE),we performed clinic and laboratory studies in 8 patients who preliminarily developed high altitude cerebral edema (HACE) and then ARDS occurred at an altitude of 4 500 m. After an initial emergency treatment on high mountains,all the patients were rapidly transported to a hospital at a lower altitude of 2 808 m. The right cardiac catheterizations were carried out within 5 h after hospitalized. The monitoring hemodynamics and oxygen dynamics were studied via a thermodilution Swan-Gaze catheter. The results showed that before treatments at the beginning of monitoring,there presented a significant pulmonary artery hypertension with a decreased cardiac function,and a lower oxygen metabolism in all the 8 patients. However,after some effective treatments,including mechanical ventilation and using dexamethasone,furosemide,etc,four days later the result of a repeated monitoring showed that their pulmonary artery pressure had been decreased with an improved cardiac function with all the oxygen metabolic indexes increased significantly. Our studies suggested that performing monitoring hemodynamics in patients with ARDS secondary to HAPE will define the clinical therapeutic measures which will benefit the outcome.

Subclinical high altitude pulmonary edema: A clinical observation of 12 cases in Yushu

During the Yushu Earthquake on April 14,2010,a high incidence of acute high altitude illness was observed in the mountain rescuers,and 0.73 % of these patients suffered from high altitude pulmonary edema,of which 12 patients developed subclinical pulmonary edema and concomitantly contracted acute mountain sickness. Symptoms and signs were atypically high heart rate with high respiratory rate,striking cyanosis,and significantly low oxygen saturation,whereas no moist rates were heard on auscultation,and Chest X-ray showed peripheral with a patchy distribution of mottled infiltrations in one or both lung fields. We believe that subclinical high altitude pulmonary edema is an earliest stage of pulmonary edema at high altitude. The possible pathogenesis and the diagnosis were discussed.