The Effects of Rhodiola Tibetica on Lung Tissue of Rats with High Altitude Pulmonary Edema

2013 ◽  
Vol 690-693 ◽  
pp. 1305-1309
Author(s):  
Wen Hua Li

Objective observation of Tibetan medicine rhodiola on high altitude Pulmonary edema in rats and HIF-1a expression changes. Method Will 50 only male SD rats randomly divided into 5 group , are often oxygen control group (Xi'an , altitude 5m ), acute hypoxia control group (Xi'an , altitude 5m ), acute hypoxia Group (naqu , elevation 4500m ), rhodiola acclimatization control group ( Xi'an , altitude 5m ), rhodiola altitude acclimatization group (naqu, elevation 4500m ) , light and electron microscopic observation of lung tissue samples , immunohistochemical detection of various groups of lung tissue HIF-la expression, RT-PCR method detection altitude hypoxia group animal lungs HIF-la mRNA expression changes. Results Acute hypoxia group lung tissue microstructure and Ultrastructure of a discernible high altitude pulmonary edema, and after the Tibetan medicine rhodiola after high altitude pulmonary edema is significantly reduced, ( as in Figure 123456). Lung tissue within the immunohistochemical detection not see HIF-la protein expression, RT-PCR detection SD big rat intraperitoneal injection of rhodiola extract 40g BGE/kg, 2h open back began to rise 4h, peak, after declining 24h, basically back to their normal control group , level rhodiola medicine acclimatization group HIF a 1 am RNA expression are clearly higher than the atmospheric oxygen control group and acute hypoxia group (p < 0.01). Conclusions Tibetan medicine rhodiola on lung tissue HIF-lamRNA expression of conducive to reduce hypoxic rats high altitude pulmonary edema.

2011 ◽  
Vol 140 ◽  
pp. 68-73 ◽  
Author(s):  
Wen Hua Li ◽  
Dong Ya Yuan ◽  
Fang Yun Sun ◽  
Feng Cang Zhao ◽  
Min Zhang ◽  
...  

Background: Studies show that rapid access to high altitude, the body inevitably will be different degrees of injury, more significant damage to heart and lung [1 ~ 3]. The high altitude hypoxia on the lung tissue to adapt to structural changes and hypoxia inducible factor-1α (HIF-1α) expression of the study rarely reported. The experimental area for a short time brought by the near sea level to higher altitudes rat lung tissue by light, electron microscopy and the expression of hypoxia inducible factor-1α changes were studied.Objective: To observe the altitude hypoxia on the ultrastructure of lung tissue and the hypoxia inducible factor-la (HIF-1α) expression.Methods: 50 rats were randomly divided into 5 groups, namely group 1 d Golmud (altitude 2 700 m), 2 d Tanggula group (altitude 5 000 m), 3 d Nagqu group (altitude 4 500 m) and 30 d Nagqu group (altitude 4 500 m), the control group (in Xi'an, elevation 5 m). 4 time-consuming experimental animals 1 d from Xi'an to the Golmud, Qinghai (altitude 2 700 m), 2 d to the Tibetan Tanggula (altitude 5 000 m), 3 d to the Naqu (altitude 4500 m), 30 d in Tibet Nagqu. Light and electron microscopy of the lung tissue samples, Western Blot method to detect the lung tissue of hypoxia inducible factor-1α expression, RT-PCR method for detection of high altitude hypoxic group, lung tissue expression of hypoxia inducible factor-1αmRNA change. Results and Conclusions: Acute hypoxia 2d Tanggula microstructure and ultrastructure of lung tissue apparent high altitude pulmonary edema, and 30d after hypoxic Nagqu group after high altitude pulmonary edema was significantly reduced lung tissue Western blotting, not Canon See HIF-1α protein expression, RT-PCR detection of HIF-1αmRNA in the 30d Nagqu group, a certain amount of expression, the other three experimental groups HIF-1αmRNA expression was not significant (P> 0.05), 30d Nagqu group HIF-lamRNA expression was significantly higher In the control group (P <0.01). The results confirmed that the lung tissue after hypoxic expression of HIF-1αmRNA increase will help reduce the hypoxic altitude pulmonary edema.


1996 ◽  
Vol 81 (2) ◽  
pp. 922-932 ◽  
Author(s):  
A. Podolsky ◽  
M. W. Eldridge ◽  
R. S. Richardson ◽  
D. R. Knight ◽  
E. C. Johnson ◽  
...  

Ventilation-perfusion (VA/Q) mismatch has been shown to increase during exercise, especially in hypoxia. A possible explanation is subclinical interstitial edema due to high pulmonary capillary pressures. We hypothesized that this may be pathogenetically similar to high-altitude pulmonary edema (HAPE) so that HAPE-susceptible people with higher vascular pressures would develop more exercise-induced VA/Q mismatch. To examine this, seven healthy people with a history of HAPE and nine with similar altitude exposure but no HAPE history (control) were studied at rest and during exercise at 35, 65, and 85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m) breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) gas at both locations. We measured cardiac output and respiratory and inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard deviation of the perfusion distribution) increased with exercise. At sea level, log standard deviation of the perfusion distribution was slightly higher in the HAPE-susceptible group than in the control group during heavy exercise. At altitude, these differences disappeared. Because a history of HAPE was associated with greater exercise-induced VA/Q mismatch and higher pulmonary capillary pressures, our findings are consistent with the hypothesis that exercise-induced mismatch is due to a temporary extravascular fluid accumulation.


2015 ◽  
Vol 4 (3) ◽  
pp. 7
Author(s):  
Xiaofeng Wang

<strong>Objective:</strong> To analyze the effect of a nursing intervention program in patients with high altitude pulmonary edema, and to provide a guideline for clinical nursing work. <strong>Methods:</strong> A total of 52 cases of patients suffering from high-altitude pulmonary edema were divided into two groups. The control group was given routine nursing intervention, while the experimental group was given a systematic nursing intervention. The disappearance of cyanosis and pulmonary rales in both groups of patients over time were compared and the results were statistically analyzed. <strong>Results:</strong> In the experimental group, both cyanosis and pulmonary rales disappeared faster compared the routine group. The comparison between patients in both groups was significantly different (<em>p</em> &lt; 0.05). The level of anxiety among patients of the experimental group is also significantly lower than the patients in the control group (<em>p</em> &lt; 0.05). In both groups, the difference was not significant (<em>p </em>&gt; 0.05) before treatment and the clinical symptom score of the experimental group was significantly lower than that in the control group (<em>p </em>&lt; 0.05). <strong>Conclusion:</strong> It is effective to implement a systematic nursing intervention program in caring for patients with high-altitude pulmonary edema and it is suitable for clinical application.


1989 ◽  
Vol 67 (5) ◽  
pp. 1982-1989 ◽  
Author(s):  
A. Kawashima ◽  
K. Kubo ◽  
T. Kobayashi ◽  
M. Sekiguchi

To verify the presence of the constitutional abnormality implicated in the pathogenesis of high-altitude pulmonary edema (HAPE), we evaluated the hemodynamic responses to hypoxia, hypobaria, and exercise in HAPE-susceptible subjects (HAPE-S). HAPE-S were five males with a history of HAPE. Five healthy volunteers who had repeated experiences of mountain climbing without any history of altitude-related problems served as controls. HAPE-S showed much greater increase in pulmonary vascular resistance index (PVRI) than the control subjects, resulting in a much higher level of pulmonary arterial pressure (Ppa), under both acute hypoxia of 15% O2 (Ppa = 29.0 +/- 2.8 vs. 17.8 +/- 0.3 Torr, P less than 0.05) and acute hypobaria of 515 Torr (32.3 +/- 2.8 vs. 19.1 +/- 0.8 Torr, P less than 0.05). Also, PVRI in HAPE-S exhibited a tendency to increase even during light exercise with supine bicycle ergometer (50 W), whereas PVRI in the control subjects significantly decreased, so that HAPE-S showed a greater increase in Ppa (delta Ppa = 16.0 +/- 1.5 vs. 4.9 +/- 1.1 Torr, P less than 0.001) and a greater decrease in arterial oxygen tension (17.8 +/- 4.7 vs. 5.6 +/- 1.7 Torr, P less than 0.05). We thus conclude that HAPE-S have a constitutional abnormality, which can be evaluated at low altitude, in the pulmonary circulatory responses to possible causative factors of HAPE such as hypoxia, hypobaria, and exercise.


2020 ◽  
Author(s):  
Yanli Zhao ◽  
Lining Si ◽  
Qifu Long ◽  
Derui Zhu ◽  
Guoping Shen ◽  
...  

Abstract Background: High altitude pulmonary edema (HAPE) is a severe form of acute mountain sickness (AMS). The results of existing studies have shown that the onset of HAPE has obvious ethnic specificity and personal susceptibility, suggesting that the occurrence of HAPE is related to genetic factors. Therefore, six polymorphisms on MIR17HG were selected to investigate the effect of mutations on MIR17HG on HAPE in Chinese Han population.Materials and Methods: 487 healthy participants (244 participants had high altitude pulmonary edema, as the case group; and 243 participants had no symptoms of HAPE, as the control group) were genotyped via the Agena MassARRAY, and the relationship between polymorphisms on MIR17HG and HAPE risk was evaluated using a χ2 test with an odds ratio (OR) and 95% confidence intervals (CIs) in multiple genetic models.Results: In the allele model, we observed that lower risk (OR = 0.74, 95%CI: 0.56 - 0.98, p = 0.036) of the A allele for rs7318578 on the MIR17HG compared with the people with the C allele. Logistic regression analysis of four models for all selected MIR17HG SNPs between cases and controls showed significant differences for rs7318578 (OR = 0.74, 95%CI: 0.56 – 0.98, p = 0.037) and rs17735387 (OR = 1.51, 95%CI: 1.03 – 2.21, p = 0.036) in the HAPE population.Conclusion: rs7318578 and rs17735387 on MIR17HG were associated with the genetic susceptibility of HAPE in Chinese Han population.


Dose-Response ◽  
2020 ◽  
Vol 18 (4) ◽  
pp. 155932582097082
Author(s):  
Jiewen Tan ◽  
Chunjin Gao ◽  
Cong Wang ◽  
Linlin Ma ◽  
Xiaomin Hou ◽  
...  

Objective: To investigate the therapeutic roles of hyperbaric oxygen exposure on high-altitude pulmonary edema and to determine whether aquaporin-1 and aquaporin-5 were involved in the pathogenesis of HAPE in rats. Methods: Rats were divided into 5 groups: The control group, the HAPE group (HAPE model), the HBO group (hyperbaric oxygen exposure), the NBO group (normobaric oxygen exposure), and the NA group (normal air exposure). Western blot and real-time PCR were used to analyze the pulmonary expressions of AQP1 and AQP5. The wet-to-dry (W/D) weight ratio and the morphology of the lung were also examined. Results: The lung W/D weight ratio in the HAPE group was increased compared with the control group. The injury score in the HBO group was noticeably lower than that in the control group. The mRNA and proteins expressions of AQP1 and AQP5 were significantly downregulated in the HAPE group. Conclusions: Oxygen exposure alleviated high-altitude hypobaric hypoxia-induced lung injury in rats. Additionally, HBO therapy had significant advantage on interstitial HAPE.


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