| Autor: |
Sheppard RL; Department of Submarine Medicine and Survival Systems Groton, Naval Submarine Medical Research Laboratory, Groton, CT, United States.; Department of Undersea Medicine, Walter Reed Army Institute of Research and Naval Medical Research Center, Silver Spring, MD, United States., Swift JM; Department of Undersea Medicine, Walter Reed Army Institute of Research and Naval Medical Research Center, Silver Spring, MD, United States., Hall A; Department of Undersea Medicine, Walter Reed Army Institute of Research and Naval Medical Research Center, Silver Spring, MD, United States., Mahon RT; Department of Undersea Medicine, Walter Reed Army Institute of Research and Naval Medical Research Center, Silver Spring, MD, United States. |
| Jazyk: |
angličtina |
| Zdroj: |
Frontiers in physiology [Front Physiol] 2018 Feb 28; Vol. 9, pp. 130. Date of Electronic Publication: 2018 Feb 28 (Print Publication: 2018). |
| DOI: |
10.3389/fphys.2018.00130 |
| Abstrakt: |
Introduction: Individuals with a known susceptibility to high altitude pulmonary edema (HAPE) demonstrate a reduced ventilation response and increased pulmonary vasoconstriction when exposed to hypoxia. It is unknown whether reduced sensitivity to hypercapnia is correlated with increased incidence and/or severity of HAPE, and while acute exercise at altitude is known to exacerbate symptoms the effect of exercise training on HAPE susceptibility is unclear. Purpose: To determine if chronic intermittent hypercapnia and exercise increases the incidence of HAPE in rats. Methods: Male Wistar rats were randomized to sedentary (sed-air), CO 2 (sed-CO 2 ,) exercise (ex-air), or exercise + CO 2 (ex-CO 2 ) groups. CO 2 (3.5%) and treadmill exercise (15 m/min, 10% grade) were conducted on a metabolic treadmill, 1 h/day for 4 weeks. Vascular reactivity to CO 2 was assessed after the training period by rheoencephalography (REG). Following the training period, animals were exposed to hypobaric hypoxia (HH) equivalent to 25,000 ft for 24 h. Pulmonary injury was assessed by wet/dry weight ratio, lung vascular permeability, bronchoalveolar lavage (BAL), and histology. Results: HH increased lung wet/dry ratio (HH 5.51 ± 0.29 vs. sham 4.80 ± 0.11, P < 0.05), lung permeability (556 ± 84 u/L vs. 192 ± 29 u/L, P < 0.001), and BAL protein (221 ± 33 μg/ml vs. 114 ± 13 μg/ml, P < 0.001), white blood cell (1.16 ± 0.26 vs. 0.66 ± 0.06, P < 0.05), and platelet (16.4 ± 2.3, vs. 6.0 ± 0.5, P < 0.001) counts in comparison to normobaric normoxia. Vascular reactivity was suppressed by exercise (-53% vs. sham, P < 0.05) and exercise+CO 2 (-71% vs. sham, P < 0.05). However, neither exercise nor intermittent hypercapnia altered HH-induced changes in lung wet/dry weight, BAL protein and cellular infiltration, or pulmonary histology. Conclusion: Exercise training attenuates vascular reactivity to CO 2 in rats but neither exercise training nor chronic intermittent hypercapnia affect HH- induced pulmonary edema. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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