6 Pages

Limnology: Lecture 1 Physical Limnology: Properties of Water


Gain access to the library to view online
Learn more


  • cours magistral - matière potentielle : 7 vii
  • cours magistral
  • cours magistral - matière potentielle : 7 vi
  • cours magistral - matière potentielle : 7 iii
  • cours magistral - matière potentielle : 7 iv
  • cours magistral - matière potentielle : 7 ii
Limnology: Lecture 7 Aquatic Ecosystems Limnology: Lecture 7
  • ecosystem metabolism a.
  • co2 sink
  • o2 source
  • dry weight
  • lake
  • co2
  • zone
  • respiration
  • o2
  • system



Published by
Reads 33
Language English
Hypoxia Decreases Exhaled Nitric Oxide in Mountaineers Susceptible to High-Altitude Pulmonary Edema
THILO BUSCH, PETER BÄRTSCH, DIRK PAPPERT, EKKEHARD GRÜNIG, WULF HILDEBRANDT, HUBERT ELSER, KONRAD J. FALKE, and ERIK R. SWENSON Department of Anesthesiology and Intensive Care Medicine, Charité, Campus Virchow-Klinikum, Humboldt-University, Berlin, Germany; and Departments of Sports Medicine, Cardiology, and Nuclear Medicine, Ruprecht-Karls-University, Heidelberg, Germany
An exaggerated hypoxic pulmonary vasoconstriction is essential for development of high-altitude pulmonary edema (HAPE). We hypothesized that susceptibility to HAPE may be related to de-creased production of nitric oxide (NO), an endogenous modula-tor of pulmonary vascular resistance, and that a decrease in ex-haled NO could be detected during hypoxic exposure. Therefore, we investigated respiratory tract NO excretion by chemilumines-cence and pulmonary artery systolic pressure (Ppa,s) by echocar-diography in nine HAPE-susceptible mountaineers and nine HAPE-resistant control subjects during normoxia and acute hypoxia (fraction of inspired oxygen [FIO]50.12). The subjects performed 2 oral breathing. Nasally excreted NO was separated from respira-tory gas by suction via a nasal mask. In HAPE-susceptible subjects, NO excretion in expired gas significantly decreased (p,0.05) during hypoxia of 2 h in comparison with normoxia (2864 versus 2162 nl/min, mean6SEM). In contrast, the NO excretion rate of control subjects remained unchanged (3166 versus 3366 nl/ min, NS). Nasal NO excretion did not differ significantly between groups during normoxia (HAPE-susceptible group, 183616 nl/ min; control subjects, 297655 nl/min, NS) and was not influ-enced by hypoxia. The changes in Ppa,s with hypoxia correlated with the percent changes in lower respiratory tract NO excretion (R520.49, p50.04). Our data provide the first evidence of de-creased pulmonary NO production in HAPE-susceptible subjects during acute hypoxia that may contribute among other factors to their enhanced hypoxic pulmonary vascular response.
High–altitude pulmonary edema (HAPE) (1, 2) is a form of noncardiogenic pulmonary edema that develops in approxi-mately 10% of randomly selected mountaineers within 24 h after rapid ascent to altitudes above 4,000 m (3). An even higher incidence rate of about 60% has been demonstrated in subjects who are susceptible to HAPE as documented by pre-vious occurrence of the disease (3). HAPE can be effectively prevented by prophylactic use of nifedipine (4) or slow ascent. Nevertheless, it remains the most common cause of death re-lated to high-altitude exposure during trekking or mountain-eering (5). The mortality rate in Himalayan mountaineers was estimated to be 50% if immediate treatment with supplemen-tal oxygen or rapid descent was impossible (6). Although knowledge of the factors influencing the devel-opment of HAPE is still incomplete, there is experimental evidence that an exaggerated hypoxic pulmonary vasocon-striction (HPV) plays an important role. An excessive rise in
(Received in original form January 31, 2000 and in revised form June 20, 2000) Presented in part at the ERS Annual Congress, Geneva, Switzerland, September 19–23, 1998. Supported by Deutsche Forschungsgemeinschaft (DFG Fa139/4-3). Correspondence and requests for reprints should be addressed to T. Busch, Ph.D., Klinik für Anaesthesiologie und Operative Intensivmedizin, Charité, Campus Vir-chow-Klinikum, Humboldt-Universität zu Berlin, Augustenburger Platz 1, D-13353 Berlin, Germany. Am J Respir Crit Care MedVol 163. pp 368–373, 2001 Internet address: www.atsjournals.org
pulmonary artery pressure has been demonstrated by invasive (7, 8) and noninvasive (4, 9) measurements at high altitude in individuals with HAPE. This rise precedes edema formation (4). Subjects who are susceptible to the disease demonstrate an increased pulmonary vascular response even during a brief hypoxia exposure at low altitude (8, 10, 11). The underlying pathophysiological mechanism for this exaggerated HPV is still unknown. There is, however, evidence that the endoge-nous vasodilator nitric oxide (NO) (12, 13) modulates hypoxic vascular reactivity. Thus, in healthy human volunteers, admin-G istration of the NO synthase antagonistN-monomethyl-L-arginine (L-NMMA) during hypoxia increases pulmonary ar-tery pressure and vascular resistance (14). Furthermore, it has been demonstrated that the exogenous administration of 40 ppm NO in hypoxic subjects prone to HAPE evokes a de-crease in pulmonary artery pressure three times larger than the decrease in HAPE-resistant subjects (9). These findings suggest that reduced endogenous NO synthesis in HAPE-sus-ceptible individuals may contribute to their heightened hy-poxic pulmonary vascular response. NO is produced endogenously within the upper and lower respiratory tract and can be measured in exhaled gas by chemi-luminescence analysis (15). We hypothesized that HAPE sus-ceptibility may be related to a decreased release of NO in the respiratory tract. To test this hypothesis, we measured NO ex-cretion in exhaled gas together with pulmonary artery pres-sure in normoxia and during acute hypoxia of 4 h in HAPE-susceptible and in HAPE-resistant mountaineers.
METHODS Study Population With written informed consent, we investigated 18 healthy male mountaineers, whose susceptibility or resistance toward HAPE was known from previous studies at an altitude of 4,559 m (3, 4, 9). All volunteers were nonsmoking natives of low altitude, free of airway in-fections, and receiving no medication. Cardiac and pulmonary dis-eases were ruled out by clinical examination and blood gas analysis. None of the subjects had resided above 2,000 m within the last 2 wk before the measurements, which were carried out in Heidelberg, Ger-many, at an altitude of 100 m above sea level. The group of HAPE-susceptible individuals consisted of nine mountaineers (mean age, 456 3 yr; weight, 7963 kg, height, 17261 cm) who had developed at least one case of radiographically documented pulmonary edema at an altitude of 4,559 m within the last 4 yr. Nine mountaineers (mean age, 3764 yr; weight, 8163 kg; height 18163 cm) who did not de-velop pulmonary edema during repeated exposure at the same alti-tude were included in the control group. The study was carried out ac-cording to the principles of the Helsinki Declaration of 1983, and approved by the Ethics Committee of the University of Heidelberg.
General Procedures The subjects were investigated in the supine position while breathing synthetic gas mixtures consisting of 21 or 12% oxygen mixed in N2. The hypoxic gas mixture corresponded to an altitude exposure of 4,500 m. Inhalation was performed via a loose-fitting face mask except for the time of NO measurements, which required oral breathing via a