The pathogenesis of high-altitude pulmonary oedema (HAPE) is disputed. Recent reports show a strong correlation between the occurrence of HAPE and pulmonary artery pressure, and it is known that the oedema is of the high-permeability type. We have, therefore, proposed that HAPE is caused by ultrastructural damage to pulmonary capillaries as a result of stress failure of their walls. However, no satisfactory electron microscopy studies are available in patients with HAPE, and animal models are difficult to find. Madison strain Sprague-Dawley rats show a brisk pulmonary pressure response to acute hypoxia and are susceptible to HAPE. We exposed 13 Madison rats to a pressure of 294 torr for up to 12.5 h, or 4 rats to 236 torr for up to 8 h. Pulmonary arterial or right ventricular systolic pressures measured with a catheter increased from 30.5 +/- 0.5 (SEM) in controls (n = 4) to 48 +/- 2 torr (n = 11). The lungs were fixed for electron microscopy with intravascular glutaraldehyde. Frothy bloodstained fluid was seen in the trachea of three animals. Ultrastructural examination showed evidence of stress failure of pulmonary capillaries, including disruption of the capillary endothelial layer, or all layers of the wall, swelling of the alveolar epithelial layer, red blood cells (RBCs) and oedematous fluid in the alveolar wall interstitium, proteinaceous fluid and RBCs in the alveolar spaces, and fluid-filled protrusions of the endothelium into the capillary lumen.(ABSTRACT TRUNCATED AT 250 WORDS)

The blood-gas barrier needs to be extremely thin for gas exchange, but also immensely strong because the capillary wall stresses become very high during exercise. Failure of the barrier causes high-permeability pulmonary edema or hemorrhage. Avoiding stress failure poses a challenging problem for some animals.

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The Challenger disaster focused attention on the hazards as well as the possibilities of man in space. The physiological effects of prolonged weightlessness include important changes in vestibular, bone, muscle, cardiovascular, blood, renal, and pulmonary function. Much has been learned from US and Soviet experiments, but large areas of ignorance remain. Exceptional opportunities for physiological research are provided by Spacelab, a pressurized laboratory planned as a payload of the Space Shuttle.

The ascent of Mount Everest (altitude 8,848 m) by two climbers without supplementary oxygen in 1978 was a feat that astonished many physiologists;indeed, measurements of maximal oxygen uptake at lower altitudes suggested that it would be impossible. Data obtained in 1981 at extreme altitudes, including the summit itself, showed that man can tolerate the extreme hypoxia only by an enormous increase in ventilation. Even so, the arterial PO2 is apparently less that 30 Torr and maximal oxygen intake only about one liter per minute. Under these conditions man is at the utmost limit of tolerance to hypoxia, and even day-by-day variations of barometric pressure probably affect performance.