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Ventilation and arterial acid-base status at rest and during steady-state work at P i O 2 100, 145 and 250 mm Hg, were studied in: (1) lowlanders at sea level and after 4, 21 and 45 days sojourn at 3100 m altitude; (2) lowlanders residing for 2–15 years at 3100 m; and (3) native altitude residents. The total ventilatory changes at rest and work in the sojourner between ambient conditions at 250 and 3100 m altitudes were attributed: (a) to (acute) hypoxia alone, particularly during moderate to severe exercise; and (b) to the secondary effects of altitude sojourn which accounted for most of the final levels of hyperventilation achieved under all conditions of rest and work, and were complete after 4 days sojourn. Because of: (a) the absence of a significant respiratory alkalosis in response to acute hypoxia at rest, and (b) the normal ventilatory acclimatization to altitude in a lowlander subject who was non-responsive to hypercapnic-hypoxic stimuli combinations, it was reasoned that current theories based on a restoration of CSF [H + ] were not sufficient to explain the hyperventilation obtained upon sojourn to 3100 m. In residents of 3100 m: (a) Exercise e was significantly lower, Pa CO 2 higher (PIo2100), and the Δe with removal of hypoxemia less than in the sojourner at 3100 m, but similar to the sojourner's results obtained during acute hypoxic exposure at sea-level; and (b) native residents and resident low-landers were similar in all respects. Sojourner-resident differences in hypoxic exercise hyperpnea at 3100 m were attributed primarily to the acquired hyper-responsiveness in the sojourner and to a lesser extent to some degree of subnormal ventilatory chemosensitivity in the resident.

There are two conventional approaches available for the investigation of placental transfer. The first is to derive a mathematical model of the placenta. On the basis of this model, the response of the placenta to a change can be predicted. The second method is to perform experiments on living animals, and observe the response of the animal to a change. Sometimes the two methods are compatible and sometimes they are not. Where there is disagreement, it is often due to the complex nature of the animal response. The response that was predicted from the mathematical model may exist, the the ability of the investigator to observe this response will be hindered by compensatory reflexes which mask the predicted response.

After major thoracic surgery it is important to provide efficient analgesia without the hazard of respiratory despression. In 1952 Fromherz and Pellmont1suggested, on the basis of animal experiments, that there may exist a ratio at which the respiratory depression induced by levorphan tartrate (Levo-Dromoran Tartrate)* could be counteracted by levallorphan tartrate (Lorfan Tartrate)† without significant loss of analgesia. Support for this theory was provided by Gross and Hamilton.2In normal human volunteers they found that on simultaneous administration less levallorphan tartrate was required to prevent respiratory depression than was necessary to affect the analgesia produced by levorphan tartrate. Cullen and Santos3reported favorably on a combination of 10 parts of levorphan tartrate and 1 part of levallorphan tartrate in patients with chronic pain. The present study represents an attempt to evaluate this combination in patients after major thoracic surgery. The aim of the study was to

Excerpt Frequent exposure to moldy organic dusts may result in serious acute or chronic lung disease. The characteristic syndrome seen in more than 80 farmers exposed to a variety of moldy forages ...