An Interactive Annotated World Bibliography of Printed and Digital Works in the History of Medicine and the Life Sciences from Circa 2000 BCE to 2022 by Fielding H. Garrison (1870-1935), Leslie T. Morton (1907-2004), and Jeremy M. Norman (1945- ) Traditionally Known as “Garrison-Morton”

15871 entries, 13811 authors and 1928 subjects. Updated: March 19, 2023

HOUSTON, Charles Snead

2 entries
  • 12996

Acute pulmonary edema of high altitude.

New Eng. J. Med., 263, 478-480, 1960.

Houston described four individuals who developed "edema of the lungs" as a result of high elevation activities. "He described chest X-rays with edema and non-specific changes on EKG. Even though these cases had been termed high altitude pneumonia in the past, Houston indicated that these cases were 'acute pulmonary edema without heart disease' " (Wikipedia article on High-altitude pulmonary edema, accessed 6-2020).

Subjects: Altitude or Undersea Physiology & Medicine
  • 12997

Operation Everest II: Man at extreme altitude.

J. Appl. Physiol., 63, 877-882, 1987.

In 1985 Houston, Sutton and Cymerman and colleagues in Canada used a decompression chamber to simulate a seven week ascent of Mt. Everest. This appears to be their first paper summarizing the overall results. Many publications were issued from the research done in this pioneering study. The first extensive collective report appears to be Houston, Cymerman, Sutton, Operation Everest II: Biomedical studies during a simulated ascent of Mt. Everest. Natick, MA: US Army Research Institute of Environmental Medicine, 1991.

"In October 1985, 25 years ago, 8 subjects and 27 investigators met at the United States Army Research Institute for Environmental Medicine (USARIEM) altitude chambers in Natick, Massachusetts, to study human responses to a simulated 40-day ascent of Mt. Everest, termed Operation Everest II (OE II). Led by Charlie Houston, John Sutton, and Allen Cymerman, these investigators conducted a large number of investigations across several organ systems as the subjects were gradually decompressed over 40 days to the Everest summit equivalent. There the subjects reached a equation M1 of 15.3 mL/kg/min (28% of initial sea-level values) at 100 W and arterial Po2 and Pco2 of ∼28 and ∼10 mm Hg, respectively. Cardiac function resisted hypoxia, but the lungs could not: ventilation–perfusion inequality and O2 diffusion limitation reduced arterial oxygenation considerably. Pulmonary vascular resistance was increased, was not reversible after short-term hyperoxia, but was reduced during exercise. Skeletal muscle atrophy occurred, but muscle structure and function were otherwise remarkably unaffected. Neurological deficits (cognition and memory) persisted after return to sea level, more so in those with high hypoxic ventilatory responsiveness, with motor function essentially spared. Nine percent body weight loss (despite an unrestricted diet) was mainly (67%) from muscle and exceeded the 2% predicted from energy intake–expenditure balance. Some immunological and lipid metabolic changes occurred, of uncertain mechanism or significance. OE II was unique in the diversity and complexity of studies carried out on a single, courageous cohort of subjects. These studies could never have been carried out in the field, and thus complement studies such as the American Medical Research Expedition to Everest (AMREE) that, although more limited in scope, serve as benchmarks and reality checks for chamber studies like OE II" (Peter D. Wagner, "Operation Everest II," High. Alt. Med. Biol., 11 (2010) 111-119).

Subjects: Altitude or Undersea Physiology & Medicine