Progressive body weight loss occurs during high mountain expeditions, but whether it is due to hypoxia, inadequate diet, malabsorption, or the multiple stresses of the harsh environment is unknown. To determine whether hypoxia due to decompression causes weight loss, six men, provided with a palatable ad libitum diet, were studied during progressive decompression to 240 Torr over 40 days in a hypobaric chamber where hypoxia was the major environmental variable. Caloric intake decreased 43.0% from 3,136 to 1,789 kcal/day (P less than 0.001). The percent carbohydrate in the diet decreased from 62.1 to 53.2% (P less than 0.001). Over the 40 days of the study the subjects lost 7.4 +/- 2.2 (SD) kg and 1.6% (2.5 kg) of the total body weight as fat. Computerized tomographic scans indicated that most of the weight loss was derived from fat-free weight. The data indicated that prolonged exposure to the increasing hypoxia was associated with a reduction in carbohydrate preference and body weight despite access to ample varieties and quantities of food. This study suggested that hypoxia can be sufficient cause for the weight loss and decreased food consumption reported by mountain expeditions at high altitude.
Alterations in skeletal muscle structure were investigated in 6 male subjects who underwent 40 days of progressive decompression in a hypobaric chamber simulating an ascent to the summit of Mount Everest. Needle biopsies were obtained from vastus lateralis of 5 subjects before and immediately after confinement in the chamber, and were examined for various structural and ultrastructural parameters. In addition, total muscle area was calculated in 6 subjects from CT scans of the thighs and upper arms. Muscle area at these sites was found to decrease significantly (by 13 and 15%) as a result of the hypobaric confinement. This was substantiated by significant (25%) decreases in cross sectional fibre areas of the Type I fibres and 26% decreases (non significant) in Type II fibre area. Capillary to fibre ratios remained unchanged following hypoxia as did capillary density although there was a trend (non significant) towards an increase in capillary density. There were no significant increases in mitochondrial volume density or other morphometric parameters. These data indicate that chronic, severe hypoxia on its own does not result in an increase in absolute muscle capillary number or a de novo synthesis of mitochondria. The trends toward an increase in capillary density and mitochondrial volume density were interpreted as being secondary occurrences in response to the pronounced muscle atrophy which occurred.
SummaryThe diagnosis of suspected venous thromboembolic disease during pregnancy is problematic because of the fear of fetal irradiation with routine diagnostic procedures. In order to develop rational guidelines, we have calculated levels of radiation exposure to the fetus for the common diagnostic procedures and conducted a literature review to examine the fetal risks associated with these levels of radiation. A small increase in the relative risk of childhood cancer is suggested by a literature review of outcomes following low dose (less than 5 rads), in utero radiation exposure. With careful use of the available procedures, a diagnosis of venous thrombosis is possible with fetal radiation exposure of less than 0.50 rads and a diagnosis of pulmonary embolism is possible with fetal radiation exposure of less than 0.05 rads. The risk of such exposure is small, both in relative and absolute terms.
In patients with severe LV dysfunction, the amount of scar was a significant independent predictor of LV function recovery after revascularization. A combination of PET and clinical parameters predicts the degree of recovery. This model is being applied in a large randomized controlled trial to determine the effectiveness of therapy guided by FDG PET.
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