MODELING UPPER AIRWAY FUNCTION

Stability of inspiratory flow through the pharyngeal airway requires an appropriate balance between collapsing forces due to subatmospheric pressure and the stiffness of the airway wall. This stiffness consists of both elastic and neuromuscular components. Neuromuscular stiffening is reflexly enhanced in response to subatmospheric airway pressure, so the system exhibits properties of negative-feedback control, for which Huang and Ffowcs Williams (p. 1759) have developed a mathematical model. Changes in model parameters produce three distinct conditions: unimpeded flow, intermittent obstruction (flutter), and sustained airway closure. The authors suggest that the increased latency and decreased strength of reflex stiffening that occur with sleep contribute to snoring and obstructive sleep apnea. The paper is discussed in an Invited Editorial by Roberts (p. 1757).

	HYPOXIA AND FATIGUE IN SINGLE MUSCLE FIBERS

Does muscle fatigue in hypoxia occur only when intracellular O₂ availability as an electron acceptor becomes limiting? Studies with isolated mitochondria suggest that such limitation occurs only when the PO₂ is very low, i.e., <1 Torr. Stary and Hogan (p. 1812) examined the development of fatigue in individual frog muscle fibers, electrically stimulated at increasing contraction rates. Fatigue developed when extracellular PO₂ was lowered to 30 Torr, a value well above that estimated to result in an anoxic core within the fiber. This result favors the conclusion that hypoxic fatigue reflects an O₂ dependence of muscle performance, even when mitrochondrial respiration is not compromised.

	PREDICTING THE RISK OF DECOMPRESSION SICKNESS

Decompression sickness (DCS) may arise when bubbles of inert gas form during whole body decompression, e.g., following a dive. The risk of DCS in relation to pressure history is empirically predictable from extensive experience with human subjects, but the predictive model cannot be reliably extrapolated to cover all conditions. Ball et al. (p. 1920) have developed a predictive model that uses data from both humans and sheep, with scaling to take the species difference into account. The results provide a practical tool for estimating DCS risk from outcomes in sheep, especially in decompression profiles too risky to test in humans.

	ESTROGEN AND DECREASED BONE FORMATION

Is the decrease in bone formation after estrogen treatment linked to a prior decrease in bone resorption? To test this possibility, Turner et al. (p. 1950) measured the effects of diethylstilbestrol on steady-state mRNA for immediate-response genes, extracellular matrix proteins, and signaling peptides in proximal tibial metaphysis and uterus. The - and -forms of the estrogen receptor were also measured. Treatment resulted in significant increases in message levels for c-fos and c-jun in bone and uterus. Estrogen transiently increased 20-fold insulin-like growth factor I mRNA in uterus and decreased the level in bone by 50%. Proline incorporation into bone matrix fell significantly in 2-3 days. Thus the rapid decrease in insulin-like growth factor I expression, decreases in mRNA levels for bone matrix proteins, and absence of rapid increases in mRNA levels for signaling peptides indicate that estrogen decreases bone formation by a mechanism not requiring prior reduction in bone resorption.

	SURFACTANT ACTIVITY AFTER AROUSAL FROM TORPOR

Torpor in the dunnart Sminthopsis crassicaudata, a small marsupial mammal, alters the lipid composition and surface activity of pulmonary surfactant. Lopatko et al. (p. 1959) studied surfactant from warm-active dunnarts and from animals killed immediately and at intervals after rapid arousal from torpor. Total phospholipid (PL), disaturated PL (DSP), and the PL/DSP ratio remained elevated 60 min after arousal, whereas cholesterol content decreased to warm-active values. In general, 60 min of arousal were insufficient for lipid composition and surface activity to return fully to warm-active levels.

	ALVEOLAR EPITHELIAL DEFORMATION IN RAT LUNGS

Previous studies showing that stretching of epithelial basement membrane (EBM) was minimal at high lung volumes may have been influenced by the lung volume history before fixation. Tschumperlin and Margulies (p. 2026) reexamined this issue using rat lungs fixed by glutaraldehyde perfusion on deflation after three pressure-volume cycles at inflation pressures between 10 and 25 cmH₂O. EBM surface area, computed from images digitized from electron micrographs, increased 5, 16, 12, and 40% above the value at 24% total lung capacity at lung volumes of 42, 60, 82, and 100% total lung capacity, respectively. Thus epithelial cells may be deformed by high inflation pressures, and the EBM may contribute to lung recoil.

	PULMONARY HEMORRHAGE IN EXERCISING HORSES

Exercise-induced pulmonary hemorrhage is a problem in the horse-racing industry and an intriguing pathophysiological puzzle. Furosemide treatment lowers the pulmonary vascular pressure increase that occurs with exercise in horses, and this is thought to decrease the incidence and severity of hemorrhage. Does this outcome reflect reduced blood volume or a redistribution of pulmonary blood flow? Erickson et al. (p. 2034) measured pulmonary flow distribution with fluorescent microspheres in resting and exercising horses with and without furosemide treatment. Furosemide resulted in increased ventral pulmonary blood flow at rest, but this change disappeared during exercise. The authors conclude that any preventive or palliative effect of furosemide on exercise-induced lung hemorrhage does not depend on pulmonary blood flow redistribution.

	BUILT FOR SPEED?

Weyand et al. (p. 2059) measured human running speed in subjects breathing air or a 13% O₂ gas. Hypoxia decreased maximal O₂ uptake by 30%, but did not affect running speed over durations lasting 60 s or less, because O₂ deficit increased to cover the energy cost. The authors conclude that maximal muscle power output is not limited by either anaerobic or aerobic power for burst activities. Based on examples in nature, in which animals that are good sprinters often do not have high aerobic capacities, the authors hypothesize that the design has evolved to minimize the cost of developing and maintaining superfluous cardioventilatory capacity.