Journal of Applied Physiology
Vol. 81, No. 4, pp. 1453-1454, October 1996

This Month in the Journal

STRAIN-INDUCED GROWTH OF IMMATURE LUNGS

HYPOXIC VENTILATORY RESPONSES OF LOW-BIRTH-WEIGHT LAMBS

HEAT STRESS ALTERS GLUCOSE KINETICS DURING EXERCISE

INTRINSIC POSITIVE END-EXPIRATORY PRESSURE BY PHARYNGEAL CONSTRICTORS?

EFFECTS OF GAS NARCOSIS ON VENTILATION AND EFFORT PERCEPTION

STIMULATION OF BREATHING BY HYPEROXIA

VOLUNTARY CONTROL OF THE BREATHING PATTERN

BRAIN STEM ACIDOSIS IN HYPOXIA

INTESTINAL PCO₂ IN ISCHEMIA

USE AND ABUSE OF MODEL ATMOSPHERES

STRAIN-INDUCED GROWTH OF IMMATURE LUNGS

Does increasing mechanical strain accelerate the postnatal growth of lungs? Zhang et al. (p. 1471) subjected weanling ferrets to 6 cmH₂O continuous positive airway pressure (CPAP) for 2 wk. Compared with control animals exposed to ambient pressure, CPAP increased total lung capacity (TLC) by 40%. This was associated with an increase in lung weight, total protein, and DNA content. Lung recoil at equal fractions of TLC, determined from deflation air- and saline-filled pressure-volume curves, did not change with CPAP. These responses indicate a remodeling of the lung parenchyma rather than simple lung distension. The paper is discussed in an Invited Editorial by Mansell (p. 1469).

HYPOXIC VENTILATORY RESPONSES OF LOW-BIRTH-WEIGHT LAMBS

In the course of normal postnatal development, neonates of several species substantially increase their ventilatory response to progressive hypoxia. Moss et al. (p. 1555) report that this developmental change is absent in lambs that have normal gestational age but low body weight at birth. This finding is unexplained but provocative in view of the increased risk of the sudden infant death syndrome in low-birth-weight human infants.

HEAT STRESS ALTERS GLUCOSE KINETICS DURING EXERCISE

During exercise in the heat, blood glucose rises more than during similar exercise in a temperate environment. This exaggerated hyperglycemia must reflect, in part, an altered balance between glucose output by the liver and glucose uptake by the exercising muscles. Hargreaves et al. (p. 1594) measured glucose kinetics in normal subjects during exercise in 20 and 40°C environments on different days. Their results indicate that the exaggerated hyperglycemia during exercise in the heat resulted from increased hepatic glucose output, with no significant difference in whole body glucose utilization.

INTRINSIC POSITIVE END-EXPIRATORY PRESSURE BY PHARYNGEAL CONSTRICTORS?

Newborn mammals exhibit active closure of the larynx during expiration, and this is augmented by permeability pulmonary edema. Diaz et al. (p. 1598) hypothesized that such active expiratory glottic closure is associated with activation of pharyngeal constrictor muscles. They tested this hypothesis by recording a variety of respiratory variables, including electromyograms of pharyngeal and laryngeal muscles, in newborn lambs after induction of permeability pulmonary edema by intravenous injection of halothane. This maneuver caused a central apnea associated with tonic and phasic thyroarytenoid and inferior pharyngeal constrictor muscle activity. After resolution of this apnea, expiratory activity appeared in glottic and pharyngeal constrictors for 1.5-5 h, even after correction of hypoxia. The authors speculate that expiratory contraction of the inferior pharyngeal constrictor may promote upper airway closure during expiration, which, in turn, might improve pulmonary gas exchange by increasing end-expiratory lung volume.

EFFECTS OF GAS NARCOSIS ON VENTILATION AND EFFORT PERCEPTION

In studies of ventilatory responses and perceptions during high-pressure dives, it is difficult to distinguish between effects of inert-gas narcosis and those related mechanically to the increase in gas density. Fothergill and Carlson (p. 1652) approached this problem by comparing, in trained divers at sea-level pressure, the effects of breathing a narcotic gas mixture (44% O₂, 23% N₂O, 15% He, balance N₂) with those of breathing a nonnarcotic mixture with closely matched physical properties (44% O₂, balance N₂). Both at rest and during exercise, with and without an inspiratory resistive load, the narcotic gas had little influence on ventilation or the perception of effort. By isolating the effects of narcosis from those of increased gas density, this approach may lead to insight regarding altered perception and performance during dives.

STIMULATION OF BREATHING BY HYPEROXIA

When a normal subject breathes an oxygen-enriched gas mixture at sea level, the ventilatory response reflects a balance of altered stimuli, including hyperoxic inhibition of peripheral chemoreceptors and hypercapnic stimulation of central chemoreceptors via reduced cerebral blood flow and the Haldane effect. Most subjects increase ventilation somewhat, thus adding arterial hypocapnia to the complex balance. Becker et al. (p. 1683) studied the steady-state responses of subjects exposed to 30 and 75% oxygen while end-tidal PCO₂ was held constant. Ventilation increased in a dose-related fashion, but the increase was markedly attenuated when end-tidal PCO₂ was allowed to fall. The authors speculate that the Haldane effect was the major cause of the hyperoxic hyperventilation.

VOLUNTARY CONTROL OF THE BREATHING PATTERN

What are the constraints on sustained voluntary patterns of breathing? Rafferty and Gardner (p. 1744) trained volunteers to modulate the timing and depth of their breathing during hyperoxic hypercapnia. Their subjects were able to sustain altered breathing patterns with increased or decreased inspiratory and expiratory durations, as well as with increased tidal volume; however, no volunteer was able to sustain ventilation with decreased tidal volume. The authors suggest that tidal volume is strongly controlled at a given level of ventilatory drive, whereas respiratory timing is more weakly controlled, permitting variations for speech and other nonmetabolic functions of breathing.

BRAIN STEM ACIDOSIS IN HYPOXIA

In the absence of peripheral chemoreceptors, hypoxia depresses ventilation. LaManna and colleagues (p. 1772) exposed anesthetized vagotomized adult rats to 5 min of 8% in N₂, followed by rapid in situ freezing of the brain stem. Their principal finding was that hypoxia acidified brain stem intracellular pH by 0.2-0.4 unit, especially in deeper structures. There were also decreases in phosphocreatine and ATP. The authors speculate that the hypoxia-induced intracellular acidification modulates respiratory brain stem structures to depress ventilation.

INTESTINAL PCO₂ IN ISCHEMIA

During progressive ischemia, tissue and venous PCO₂ values rise, initially reflecting the widening difference in CO₂ content between arterial and venous blood. Beyond a critical restriction of O₂ delivery, however, O₂ consumption is reduced, and lactic acid reacts with tissue bicarbonate to release CO₂ molecules in excess of those produced by metabolism, thus raising tissue and venous PCO₂ dramatically. Rozenfeld et al. (p. 1834) report detailed studies of this phenomenon in anesthetized dogs with induced intestinal isch-emia. The results are of interest with regard to tissue gas exchange, acid-base balance, and the monitoring of ischemic organs and tissues.

USE AND ABUSE OF MODEL ATMOSPHERES

Life at high altitudes is critically dependent on the ambient PO₂ and thus on the ambient barometric pressure. The extent to which barometric pressure falls with increasing altitude has been accurately measured and modeled by atmospheric scientists, but physiologists have often misused model atmospheres, sometimes making large errors. As reviewed and analyzed by West (p. 1850), the most frequent error has been to use the aviation industry's Standard Atmosphere, which incorporates a particular profile of temperature with altitude, to predict barometric pressure at locations where the temperature profiles are different. When temperature is taken into account by using models for specific latitudes and seasons, barometric pressure at any altitude can be estimated with satisfactory accuracy.