PULMONARY CHEMOREFLEX RESPONSES TO INTRAVENOUS LACTIC ACID 
Lee et al. (p. 2349) report experiments in which lactic acid was
injected intravenously in anesthetized rats. Lactic acid injections
elicited apnea, bradycardia, and hypotension
the classic triad of
responses to C-fiber stimulation in the lungsfollowed by a period of
hyperpnea. The apneic and bradycardiac responses were completely
abolished by vagotomy or by perineural capsaicin treatment of the vagi
to block the conduction of C fibers. Carotid body chemoreceptor
denervation attenuated the hyperpneic response. Single-unit recordings
from vagal C fibers showed bursts of activity after lactic acid
injections. The results implicate pulmonary C fibers in the immediate
responses to lactic acid injection and raise questions about possible
responses to endogenous lactic acid. The paper is discussed in an
Invited Editorial by Sant'Ambrogio (p. 2347).
RECRUITMENT PATTERN OF ABDOMINAL MOTOR UNITS
The regulation of the periodic contraction of muscles of the
respiratory pump is essential for proper ventilation. Increases in
muscle contraction can be produced by increasing the firing rate of
motoneurons that are already active, by recruiting inactive motoneurons, or both. Mateika et al. (p. 2428) examined the effects of
chemoreceptor activation on individual motoneurons innervating the
external oblique (expiratory) muscle by recording single motor unit
activities in spontaneously breathing cats. Silent during the first
~30% of expiration, these motor units abruptly began to fire, with
the rate increasing throughout the remainder of the phase. The increase
in ventilation produced by isocapnic hypoxia was supported by increased
firing in motor units active during normoxia as well as by the
recruitment of motor units that were previously silent.
NITRIC OXIDE DECREASES LUNG INJURY AFTER INTESTINAL ISCHEMIA
Injury to a primary organ releases mediators into the blood stream that
may damage other organs. Terada et al. (p. 2456) have shown that
production of nitric oxide (NO) by the lungs protects them from such
secondary injury. When anesthetized rats were subjected to 30 min of
intestinal ischemia followed by 2 h of reperfusion, there was no
increase in lung albumin leak. However, when NO synthesis was
inhibited, then the same intestinal injury induced lung leak. This was
prevented by inhalation of NO. The protective effect of NO appears to
be due to decreased pulmonary neutrophil retention.
A REVISED CONCEPT OF LUNG ARCHITECTURE
The classic view of the structure of the mammalian lung holds that each
branch of the bronchovascular tree lies within a parenchymal cone,
which is, in turn, surrounded by a septum. As the bronchovascular tree
branches to smaller and smaller units, the surrounding cone/septal unit
that encloses it becomes smaller and smaller. Verbeken et al. (p. 2468)
provide evidence that this classic view is incorrect. The authors
reconstructed the total septum system in three dimensions and projected
it onto a corresponding airway tree. The results reveal that branches
of the bronchovascular tree do not lie within the parenchymal cone but,
rather, course in the septum and feed the parenchyma to the side. In
centrilobular emphysema, tortuosities of both intra-acinar and
interlobular septa appear, associated with distortion of
corresponding intraseptal bronchioles.
SURFACTANT INHIBITION BY PLASMA
Surfactant recovered from preterm lambs after surfactant treatment has
been reported to have decreased sensitivity to inhibition by plasma.
Ikegami et al. (p.2517) investigated the inhibition by plasma of
1) endogenous surfactant from
preterm lambs and 2) surfactant from
preterm lambs that had been treated with an organic solvent-extracted
sheep surfactant. Surfactant recovered from 134-day-gestation lambs was
less sensitive to inhibition than surfactant recovered from 121- and
128-day-gestation lambs after surfactant treatment. The authors
interpret the results as indicating that lung maturation influences the
inhibition of surfactant by plasma.
OPIOID-MEDIATED MECHANISMS IN HEAT STROKE
Intraperitoneal heating (IPH) of guinea pigs produces heat stroke
characterized by ear-skin vasoconstriction and post-IPH hypothermia.
Romanovsky and Blatteis (p. 2565) hypothesized that these phenomena
involve endogenous opioid agonists. Unanesthetized lightly restrained
guinea pigs, chronically implanted with intraperitoneal thermodes and
intrahypothalamic thermocouples, received naltrexone before IPH-induced
heat stroke. Naltrexone prevented the hyperthermia-induced vasoconstriction and attenuated the hyperthermia-induced hypothermia, indicating that both phenomena are opioid dependent. The latter response is speculated to reflect opioid-mediated inhibition of metabolism, and the former is thought to result from
opioid-induced hemodynamic changes. Opioid antagonists may have
therapeutic value in heat stroke.
CONTROL OF AMNIOTIC FLUID VOLUME
Amniotic fluid volume is maintained by a balance between fetal fluid
production as lung liquid and urine and fluid removal by fetal
swallowing and intramembranous transport. Mann et al. (p. 2588) induced
sustained antidiuresis in ovine fetuses by intra-amniotic injection of
a specific vasopressin V2-receptor
agonist. Despite the marked reduction in fetal urine flow, amniotic
fluid volume did not change. The results suggest that osmotically
driven intramembranous fluid movement may contribute to amniotic fluid
volume homeostasis.
WINDCHILL REVISITED
Wind increases the risk of frostbite during exposure to subfreezing air
temperatures. This well-known phenomenon was quantified in 1945 by
Siple and Passel, who studied the time required for water in a cylinder
to freeze during exposure to various combinations of airspeed and
temperature and developed a windchill index for predicting the risk of
frostbite. Danielsson (p. 2666) has reexamined this problem by using
modern heat transfer theory and tissue freezing data from the
literature. The results indicate that the windchill index
systematically underestimates the effect of airspeed. The new analysis
shows that there is little risk of finger frostbite at air temperatures
above 
10°C, regardless of airspeed, but that this risk is
very high below 25°C, even in still air.
NONINVASIVE ESTIMATION OF STROKE VOLUME DURING EXERCISE
Although noninvasive techniques have been used to estimate cardiac
output during exercise, they often intrude on the subjects' spontaneous ventilation and gas exchange. Whipp et al. (p. 2674) hypothesized that the exercise stroke volume and, hence, cardiac output
can be accurately estimated by the response pattern of two easily
determined variables, oxygen uptake and heart rate. This prediction was
tested in 23 healthy subjects who underwent a 3-min incremental
exercise test. Arterial and mixed venous oxygen contents were
determined from indwelling catheters. The predicted stroke volume
closely reflected the measured value
(r = 0.80). Thus, in healthy subjects,
exercise stroke volume may be estimated with reasonable accuracy from
measurement of oxygen uptake and heart rate taken over a range of
exercise intensities.
CHEST WALL VOLUME ANALYSIS WITH USE OF A THREEDIMENSIONAL
OPTICAL METHOD
Cala et al. (p. 2680) evaluated an optical reflectance system that
tracks reflective markers with four television cameras as a method of
estimating lung volume during breathing. Hemispherical markers were
arranged circumferentially in seven rows on the chest wall of two
standing subjects. Marker coordinates were computed by grid
calibration, and chest wall surface and volume were calculated. During
tidal breathing, vital capacity maneuvers, and
CO2-stimulated hyperpnea, lung
volumes measured by this method compared favorably with those measured
by spirometry.
PULMONARY CHEMOREFLEX RESPONSES TO INTRAVENOUS LACTIC ACID
