A NEW MODEL OF PULMONARY O2 TRANSFER 
The quantitative understanding of
O2 uptake in the lungs has
progressed greatly over the past 40 years owing to a fruitful interplay
between experimental and theoretical analyses. Frank et al. (p. 2036)
present a theoretical advance in their report of a two-dimensional
finite-element model of O2 uptake
by equally spaced red blood cells in pulmonary capillaries, designed to
represent the sheet flow characteristics of the pulmonary
microcirculation. The results of the model provide insight about the
importance of the hematocrit and the unimportance of the plasma protein
concentration in determining the membrane and erythrocytic components
of the pulmonary diffusing capacity. The paper is discussed in an
Invited Editorial by Popel (p. 1717).
HEAD POSITION AND CARDIOVASCULAR CONTROL
The role of the otolith receptors and neck mechanoreceptors in the
control of the cardiovascular system is unclear. Normand et al. (p.
1734) examined this problem in human subjects, measuring blood flow in
the calf and forearm and arterial pressure and heart rate under resting
conditions in two body positions (lying prone and on one side) and
three neck positions (reference, flexion, and extension). The results
show a complex dependency of cardiovascular variables on neck position,
with different responses in the two body positions. The authors
conclude that both otolith receptors and neck mechanoreceptors are
involved in cardiovascular control.
CARDIOPULMONARY BYPASS ALTERS ENDOTHELIAL FUNCTION
The pulmonary vascular bed becomes hyperreactive to vasoconstrictor
agents after cardiopulmonary bypass (CPB). Zanaboni and colleagues (p.
1776) investigated the effects of CPB on endothelium-dependent pulmonary vasodilator processes in conscious dogs. Continuous left
pulmonary vascular pressure-flow plots were constructed, and responses
to acetylcholine, bradykinin, and sodium nitroprusside were evaluated
before and after CPB. The vasodilator response to acetylcholine was
attenuated after CPB, whereas the responses to bradykinin and sodium
nitroprusside were unchanged. The authors conclude that CPB causes a
selective defect in endothelial function in the pulmonary
vasculature.
AEROBIC CAPACITY IN AGING ATHLETES
Åstrand and associates (p. 1844) report an unusual set of
data: measurements of peak O2
uptake and related variables in male and female athletes studied first
in their twenties and then repeated 21 and 33 yr later. Peak aerobic
power decreased significantly during the 21 yr after the initial
measurements but was not further reduced over the next 12 yr. Peak
heart rate during exercise diminished with age, reflecting the reduced
peak O2 uptake: the average heart rate at an O2 uptake of 1.5 l/min
was the same at all ages.
TRANSIENT RESPONSES TO EXERCISE AFTER HEART TRANSPLANT
Heart transplant recipients (HTR) are often capable of moderate
exercise after transplantation, but the metabolic and circulatory transients at the onset and cessation of exercise are altered by the
surgical denervation of the heart. Grassi et al. (p. 1952) measured
transient responses to several exercise protocols in HTR and control
subjects. The half time of on- and off-kinetics of
O2 consumption,
CO2 production, ventilation, and
cardiac output were all longer in HTR than in the controls. At the
onset of a second bout of exercise, 5 min after cessation of a first
bout, HTR showed shorter half times for cardiac output but no change in
half times for the other variables, compared with the initial onset of
exercise. The authors suggest that this "priming effect" of the
initial bout on the circulatory response to the second bout may reflect
higher heart rate and catecholamine levels resulting from the initial
exercise period. The lack of a priming effect on
O2 consumption half time suggests
that this variable depends more on the kinetic responses of metabolic
processes in muscle than on the circulatory delivery of
O2.
AUTOTRANSFUSION BY SPLENIC CONTRACTION IN SEALS
Diving mammals such as seals share a need for activity-augmented
O2 supply with terrestrial
athletes such as the horse and dog. In both, the spleen acts as a
reservoir of red blood cells that can rapidly augment circulating blood
volume and systemic hematocrit. This has obvious potential for
enhancing tissue O2 supply.
Because diving mammals must hold their breath, the question arises as
to the control mechanisms and blood volume- and hematocrit-enhancing potential of their spleens for increasing
O2 supply and thus prolonging diving time. The report of Cabanac et al. (p. 1989) shows that blood
volume in seals can be enhanced 13% by splenic contraction, which is
controlled by 
-adrenergic stimulation (as in the horse). Although
the hematocrit of this blood is >85%, diving time would be extended
by only ~1.5 min if all of the
O2 stored in splenic red blood
cells were consumed.
NEONATAL LUNG INJURY INDUCED BY ANTIBODY TO SURFACTANT PROTEIN B
Without surfactant protein B (SP-B), lamellar bodies are not converted
into tubular myelin, and pulmonary surfactant malfunctions. When
Grossmann et al. (p. 2003) exposed the lungs of neonatal rabbits to a
monoclonal antibody to SP-B, respiratory system compliance fell to a
level comparable to that of surfactant-deficient newborns. Changes in
the lungs included alveolar edema or collapse, necrosis, and
desquamation of airway epithelium and the formation of hyaline membranes. Serum proteins and granulocytes appeared in the alveolar air
spaces. The authors suggest that these pathological changes reflect a
combination of direct inactivation of surfactant and an inflammatory
response triggered by the immune reaction.
TRIIODOTHYRONINE ATTENUATES SURFACTANT DAMAGE DURING
SEPSIS
Sepsis both induces hypothyroidism and decreases surfactant function.
The work of Ksenzenko et al. (p. 2020) suggests that the hypothyroidism
may contribute to the changes in surfactant. Sepsis was induced in rats
by cecal ligation and puncture, which led to reductions in dynamic lung
compliance and surfactant adsorbtion. The relative quantities of
different phospholipids in surfactant were changed, and the fatty acid
composition and saturation of most phospholipids were altered.
Treatment of septic rats with triiodothyronine attenuated all these
changes.
WHAT LIMITS THE STABILITY OF MICROBUBBLES?
Understanding the in vivo stability of small gas bubbles is important
for their use as ultrasonic contrast agents and carriers of gas (e.g.,
oxygen) to tissues, as well as for avoiding decompression sickness.
Considering three mechanisms that contribute to microbubble stability,
i.e., liquid surface tension, surfactant effects, and the environmental
pressure, Van Liew and Raychaudhuri (p. 2045) have derived the
theoretical relationship between bubble radius and stability, as
characterized by the net pressure within the bubble. The model allows
identification of the range of radii for stable bubbles as the
parameters of the stabilizing mechanisms change. This work provides a
framework for the selection of conditions to control bubble stability
for specific applications in research and clinical settings.
A NEW MODEL OF PULMONARY O2 TRANSFER
