Objective: To evaluate the clinical therapeutic effects of furosemide and captopril on High
altitude pulmonary edema( HAPE ). Methods 10 patients with HAPE underwent Swan-Ganz
catheter and the parameters of hemodynamics were measured before and after administration of
furosemide and captopril. The state of HAPE was assessed according to the Lake Louise acute
mountain sickness scoring system. Results: After furosemide administration, mPAP and the Lake
Louise scores of HAPE decreased significantly. Blood pressure, heart rate and cardiac output
were not changed significantly after furosemide administration. Although captopril could also
decrease the mPAP of HAPE, the change was not significant. MSAP of HAPE decreased
significantly compared to before administration. Conclusion: Furosemide may improve the
clinical symptoms of patients with HAPE. It also can selectively decrease the pulmonary
hypertension in HAPE without causing systemic vasodilation.
142.
THE ROLE OF THE AUTONOMIC NERVOUS SYSTEM IN CARDIOVASCULAR
RESPONSES TO HYPOXIA. Chun Liu
1
, George Balanos
1
, Keith Dorrington
1
, Peter Robbins
1
.
University Laboratory of Phsyiology, Oxford University
1
.
This study aims to clarify the contribution of the autonomic nervous system to the
cardiovascular responses to acute systemic hypoxia. Cardiac output (CO), heart rate (HR), mean
blood pressure (MBP) and middle cerebral arterial blood flow (MCAF) responses to 10 min
euoxia, then 20 min isocapnic hypoxia followed by 10 min euoxia, and the corresponding control
(40 min euoxia) were compared in four protocols: (1) voluntarily controlled constant ventilation
(VE) in the presence of placebo; (2) spontaneous breathing in the presence of placebo; (3)
voluntarily controlled constant VE in the presence of cholinergic- and b-adrenergic receptor
blockade; (4) spontaneous breathing in the presence of cholinergic- and b-adrenergic receptor
blockade. Heart rate, CO and MCAF significantly increased in response to isocapnic hypoxia
without cholinergic- and b-adrenergic receptor blockade (p<0.01, p<0.05 and p<0.05 vs. euoxia,
respectively). Cholinergic- and b-adrenergic receptor blockade increased HR and CO, but not
MCAF in euoxia (p<0.01, p<0.05 and p0.05 vs. placebo, respectively), and they abolished the
increases in HR and CO, but not the increase in MCAF in response to hypoxia (p0.05, p0.05 and
p<0.05 vs. euoxia, respectively). Hypoxia caused no change in MBP, with or without cholinergic-
and b-adrenergic receptor blockade. Maintenance of constant VE had no effect on these
responses. We conclude that via cholinergic-receptors and/or b-adrenergic receptors, the
autonomic nervous system contributes substantially to the regulation of cardiac responses to
hypoxia, but participates less in the regulation of the cerebral and peripheral circulatory responses
to hypoxia.
143.
MATERNAL AND FETAL RESPONSES TO CHRONIC HYPOXIA. Lawrence Longo
1
. Center
for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, California
1
.
Background. For the pregnant woman at high altitude, in an attempt to maintain homeostasis,
acclimatization involves major alterations in the function of various organ systems of both mother
and fetus. Although responses to chronic hypoxia are of great importance, little is known of the
cellular and subcellular mechanisms by which these occur. Results. In the pregnant woman,
chronic hypoxia is associated with, among other things, increased ventilation, arterial oxygen
saturation, and significant changes in uterine artery function and uteroplacental blood flow. For
the fetus, in addition to growth restriction, are marked alterations in cardiac function and
myocardial calcium handling mechanisms. Importantly, the responses of the cerebrovasculature
and their signal transduction mechanisms are significantly modified in terms of both Ca2+ -
dependent and Ca2+ -independent pathways. Conclusions. These results highlight important
changes in the heart and cerebrovasculature in response to chronic hypoxia. They also emphasize
the subtle nature of altered signal transduction mechanisms in these tissues. In addition, they
underscore the significant differences in these responses between mother and fetus. They also
point out possible mechanisms that underlie problems such as acute mountain sickness, high
altitude cerebral edema, and related conditions. Finally, these results underscore the need for
