systolic pressure are both correlated whether not % hemoglobin saturation. We can conclude with
this results that the test in the hypobaric chamber is more demanding as subjective and
physiological aspects that the test in the natural condition.
218.
THE TREATMENT AND MONITORING FOR ACUTE HIGH ALTITUDE PULMONARY
EDEMA. Ma Si-Qing
1
, Zhang Hai-Ming
1
, Yang Zheng-Ping
1
. Intensive Care Unit, Qinghai
Provincial People's Hospital, Qinghai, China
1
.
To investigate the changes of hemodynamics of high altitude pulmonary
edema_HAPE_and its relation with HAPE. Methods: 8 cases of HAPE came from an altitude
of 4000m and were monitored by Swan-Ganz catheter and thermodilution at moderate altitude
(2800m). Results: The mean pulmonary artery pressure (mPAP), right atrial pressure (RAP),
pulmonary vascular resistance index (PVRI), right ventricular stroke work index (RVSWI) and
pulmonary artery wedge pressure (PAWP) were higher on the 1st day, but were decreased on the
4th day (41.63±3.02 & 18.05±2.88 mmHg; 13.85±1.51 & 6.87±0.99 mmHg; 496.50±100.22 &
262.65±17.23; 22.17±1.51 & 11.21±1.89 P<0.01; 14.00±4.21 & 8.88±2.23 mmHg, P<0.05,
respectively). The stroke volume index (SVI), left ventricular stroke index (LVSWI), total
peripheral vascular index (SVRI) and cardiac index (CI) were lower in the 1st day, however,
there was an increase of the SVI, LVSWI, SVRI and CI by the 4th day (38.05±0.36 &
47.73±0.55; 50.18±6.78 & 61.03±7.81; 1652.25±424.89 & 1749.25±358.93 P<0.01; 4.20±0.38 &
4.28±0.42 P<0.05, respectively). Conclusions: There were obvious disorders of hemodynamics
during the acute high altitude pulmonary edema, all of these causing severe hypoxia and
pulmonary artery hypertension (HAPH). This suggests, therefore, that emergent transfer from
high altitude to moderate altitude (<3000 m) followed by immediate ventilator support so as to
increase PaO2 and ameliorate HAPH were the key to effective treatment.
219.
BRAIN-DERIVED ERYTHROPOIETIN IMPROVES THE HYPOXIC VENTILATORY
RESPONSE OF TRANSGENIC MICE IN A GENDER-SPECIFIC MANNER. Jorge Soliz
1
, Max
Gassmann
1
. University of Zurich
1
.
Although normally expressed by glial and neuronal cells, no physiological functions of this
brain-derived erythropoietin (Epo) have been described so far. Here, we describe the expression
of Epo receptor in central breathing control areas as well as the noradrenergic neurons in the
brainstem. Using a transgenic mouse line (termed tg21) that overexpresses human Epo in brain,
we investigated the role of brain-derived Epo in the modulation of respiratory responses to
hypoxia. First, we discovered that in contrast to wild type (wt) animals, tg21 showed a dramatic
increase of the hypoxic ventilatory response (HVR) at 6% O2, and an inverted ventilatory pattern
(higher tidal volume, lower respiratory rate) in hypercapnia (5% CO2). Second, we found a
marked sexual dimorphism and differences between tg21 and wt lines in tyrosine hydroxylase
(TH) activity in vivo and endogenous levels of norepinephrine in brainstem noradrenergic cell
groups (A1C1, A2C2, A5). Third, we observed that after sustained hypoxia (10% O2 for 72
hours), HVR was significantly improved in transgenic males, but dramatically reduced in
transgenic females compared to corresponding wt controls. These results suggest that brain-
derived Epo improves the HVR to severe acute hypoxia and plays a crucial sexual dimorphic role
in the acclimatization process to chronic hypoxia. At least part of these findings can be explained
via Epo-mediated modulation of central catecholamines. Taken together our data implies that
Epo, which is physiologically expressed in mammalian brain including humans, participates on
the systemic control of oxygen homeostasis and could have important participation in high
altitude disorders.
220.
CORRELATION OF URINE, BLOOD OSMOTIC PRESSURE, URINE AND BLOOD
OSMOTIC RATIO AND INDICATIORS OF HEMORHEOLOGY AT DIFFERRENT
