It has been known for a long time that under some conditions of the establishment of
adaptation mechanisms to a special stressor could induce non-special adaptation to other
stressors, which was considered a cross-adaptation. It is confirmed that the hypoxia-adaptation
could be induced by other stressor-adaptation, but its mechanism remains unclear. HSP70 is a
famous stress protein and works abundantly in cellular stress response process. In the present
study we established the animal model of hypoxia-restraint cross adaptation and the improvement
of cardiovascular function as the important physiological marker of the cross-adaptation. Either in
plasma or in cardiomyocytes of the hypoxia-restraint cross-adaptive rats there was a significant
elevation of HSP70 level, which was promoted by the stress, induced activation of corticosterone-
ERK-HSF pathway and correlated with the improvement of cardiovascular function. It is noticed
that mitochondria did critical work in mediating stress induced death signal transduction pathway
in cardiomyocytes. Further research found the elevation of HSP70 protected the mitochondria
from stress injury. HSP70 not only inhibited opening of mitochondria membrane permeability
transition pore (MPTP), which in turn decreased the release of cytochrome C and the activation of
caspase cascade, but also inhibited the FAS expression on cardiomyocyte membrane and blocked
the FAS-Caspase-8- mitochondria pathway. HSP70 therefore decreased the cardiomyocyte
apoptosis and necrosis induced by hypoxia and protected the cardiovascular function in hypoxia
body. As a result, the mechanism of cross-adaptation was established. Transfected anti-hsp70
ad.virus to cardiomyocyte decreased the preconditioning induced increase of HSP70 synthesis,
the physiological effects of cross-adaptation on stressed cardiomyocyte reduced or disappeared.
These results indicated that HSP70 play an important role in cross-adaptation mechanism. And it
is suggested that HSP70 might be as a molecular marker to evaluate the cross-adaptation and also
as an important drug-aim protein for exploring the new therapeutics of hypoxia injury.
140.
MICE BONE MARROW APOPTOSIS IN HIGH ALTITUDE HYPOXIA. Ji Lin-Hua
1
, Jia Nai-
Yong
1
, Li ZHan-Quan
1
. Dept. of Hematology, Qinghai Medical College Hospital, Xining,
Qinghai, P.R. China.
1
.
The pathogenesis of High Altitude Polycythemia (HAPC) is still unclear. Former studies have
mainly concentrated on proliferation. The balance of proliferation and apoptosis maintains body's
normal physical function. The aim of this study was to understand the effects mediated by high
altitude hypoxia on mice bone marrow cells and to master the role of apoptosis in the
pathogenesis of HAPC. Methods Select white pure American NIH race male mice at an altitude
of 1518.3m as control group. Mice living at altitude of 3870.0m for 1day, 4 days, 7 days, 14 days
comprise the four experimental groups. TUNEL apoptotic cell detection and the electro-
microscope methods were used to study the bone marrow cells' apoptosis. The apoptotic cells
index (AI) was calculated. Results: The main cause of death of mice bone marrow cells under the
high altitude hypoxia state was apoptosis which was investigated by the electro-microscope
method. With the elevation of altitude and the increase in duration of living at high altitude, the
AI of mice bone marrow cells increased at the early phase and perhaps decreased slowly at the
later period. The AI was 4.90% in Control group, 5.67%, 11.81%, 20.38% and 13.88%
respectively groups for living at altitude of 3870.0m for 1day, 4 days, 7 days, and 14 days. The
AI showed a positive correlation with the increase of hemoglobin (r=0.75). Conclusion These
results suggest that high altitude hypoxia not only induces cell proliferation, but also effects
apoptosis. Apoptosis is probably a protective compensatory response in order to adapt to the
hypoxic environment. Apoptosis may be related to the mechanism of HAPC.
141.
THERAPEUTIC EFFECTS OF FUROSEMIDE AND CAPTOPRIL ON HIGH ALTITUDE
PULMONARY EDEMA. Fuyu Liu
1
, Xinbing Mou
2
, Yuqi Gao
1
, GAnglin Ye
2
, Xiaobo Zhou
2
,
Guanglin Cheng
2
. Department of Pathophysiology and High Altitude Physiology, Third Military
Medical University, Chong
1
, High Altitude Medical Research Center, The Military General
Hospital of Tibet, Tibet, China
2
.
