271.
INTERMITTENT HYPOXIA ACTIVATED PROLACTIN RELEASE IN RAT PITUITARY*.
Jian-Fen Xu
1
, Xue-Qun Chen
1
, Ji-Zeng Du
1
. Zhejiang Univ.
1
.
We have previously reported that continual hypoxia (10.8% O2) enhanced prolactin (PRL)
release from rat pituitary into circulation. To understand if intermittent hypoxia could also play an
activated role in pituitary PRL, male adult rats were exposed to a simulated hypobaric hypoxia at
altitude of 2km (16.0% O2) or 5km(10.8% O2), and the immunostaining PRL levels in pituitary
and the levels of PRL in plasma were measured by immunocytochemistry and RIA, respectively.
The immunostaining PRL content in pituitary markedly increased by 2.58% (102.58±0.59%,
P<0.05) and decreased 2.32% (97.68±0.8%, P<0.05), vs. its control during the intermittent
hypoxia 2 km for 1 d and 5d, respectively, and the level of PRL in plasma increased significantly
both for 2 and 5d. Intermittent hypoxia of 5 km for 1-10 d markedly decreased the
immunostaining PRL content in the pituitary( 98.78±0.94%, P<0.05; 97.55±0.93%, P<0.05;
98.36±1.85%, P<0.05) vs. control groups, respectively, and increased PRL level in plasma. The
changes of PRL in pituitary and plasma returned to control level after 15d. Chronic continual
hypoxia 2 km for 2d and 5d significantly reduced immunostaining PRL in the pituitary
(94.92±1.85%, P<0.05; 97.01±1.81%, P<0.05) vs. control group, respectively, while, plasma PRL
levels at 2 km for 1d, 2d and 5 d were significantly increased. Continual hypoxia at 5 km for 1-
25d significantly chronically enhanced plasma PRL. The data suggest that both intermittent and
continual hypoxia chronically enhanced PRL release in pituitary and increased plasma PRL of
rats with a time course and intensity dependent manner of stress hypoxia, suggesting that hypoxia
activated PRL may be one of the mechanisms to support the animal survival through keeping
homeostasis. * This work is supported by the grant from NSFC (Major Project No. 30393134 and
Project No. 30070289; 30270232).
272.
EFFECT OF DEXAMETHASONE ON EXPRESSION OF VASCULAR ENDOTHELIAL
GROWTH FACTOR IN CHRONIC HYPOXIA PULMONARY HYPERTENSION RATS. .
Chen Yan-fan
1
, Chen Shao-xian
1
, Fang Xiao-fang, The First Affiliated Hospital of Wenzhou
Medical College. Wenzhou, China
1
.
To explore the roles of vascular endothelial growth factor (VEGF) in hypoxia pulmonary
hypertension and effects of dexamethasone. Methods: Thirty SD rats were randomly divided into
normol control group (N), hypoxia hypercapnia group(F), hypoxia hypercapnia + dexamethasone
group (D). The level of VEGF in serum and lung tissue are measured by ELISA, the expression
of VEGF,VEGFmRNA were observed by immunohistochemistry and in situ hybirdization, the
ultrastructure of pulmonary arterioles was observed by electron microscopy. Results : Mean
pulmonary arterial pressure(mPAP) weight ratio of RV to LV+Sthe level of VEGF in serum and
lung tissue of group F were significantly higher than that of group N and group D (P <0.01).
Electron microscopy showed proliferation of smooth muscle cells and collagenous fibers of
pulmonary arterioles in rats of group F, and dexamethasone could reverse the changes mentioned
above. Expression of VEGFand VEGFmRNA in pulmonary arterioles were significantly higher
in rats of group F than that of group N_P< 0.01, they were significantly decrease in rats of group
D. Conclusion: Dexamethasone can decrease the pulmonary hypertension.by inhibiting the
expression of VEGF in pulmonary arteria .
273.
PRELIMINARY STUDY ON ALTERNATION OF HOME-KEEPING GENES WITHIN
NEURON AFTER HYPOXIA. Yingzhong Yang
1
, Lingling Zhu
2
, Wenhong Fan
2
, Yan Wu
2
,
Xiaotang Jing
2
, Rili Ge
1
, Ming Fan
2
. Qinghai High Altitude Medical Institute
1
, Institute of Basic
Medical Sciences
2
.
Objective: To compare alternation of gene expression among routine home-keeping genes
and to determine suitable one for inner standard for RT-PCR in hypoxia research. Methods: 1)
Wistar rats were divided into anoxia, intermittent hypoxia and control group. RNA from cortex,
hippocampus, pituitary were extracted for further analysis. 2) Neural stem cells from embryonic
