much increased vs. in O.curzoniae and mice by CoCl2 challenge. In contrast, the liver IGFBP-1
protein in O.curzoniae was significantly increased and lasted for 6-12h with injection of CoCl2,
compared with M.oeconomus, suggesting hypoxia-increased IGFBP-1 in O.curzoniae may be a
mechanism to restrict IGF-mediated inhibitory role in growth and development through a limited
availability of plasma IGF. O.curzoniae is a well-acclimatized species on the Tibetan plateau,
and is a good model for studying hypoxia. This work is supported by the grant from NSFC
(Major Project No. 30393134 and Project No. 30270232).
35.
INTERMITTENT HYPOXIA ACTIVATES PROLACTIN RELEASE IN RAT PITUITARY . Ji-
Zeng Du
1
. Zhejiang University
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 do this,
male adult rats were exposed to hypobaric hypoxia equivalent to 2km (16.0% O2) or 5km(10.8%
O2), and PRL levels in the pituitary and plasma were measured by immunocytochemistry and
RIA, respectively. The immunostaining PRL content in the 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 contro,l
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 of 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 enhance PRL release in the pituitary and increased
plasma PRL of rats, with a time course and intensity dependent on the hypoxic stress.This
suggests that hypoxia-activated PRL may be a mechanism to support animal survival through
keeping homeostasis. This work is supported by the grant from NSFC (Major Project No.
30393134 and Project No. 30070289; 30270232).
36.
ISCHEMIA AND DIABETIC COMPLICATIONS. Kostyuk Elena
1
, Kostyuk Platon
1
, Potapenko
Yevgeniy
1
, Stepanova Inna
1
. Bogomoletz Institute of Physiology, National Academy of Sciences,
Ukraine
1
.
An important question is whether ischemia can play any significant role in such chronic
diseases as diabetes mellitus and in its complications like neuropathy, which in the case of
diabetes mellitus may be secondary to lactic acidosis. We applied a solution of pH 6.0 to the
sensory neurons of rat spinal ganglia in combination with depolarization with high-potassium
solution. In this case, the intracellular calcium transients changed the dynamics of their decay
phase. The formation of a plateau was observed, and cytosolic calcium returned to the basal level
with a large delay. This fact might indicate that acidosis changes functioning of the calcium-
regulating intracellular structures endoplasmic reticulum and mitochondria.When the action of
mitochondria was switched-off with protonophore CCCP, the plateau formation became smaller,
but it was still present, indicating the possible involvement of the endoplasmic reticulum.
Application of thapsigargin, which blocks uptake of calcium ions by the reticulum, made this
plateau disappear completely; so the endoplasmic reticulum retains its function during acidosis.
Probably the most interesting and difficult to explainfact is that even in the case of great
dysfunction of mitochondria, the endoplasmic reticulum is still active and still plays a role in
intracellular calcium homeostasis. The described alterations in calcium signaling may lead to
changes in the synaptic transmission of nociceptive volleys. Thus we can speculate that changes
in intracellular calcium exchange may be a component leading to neuropathic diabetic
complications.
