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International Society for Mountain Medicine - VIWCMM Abstracts (Page 46)

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International Society for Mountain Medicine - VIWCMM Abstracts
100.
OPTICAL AND ELECTRON MICROSCOPY FINDNGS IN DEATH CASES WITH ACUTE
HIGH ALTITUDE PULMONARY EDEMA. Wang Jian-Guo
1
, Wang Zhan-Hai
1
, Tang Guo-
Dong
2
. People's Hospital of Qinghai, Xining, Qinhai, People's Hospital of Qinghai, Xining,
Qinhai.
The lung tissue in 3 deaths with high altitude pulmonary edema were studied using optical
and electron microscopy in order to clarify the pathologic features of high altitude pulmonary
edema and furnish morphological evidence for its pathogenesis. By optical microscopy, all
alveoli were opened, alveolar septa were broadened, capillaries in alveolar septa were dilated and
congested, the connecting space of capillary endothelial cells was broadened, the basement
membrane of blood vessels was widened and blurred, inside and outside elastic membrane of the
larger pulmonary vasculature were obviously inflamed, the vascular wall was loosened and
fissured. These results suggest that acute high altitude hypoxia can result in pulmonary edema by
bringing on pulmonary vascular morphological change to make plasma or red cells infiltrate into
the pulmonary interstitium and alveoli. Rather than having an intact blood-gas barrier, the
patients developed a "tap hole" which produced a high protein exudative pulmonary edema.
Therefore, the pulmonary vascular morphological changes have important significance in the
formation of acute high altitude pulmonary edema. By the electron microscopy, it was also found
that the partial nuclear space and nuclear pore of alveolar epithelial cells were broadened and
augmented, the partial chondriosome became denatured and endoplasmic reticulum distended in
cytoplasm, the micro villi of type II alveolar epithelial cells were destroyed and disappeared, and
the cell connecting space was widened. These indicate that physiological function of the alveolar
epithelial cells have suffered a certain degree of damage.
101.
CALCIUM HOMEOSTASIS CHANGES IN RAT CARDIOMYOCYTES FOLLOWING
CHRONIC HYPOXIA . Pei Jian-Ming
1
, Chen Jiu-Hua
1
, Sun Xin
1
, Wang Yao-Min
1
. Department
of Physiology;Fourth Military Medical University;Xi'an, China
1
.
There is evidence suggesting that the Ca2+ handling may be altered following chronic
hypoxia. The main purpose of the present study was to determine intracellular calcium handling
in the rat heart during chronic hypoxia. Spectrofluorometry was used to measure intracellular
calcium ([Ca2+]i) responses to electric field and caffeine stimulation in single myocytes isolated
from right ventricles of chronically hypoxic (CH) rats breathing 10% oxygen for 4 weeks and
those of the age-matched controls. The protein expression of sarcoplasmic reticulum Ca2+-
ATPase (SERCA) and its ryanodine receptor (RyR) were measured. It was found that Ca2+
homeostasis reaches a new equilibrium after 4 weeks of CH. The Ca2+ content in SR, as
indicated by the amplitude of the caffeine induced [Ca2+]i transient, is reduced but the cytosolic
Ca2+ remains the same. The amplitude and decay of the electrically induced [Ca2+]i transient are
also reduced, indicating that the SR functions namely, release of Ca2+ from SR during excitation
contraction coupling and uptake of Ca2+ via the Ca2+ ATPase back to SR, are reduced. The time
of 50% decline of the caffeine induced [Ca2+]i transient, which indicates the Na+-Ca2+
exchange activity, is also reduced. Further study showed that expression of SERCA was
suppressed by CH while expression of RyR was not altered. The results indicate that the
attenuated Ca2+-ATPase is mainly responsible for impaired Ca2+ handling in CH.
102.
THE EFFECTS OF NALOXONE AND PICROTOXIN INJECTED INTO THE FOURTH
VENTRICLE ON DECREASED MAP INDUCED BY ACUTE HYPOXIA IN RABBITS. Wang
Jian-Xin
1
, Xu Cun-He
2
, Li Sheng-Hua
1
. Dept. of Physiology, Qinghai Medical College, Xining,
Qinghai, P. R.China
1
, The Affiliated Hospital of Qinghai Medical College, Xining, Qinghai, P.R.
China
2
.
Objective: To study the function of chemical substances on the circulatory response of the
central nervous system to acute hypoxia. Method: Rabbits were anesthetized with Urethan and
Chloralose, immobilized with gallamine triethiodide and ventilated artificially to simulate high

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