was low (<1%). This was attributed to various coronary protective factors in our highlands
including: low sugar intake (salted tea), low fat intake, serenity, very low rate of smoking, lack of
news media ('worry factors'), lack of roads and transport forcing 6-14 km. walk a day to work.
Incidence of chronic mountain sickness (CMS) is less than 1 % in the highlands of Pakistan. This
is probably due to lower altitudes and predominantly Aryan descent of the population. A
prospective study is being undertaken during summer 2004 to determine the prevalence and
pattern of CMS in the highlands of HKH, to test Wu's scoring system and to find out possible
factors, including racial, altitude and hematological, for the very low incidence of CMS factors.
Preliminary results will be presented in the VI WCMM.
98.
AN OVERVIEW OF HIGHLANDERS HEALTH HAZARDS IN THE HINDUKUSH,
KARAHORAM AND HIMALYAYA (HKH). Hajira Ilyas
1
. MMM_IMRC, Pakistan Heart
Foundation
1
.
Geo-strategically the researchers in Pakistan potentially have a melting pot for the study of
highlanders' health and high altitude medicine. Health hazards amongst the highlanders of Khot,
Mastuj, Kalash (Hindukush), Misgar, Chapursan and Shimshal (Karakoram) and Lalazar and
Astor (Himalaya) have been reported (MMM-I, 1986, MMM-II, 2004).* The common medical
ailments include anemia, worms, arthritis, skin problems, arthritis and respiratory diseases. They
are relatively protected from cardiovascular disorders, mainly because of dietary habits and
strenuous living conditions. However, accidents are a major cause of disability. Expeditions are
advised to provide quality health cover for these super athletes to prevent them from a gladiators'
fate. Iodine deficiency disorders are common and require effective large scale prevention. Keshan
disease has not been found in the highland of the HKH. Incidence of chronic mountain sickness
(CMS) is less than 0.5 % in the highlands of Pakistan. This is probably mainly due to the
predominantly Aryan descent of the population, lower altitudes of habitation and lower levels of
polycythemia.
99.
HYPOXIC EXPOSURE PROMOTES SECRETION OF ENDOTHELIN-1 FROM CULTURED
ENDOCARDIAL ENDOTHELIAL CELLS. Liu Jian
1
, Xu Shu-Min
2
, Zeng Qiang
2
, Wang Pei-
Yong
1
. Department of Pathophysiology and High Altitude Physiology, College of High Altitude
Military Medici
1
, Institute of Geriatrics, The Great Wall Hospital, Beijing
1
008
532
.
The endocardial endothelium is an important modulator for regulating cardiac function. Our
previous work proved that endocardial endothelial cells (EECs) from the right ventricle of
newborn calves are an abundant source of endothelin-1 (ET-1). In this experiment, the regulation
of ET-1 secretion from cultured right ventricle EECs and its response to hypoxia were
investigated. Primary EECs were harvested from the right ventricle of newborn calves by the
scraping method, then they were cultured and passed in RPMI-1640 medium with 20 fetal bovine
serum at 37 in 5% CO2 incubator under normoxic or hypoxic conditions. Positive ET-1 in passed
EECs was shown by immunohistochemical staining with ET-1 antibody. ET-1 released from
EECs into the medium was measured with radioimmunoassy. Staining with specific ET-1
antibody was shown to be positive for ET-1 in passaged EECs. The rate of ET-1 release was
negatively correlated with cell density and incubating duration (r=-0.954 and -0.988 respectively,
p<0.001). After 6 h to 12 h incubation in hypoxic conditions (0.5-0.7 %O2), the rate of ET-1
release increased about 2 fold (p<0.001). Release of ET-1 from EECs was surpressed by the
addition of sodium nitroprusside (1 mmol/L), and enhanced by the addition of the NO synthase
inhibitor L-nitro-arginine (2.5 mmol/L), under either normoxia or hypoxia. The present findings
indicate the release of ET-1 from EECs was negatively modulated by endogenous NO, while
hypoxia stimulates ET-1 release by inhibiting NO synthase. Further studies are needed to
elucidate the involvement of ET-1 secretion from right ventricle EECs in the development of
hypoxic pulmonary artery hypertension and right ventricular hypertrophy.
