with ig NS 5.0ml/kg/day), a treated group (hypoxic rats treated with ig Ipt 0.75 mg/kg/day) and a
treated group (hypoxic rats treated with ig Ipt 1.5 mg/kg/day). After 4wk, the expression of
KATP protein in the pulmonary artery smooth muscles was analyzed with Western blot, gas
chromatography, immunohistochemistry and two dimension electrophoresis. Results: The
subunits of KATP protein expression in the pulmonary artery smooth muscles in the hypoxic
group were significant lower than the control group (P<0.01). Chronic iptakalim treatment could
reverse these changes in dose-dependent manner, in which the higher dose of iptakalim reversed
more effectively than the lower dose did. Conclusions: The subunits protein expression of KATP
channels were inhibited by chronic hypoxia, and Iptakalim could the remodeling of KATP
channels in the pulmonary artery smooth muscles of rats with chronic hypoxic pulmonary artery
hypertension. The result indicated that KATP channels in the pulmonary artery smooth muscles
play important roles in chronic hypoxic pulmonary hypertensive rats. It is therefore suggested that
Iptakalim might be promising in the treatment of patients with hypoxic pulmonary hypertension.
309.
CHRONIC MOUNTAIN SICKNESS AMONG THE CHIPAYA AFTER 2500 YEARS OF
HIGH ALTITUDE EXPOSURE. Gustavo R. Zubieta-Calleja (Jr)
1
, Michael Moretti
1
, Luis
Zubieta-Calleja
1
, Nancy Zubieta
1
, Gustavo Zubieta-Castillo (Sr)
1
. High Altitude Pathology
Institute IPPA
1
.
The Chipaya culture has thrived in its high-altitude landscape for more than 2,500 years.
Over the course of its history, hydrological conditions and conflict with neighboring cultures have
forced the community which now numbers approximately 2,000 to a corner of Bolivia´s high
plateau at 4,000 m, where water is plentiful and they enjoy relative isolation from other cultures.
Lifestyle and struggle for survival have segregated them both socially and, to a great extent,
genetically, making them a very unique high altitude population, apart from the more prevalent
Quechua and Aymara populations. Blood tests were performed on nine subjects, (age = 44.8 ±
23.93) in which the mean hematocrit was 51.5 % ± 7.07. Of these, two revealed an elevated
hematocrit of 60 and 65 %, respectively. As many current global studies indicate successful
genetic adaptation has occurred among high altitude populations such as the Tibetans, it is
surprising to discover that CMS is present among the high-altitude Chipaya. If we assume that
adaptation to high altitudes is genetic as suggested by the literature, there could be no "loss of
adaptation" as the condition of CMS is described by many authors. Quite to the contrary, we
believe this traduces that there is acardio-pulmonary disease in this population (as in any other,
regardless of the altitude of residence) but with "adaptation within disease" to the hypoxic
environment. Cnclusion: CMS is present among the Chipaya, who have lived at high altitude for
thousands of years and since they were successfully adapted to such elevations genetically, we
would expect to find no CMS.
310.
HYPOVENTILATION IN CMS: A MECHANISM TO PRESERVE ENERGY. Gustavo R.
Zubieta-Calleja (Jr)
1
, Gustavo Zubieta-Castillo (Sr)
1
, Luis Zubieta-Calleja
1
, Nancy Zubieta
1
. High
Altitude Pathology Institute (IPPA)
1
.
Initial hyperventilation and tachycardia during acute exposure to high altitude hypoxia, are
followed a few months later by increased polycythemia and hypoventilation as the main
mechanisms of adaptation. In chronic mountain sickness CMS), of multiple ethiopathogenesis,
increased polycythemia and hypoventilation are dramatic and this is why hypoventilation has
consistently been reported by several authors. In fact, CMS has been attributed to
hypoventilation. During rest, arterial oxygen content (CaO2) and arterial oxygen saturation
(SaO2) are sufficient to maintain oxygen supply for the basal metabolism of tissues. Oxygen
consumption (VO2), CaO2, hypoventilation during rest and progressive hyperventilation during
the different stages of exercise, are regulated mainly by the respiratory center. CaO2 regulation is
fundamental, since increased respiratory and cardiac frequency on a previously increased
hematocrit would result in hyperoxia. It is evident that during exercise, SaO2 is low, but CaO2 is
normal. Subjects with increased polycythemia who arrive at sea level suffer from increased CaO2
