Pulmonary artery pressure in Ladakhi men on exposure to acute hypoxia after a stay at sea level.

We had observed that very few Ladakhi soldiers (native highlanders: NHL) are hospitalized for high altitude pulmonary oedema. We hypothesized that this may happen because pulmonary artery pressures of NHLs do not increase even after exposure to acute hypoxia. The aim of this study was to test the above hypothesis by non-invasive echocardiographic assessment of pulmonary arterial pressure in freshly inducted Ladakhi soldiers and comparing it with that in freshly inducted lowlander soldiers (LL). The pre-ejection period and acceleration time ratio as measured from the pulmonary artery Doppler signal was used to compute mean pulmonary arterial pressure. In NHL this pressure on day 1 of induction was significantly lower at 25.8 +/- 6.5 mmHg as compared to 31.9 +/- 9.5 mmHg in LL (P = 0.0002). Another finding of interest was the very low Lake Louise acute mountain sickness score in the NHL (0.278 +/- 0.461 on day 2). This appears to be further evidence that the natives of Ladakh are adapted to hypoxia and not merely acclimatized.

Beta-adrenoreceptor blockade attenuates heat-induced tachycardia,but not the tolerance to the stress.

Ten healthy males (age 34 +/- 3 yr 9 SE) underwent 40 min of heat exposure (WD 39.7.C) after 2 hours of ingesting 120 mg of Propranolol (Inderal; ICI), or a placebo, in a random manner, the exposures being about a week apart. That there was no placebo effect was ensured by giving a control run (no medication). In the placebo trials, the end-experiment heart rate had increased by 52%, while after propranolol the increase was only 43%. Regression analysis showed that with the placebo, the HR increased by 22 beats/min/o rise in core (aural) temperature, while with propranolol, the rise (14 beats/min) was significantly lower (P < 0.02). The various heat strain indices viz the Craig's Index, the Body heat storage (Kilocals/m2/hr), and the effective heat storage were also similar for both the treatments. We conclude that beta-adrenoreceptor activity plays a significant role in producing tachycardia of heat exposure in humans, but blocking this activity with propranolol does not affect tolerance to heat stress.