PubMed · 6677813
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R J Shephard. 1983. Vitamin E and athletic performance.. https://pubmed.ncbi.nlm.nih.gov/6677813/
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Patients with chronic congestive heart failure (CHF) have impaired oxygen delivery to working muscles. The Dead Sea, the lowest site on earth, is distinguished by natural oxygen enrichment, low humidity, high barometric pressure, and temperature with increased bromide and magnesium concentrations in the inspired air. The aim of this study is to examine the effects of descent to the Dead Sea on patients with CHF. Twelve patients with CHF and 4 age-matched healthy controls underwent complete echocardiographic studies at rest as well as treadmill and metabolic stress tests, both in Haifa, 130 m above sea level and 3 days after descent to the Dead Sea, 402 m below sea level. Significant changes in parameters at the Dead Sea compared with Haifa included time on treadmill, which increased from 612+/-198 to 672+/-1 86 seconds (p <0.05); the Borg scale decreased by 1 to 2 grades (p <0.05); and oxygen saturation increased by 3% throughout exercise (p <0.05). Systolic blood pressure decreased by 9 mm Hg at rest (p <0.05) and increased by 14 mm Hg at peak exercise at the Dead Sea in patients with CHF (p <0.05). Cardiac output at rest increased by 300 ml/min (p <0.05). Maximum oxygen consumption (VO2max) increased by 126 ml/ min (p <0.05), and even more so in patients with more severe exercise-induced oxygen desaturations, which was associated with lower peak minute ventilation to CO2 production ratio (p <0.05). Thus, descent to the Dead Sea acutely improved exercise performance due to better oxygenation and loading conditions in patients with CHF.
The effects of SB 217242, a non-peptide endothelin (ET) receptor antagonist, were investigated against hypoxia-induced cardiopulmonary changes in high altitude-sensitive rats. In isolated pulmonary artery rings, SB 217242 (30 n m) antagonized ET-1-induced contractions with a p KB of 8.0. There was no difference in the sensitivity to ET-1 or the potency of SB 217242 in pulmonary artery from normoxic rats vs. rats exposed to hypoxia (9% O2) for 14 days. However, there was a marked reduction in the maximum response to ET-1, but not to KCl or phenylephrine, in pulmonary artery from hypoxic rats; this phenomenon was inhibited by treatment of animals with SB 217242 (10.8 mg/day, ip by osmotic pump) for the 14-day hypoxic period. Furthermore, there was a significant reduction in carbachol-induced, endothelium-dependent relaxation of precontracted pulmonary artery from hypoxic animals; SB 217242 treatment during the hypoxic period did not influence this difference. Vehicle-treated rats exposed to 14-day hypoxia had 173% higher pulmonary artery pressures and 75% higher right/left+septum ventricular mass ratios compared to normoxic animals. SB 217242 (3.6 or 10.8 mg/day, ip) markedly reduced (80 and 95%, respectively) hypoxia-induced increases in pulmonary artery pressure. Right ventricular hypertrophy was inhibited by 40% at the 10.8 mg/day dose. Marked medial thickening and luminal stenosis of small and medium-sized pulmonary arteries was observed in hypoxic rats. The SB 217242-treated, hypoxia-exposed rats had comparable small and medium-sized arteries to normoxic rats. Rats treated with SB 217242 (10.8 mg/day) for the last 14 days of a 28-day hypoxic exposure had significantly lower pulmonary artery pressures than those of vehicle-treated rats. In addition, the effects of the selective ETA receptor antagonist, SB 247083, and the selective ETB receptor antagonist, A-192621 (3.6 or 10.8 mg/day, ip), were compared against hypoxia-induced increases in pulmonary artery pressure and plasma ET concentrations. SB 247083, but not A-192621, inhibited hypoxia-induced pulmonary hypertension, whereas A-192621, but not SB 247083, significantly exacerbated hypoxia-induced increases in ET concentrations, suggesting that hypoxia-induced pulmonary pressor responses are mediated via ETA receptor activation, while ETB receptor blockade may alter clearance of hypoxia-induced elevated plasma ET. The inhibitory effects of SB 217242 on the functional and remodeling changes induced by hypoxia provide further evidence that ET may play a central role in pulmonary hypertension and that ET receptor antagonists may have a utility in the treatment of this disease.
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