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1 erature, and this response was unaffected by respiratory alkalosis.
2  acclimatization, but elicits hypocapnia and respiratory alkalosis.
3 re examined in hyperthermia with and without respiratory alkalosis.
4 al hypoperfusion primarily from heat-induced respiratory alkalosis.
5 mic hyperinflation, ineffective efforts, and respiratory alkalosis.
6  +/- 2.7 mEq/L), consistent with compensated respiratory alkalosis.
7                                     For both respiratory alkalosis (5%--> 3% CO(2)) and metabolic alk
8 egulate any changes in NVC; and (2) stepwise respiratory alkalosis and acidosis would each progressiv
9  learned techniques resulted in intermittent respiratory alkalosis and hypoxia resulting in profoundl
10 her pH (P = 0.0037) than 1,400 m, suggesting respiratory alkalosis and only partial renal compensatio
11                                 However, how respiratory alkalosis and the resultant metabolic compen
12 .5-2.0 degrees C, this was not influenced by respiratory alkalosis, and (2) although biomarkers of pr
13 sistent with a combined influence of Q10 and respiratory alkalosis; and (2) the net cerebral release
14 Acid-base disturbances, such as metabolic or respiratory alkalosis, are relatively common in critical
15 progesterone and estradiol contribute to the respiratory alkalosis common in cirrhotic patients.
16                       In this model an early respiratory alkalosis developed, followed by a metabolic
17 nder normo- or hypercapnic conditions; under respiratory alkalosis (e.g. hypoxia) RTN neurons are sil
18                       It was unknown whether respiratory alkalosis impacts the global cerebral metabo
19  insight into a potential beneficial role of respiratory alkalosis in heat stress.
20       At core temperature + 2 degrees C with respiratory alkalosis, microvesicles derived from endoth