Atmospheric chemistry of 3-pentanol: kinetics, mechanisms, and products of Cl atom and OH radical initiated oxidation in the presence and absence of NOX.

Smog chamber/FTIR techniques were used to study the atmospheric chemistry of 3-pentanol and determine rate constants of k(Cl+3-pentanol) = (2.03 +/- 0.23) x 10 (-10) and k(OH+3-pentanol) = (1.32 +/- 0.15) x 10 (-11) cm (3) molecule (-1) s (-1) in 700 Torr of N 2/O 2 diluent at 296 +/- 2 K. The primary products of the Cl atom initiated oxidation of 3-pentanol in the absence of NO were (with molar yields) 3-pentanone (26 +/- 2%), propionaldehyde (12 +/- 2%), acetaldehyde (13 +/- 2%) and formaldehyde (2 +/- 1%). The primary products of the Cl atom initiated oxidation of 3-pentanol in the presence of NO were (with molar yields) 3-pentanone (51 +/- 4%), propionaldehyde (39 +/- 2%), acetaldehyde (44 +/- 4%) and formaldehyde (4 +/- 1%). The primary products of the OH radical initiated oxidation of 3-pentanol in the presence of NO were (with molar yields) 3-pentanone (58 +/- 3%), propionaldehyde (28 +/- 2%), and acetaldehyde (37 +/- 2%). In all cases the product yields were independent of oxygen concentration over the partial pressure range 10-700 Torr. The reactions of Cl atoms and OH radicals with 3-pentanol proceed 26 +/- 2 and 58 +/- 3%, respectively, via attack on the 3-position to give an alpha-hydroxyalkyl radical, which reacts with O 2 to give 3-pentanone. The results are discussed with respect to the literature data and atmospheric chemistry of 3-pentanol.

The cerebral metabolic ratio is not affected by oxygen availability during maximal exercise in humans.

Intense exercise decreases the cerebral metabolic ratio of O(2) to carbohydrates (glucose + (1/2) lactate) and the cerebral lactate uptake depends on its arterial concentration, but whether these variables are influenced by O(2) availability is not known. In six males, maximal ergometer rowing increased the arterial lactate to 21.4 +/- 0.8 mm (mean +/- s.e.m.) and arterial-jugular venous (a-v) difference from -0.03 +/- 0.01 mm at rest to 2.52 +/- 0.03 mm (P < 0.05). Arterial glucose was raised to 8.5 +/- 0.5 mm and its a-v difference increased from 1.03 +/- 0.01 to 1.86 +/- 0.02 mm (P < 0.05) in the immediate recovery. During exercise, the cerebral metabolic ratio decreased from 5.67 +/- 0.52 at rest to 1.70 +/- 0.23 (P < 0.05) and remained low in the early recovery. Arterial haemoglobin O(2) saturation was 92.5 +/- 0.2% during exercise with room air, and it reached 87.6 +/- 1.0% and 98.9 +/- 0.2% during exercise with an inspired O(2) fraction of 0.17 and 0.30, respectively. Whilst the increase in a-v lactate difference was attenuated by manipulation of cerebral O(2) availability, the cerebral metabolic ratio was not affected significantly. During maximal rowing, the cerebral metabolic ratio reaches the lowest value with no effect by a moderate change in the arterial O(2) content. These findings suggest that intense whole body exercise is associated with marked imbalance in the cerebral metabolic substrate preferences independent of oxygen availability.