The effects of the administration of 100% oxygen on minute ventilation (VE) and arterial blood gases were studied in patients with chronic obstructive pulmonary disease during acute respiratory failure. The administration of O2 resulted in an early decrease in VE, which averaged 18% +/- 2 SE of the control VE, and was due to a decrease in both tidal volume (VT) and respiratory frequency (f). This was followed by a slow increase in VE, such that after 15 min of breathing O2, VE rose to 93 +/- 6% of the control room air value, with both VT and f similar to control values. Despite the small difference between VE while breathing room air and that at the fifteenth minute of O2 inhalation, PaCO2 increased by 23 +/- 5 mmHg, and no significant correlation was found between the changes in VE and PaCO2. By the fifteenth minute of O2 inhalation the PaO2 averaged 225 +/- 23 mmHg, and it was concluded that despite the removal of the hypoxic stimulus of O2 inhalation, the activity of the respiratory muscles remained great enough to maintain VE at nearly the same degree as that while breathing room air. Consequently, the changes in PaCO2 after the administration of O2 were mainly due to increased inhomogeneity of VA/Q distribution within the lungs.

We studied the effects of hypophosphatemia on diaphragmatic function in eight patients with acute respiratory failure who were artificially ventilated. Their mean serum phosphorus level was 0.55 +/- 0.18 mmol per liter (normal value, 1.20 +/- 0.10). The contractile properties of the diaphragm were assessed by measuring the transdiaphragmatic pressure generated at functional residual capacity during bilateral supramaximal electrical stimulation of the phrenic nerves. Diaphragmatic function was evaluated in each patient before and after correction of hypophosphatemia, which was achieved by administration of 10 mmol of phosphorus (as KH2PO4) as a continuous infusion for four hours. After phosphate infusion, the mean serum phosphorus level increased significantly (1.33 +/- 0.21 mmol per liter, P less than 0.0001). The increase in serum phosphorus was accompanied by a marked increase in the transdiaphragmatic pressure after phrenic stimulation (17.25 +/- 6.5 cm H2O as compared with 9.75 +/- 3.8 before phosphate infusion, P less than 0.001). Changes in the serum phosphorus level and transdiaphragmatic pressure were well correlated (r = 0.73). These results strongly suggest that hypophosphatemia impairs the contractile properties of the diaphragm during acute respiratory failure, and they emphasize the importance of maintaining normal serum inorganic phosphate levels in such patients.

From time-resolved measurements of the decay of singlet molecular oxygen phosphorescence at 1270 nm in D,O, direct estimates have been gained for the rate constants of the singlet oxygen reactions with a group of sulphur compounds in the pD range 5 to 13. In the case of most of the thiols, the results are consistent with singlet oxygen reacting exclusively with the thiolate anions. At the normal physiological pH 7, the apparent rate constants (in units of M-' s-') were 8.9 x loh (cysteine), 2.5 x lo6 (N-acetyl cysteine), 2.9 x lo6 (glutathione), 3.0 x lo5 (2-mercaptoethanol), 2.3 x lo7 (ergothioneine) and 2.7 x lo6 (2-mercaptopropionyl glycine). For methionine the rate constant, 1.4 x lo7, was independent of pD in the range studied. These sulphur compounds, in particular Nacetyl cysteine and ergothioneine, or related compounds, might be considered as possible candidates for protection against skin photosensitivity side effects associated with the photodynamic therapy of solid tumours and as observed in the disease erythropoietic protoporphyria.Jori. G . and J. D. Spikes (1984) Photohiochcmistry of