The gas composition of intravascular bubbles produced by decom pression was investigated in rabbits using gas chromatography. The animals were exposed to 8 ATA for 30 min. All samples of bubbles were taken from the animals under 0.2 ATA pressure gradient so that no air could enter the sampling system from the outside.
The percentage of carbon dioxide in the bubbles tended to decrease at first and then increased with post-decompression time. On the other hand, the percentage of oxygen tended to change in the opposite manner.
Actual analysis of bubbles in the living decompressed animals indicates that carbon dioxide may be an outstanding factor in the initiation and ealy growth of bubbles. In view of this, Haldane’s classical maximum supersaturation limit for avoiding decompression sickness should be examined and possibly modified for gases other than nitrogen.
Prostaglandins participate in the pathophysiology of endotoxin shock; however, their exact role has not yet been clear. In this study, we investigated the role of the proaggregatory vasoconstrictor, thoromboxane A2 (T×A2), an arachidonic acid metabolite, during canine endotoxin shock. The central venous plasma levels of thromboxane B2 (T×B2), the stable metabolite of T×A2, was measured by radioimmunoassay. We also investigated the therapeutic effect of reduced glutathione (GSH), a potential cell-stabilizing sulfhydryl compound, in canine endotoxin shock. Sixty minutes after the intraveous administration of E. coli endotoxin (1 mg/kg), the plasma T×B2 levels were significantly increased from 68.8±49.0 pg/ml to 318.3±117.2 pg/ml (N=5) in the control group and from 67.9±68,4 pg/ml to 222.6±133.2 pg/ ml (N=5) in the GSH (300 mg/kg/hr) group. The levels in the GSH group were somewhat lower than in the control group for 60 to 180 minutes after the injection of endotoxin. Thromboxane A2 value appear not to relate to early thrombocytopenia and pulmonary hypertension but to relate to the change of late coagulopathy and of pulmonary vascular resistance. The administration of GSH suppressed the lactic acidemia significantly, however there was a much more decrease in the mean arterial pressure in the GSH group than in the control group. In addition, there was a tendency to inhibit the increase of the serum β-glucronidase activity in the GSH group.