Abstract
Renal cortical capillary saturation was found to decrease from 83 per cent to in average 68 per cent in severe haemorrhagic shock in dogs. There was a close agreement between the oxygen saturation in the cortical capillary blood and the renal venous blood, which means that no significant shunting occured with respect to oxygen. The data suggest that damaging renal hypoxia does in all probability not occur in acute haemorrhagic shock despite the marked reduction in renal blood flow (renal ischemia) occurring in this condition. The hypoxia theory regarding the initiation of the clinical syndrome af acute renal failure following shock is questioned and it is concluded that the noxious agent so far has not been identified.
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