Blood in the gastrointestinal tract delays and blunts the PCO2 response to transient mucosal ischaemia.

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To determine whether the presence of blood in the gastrointestinal tract impairs the detection of splanchnic mucosal ischaemia by reducing the rate and magnitude of rise in gut luminal PCO2. Prospective observational study. University Research Laboratory. Four adult male Wistar rats with four controls from a concurrent study. Four adult male Wistar rats were anaesthetised with sodium pentobarbitone and ventilated with oxygen and isoflurane to an initial PaCO2 of 30-40 torr. Electrochemical-fiberoptic gas sensors inserted into silastic tubing placed in the ileal lumen measured luminal PCO2 at 1-s intervals. Distal aortic pressure was monitored continuously. Six 2-min episodes of aortic hypotension were induced in each rat to a mean pressure of 30 mmHg by intermittent elevation of a silk sling placed around the proximal aorta. Before the last three episodes in each rat 0.75-1.0 ml blood was injected into the ileal lumen via a 25-gauge needle. Four control rats from a concurrent experiment were treated in an identical fashion except that the rats were subjected to five ischaemic episodes, and there was no intraluminal injection of blood, although a 20-gauge cannula was placed in the proximal ileal lumen. The presence of blood in the lumen significantly decreased the ischaemic deltaPCO2 response from 33 +/- 8 to 15 +/- 4 torr (P < 0.001) and also significantly increased the peak response time from 188 +/- 12 to 227 +/- 24 s (P < 0.001). The corresponding measurements in the concurrent controls differed only from the values after blood injection in the experimental group. In this animal model the presence of intraluminal blood significantly delayed the rate and the amplitude of luminal PCO2 increases in response to transient ischaemia. This raises questions about the validity of luminal CO2 measurements as an indicator of splanchnic ischaemia in the presence of gastrointestinal haemorrhage.