Effects of hypotension induced by adenosine on brain surface oxygen pressure and cortical cerebral blood flow in the pig.

Six pigs were anaesthetized with ketamine in combination with fentanyl and droperidol and paralysed with pancuronium. The pigs were tracheotomized and ventilated mechanically. Mean arterial blood pressure, MABP, was lowered from 97 +/- 21 mmHg stepwise to 58 +/- 2, 33 +/- 4 and 22 +/- 4 mmHg by intravenous infusion of adenosine (4-8 mg kg-1 min-1). Regional cerebral blood flow (rCBF) was measured directly onto the cortex of the brain by local atraumatic application of 133xenon. Brain surface oxygen pressure (PtO2) was obtained using a multiwire oxygen surface electrode. At the level of 60 mmHg, rCBF showed a significant increase, while flow values were not changed from initial values with further hypotension. Ten minutes after adenosine was discontinued, rCBF showed a rebound effect with higher values than initially. During normotension mean cortical PtO2 varied between 2.1 KPa and 3.9 kPa. During adenosine infusion PtO2 was increased at MABP-levels of 60 and 30 mmHg, while at 20 mmHg a decrease was seen in all animals. After discontinuation of the adenosine infusion, PtO2 values were higher than those measured at the initial normotension, a similar rebound phenomenon as seen with rCBF. During the experiments all hypotensive levels could be maintained at constant level without progressively increasing infusion rates, indicating no tachyphylaxis during these time periods. After discontinuation of the drug, blood pressure did not fully reach pre-hypotensive level within 10 min. Thus, hypotension induced by adenosine down to a MABP of 30 mmHg in animal experiments does not cause deterioration in either cerebral blood flow or oxygen pressure.