ABSTRACT
BACKGROUND: Induced hypertension has long been considered a potential adjunct to the management of focal cerebral ischemia. Whether induced hypertension causes an increase in cerebral blood flow(CBF), dependent on cerebral perfusion and/or an intracerebral redistribution of CBF by a vasoconstrictive effect of vasoconstrictor is controversial. In this study, effect of phenylephrine induced hypertension on the cerebral hemodynamics and mechanism of reduced ischemic area were studied. METHODS: Six mongrel dogs weighing between 13 and 18 kg were anesthetized with halothane 0.5 vo1%-N2O 1 L/min-O2 1 L/min. Ventilation was controlled to maintain PaCO2 within 35~40 mmHg. Cerebral blood flow was measured and calculated by the posterior sagittal sinus outflow method. Cerebral metabolic rate for oxygen(CMRO2) was calculated. Intracranial pressure(ICP) was also measured. Phenylephrine was infused to increase mean arterial blood pressure(MAP) to a level 30% above baseline value and MAP was held constant for 20 minutes before CBF, ICP, CMRO2 determination. These parameters were measured at 10, 20 minutes after induced hypertension. RESULTS: Induced hypertension resulted in increased MAP and decreased heart rate. There were no differences between baseline, hypertension 10 min, and hypertension 20 min in terms of PaCO2, PaO2, hematocrit and temperature. CBF was not changed after induced hypertension(39.1+/-9.7 vs 40+/-10 vs 40.2+/-10.1 ml 100g(-1) min(-1) (meanv+/-SD) at baseline, hypertension 10 min, hypertension 20 min, respectively). Cerebral metabolic rate was not changed also after induced hypertension. ICP increased after induced hypertension significantly(20.5+/-12.5 vs 26+/-15.3 vs 29.8+/-17 mmHg at baseline, hypertension 10 min, 20 min, respectively). CONCLUSIONS: Phenylephrine is a cerebral vasoconstrictor and that causes redistribution of cerebral blood flow to ischemic brain area.