CEREBRAL BLOOD-FLOW DECREASED BY ADRENERGIC-STIMULATION OF CEREBRAL VESSELS IN ANESTHETIZED NEWBORN PIGS WITH TRAUMATIC BRAIN INJURY

Changes in cerebral blood flow (CBF), pial arteriolar diameter, and ar terial blood pressure, gases, and pH were examined before and for 3 ho urs after fluid-percussion brain injury in a-chloralose-anesthetized p iglets. The brain injury was induced by a percussion of 2.28 +/- 0.06 atm applied for 23.7 +/- 0.5 msec to the right parietal cortex. Region al CBF was measured with radiolabeled microspheres, and changes in pia l arteriolar diameter were monitored in the left parietal cortex using closed cranial windows. Immediately following brain injury, mean bloo d pressure transiently (for approximately 10 minutes) either increased or decreased and then exhibited a prolonged decrease in all of the an imals. The brains showed changes consistent with traumatic brain injur y such as subarachnoid hemorrhage, contusions, or reactive axonal swel ling; none showed histological evidence of a global alternative pathog enetic mechanism such as hypoxic ischemic damage. While CBF of uninjur ed control animals did not change over a 3-hour observation period, af ter brain injury blood flow decreased 30% +/- 1% below the baseline le vel within 10 minutes and remained there for 2 to 3 hours posttrauma. After adrenergic blockade, CBF did not decrease at any time during the 3-hour period in either the uninjured control or the injured animals. Concomitant with the decreased blood flow after brain injury, pial ar teriolar diameter decreased 14% below the preinjury level. However, in piglets treated with adrenoceptor antagonists, uninjured control and brain-injured animals did not show a decrease in pial arteriolar diame ter. The present results support the hypothesis that increased sympath etic outflow to the cephalic vasculature following the fluid-percussio n brain injury causes cerebral vasoconstriction decreasing pial arteri olar diameter and regional CBF.