CEREBRAL REACTIVE HYPEREMIA AND ARTERIAL-PRESSURE IN ANESTHETIZED GOATS

The effects of arterial pressure on cerebral reactive hyperaemia were studied in anaesthetized goats measuring electromagnetically middle ce rebral artery flow and performing arterial occlusions of 5-30 s. Under normotension (mean arterial pressure, MAP = 11+/-0.3 kPa), reactive h yperaemia (peak hyperaemic flow to control flow and repayment to debt ratios) increased, and cerebrovascular resistance during peak hyperaem ic flow decreased, as ischaemia duration lengthened; the virtual maxim al changes were obtained after 20 s ischaemia. During hypertension by aorta constriction (MAP = 18 +/- 0.7 kPa) or by i.v. infusion of norad renaline (MAP = 19 +/- 0.8 kPa) middle cerebral artery flow did not ch ange significantly and cerebrovascular resistance increased 25 and 46% , respectively (P < 0.05). During both types of hypertension reactive hyperaemia was over 50% higher, and the decrement in cerebrovascular r esistance during peak hyperaemic flow was also higher, than under norm otension. During hypotension by constriction of the inferior vena cava (MAP = 5 +/- 0.5 kPa) or by i.v. infusion of isoproterenol (MAP = 6 /- 0.5 kPa), middle cerebral artery flow decreased 35% or did not chan ge, and cerebrovascular resistance decreased 41 and 45%, respectively (P < 0.05). In these conditions, reactive hyperaemia and the decrement in cerebrovascular resistance during peak hyperaemic flow were reduce d 80%, and it was similar in both types of hypotension. The absolute l evels of cerebrovascular resistance obtained during peak hyperaemia we re similar during normotension, hypertension and hypotension. Thus, ar terial pressure is a main determinant of postocclusive cerebral reacti ve hyperaemia, and myogenic mechanisms may be of significance in deter mining the early stage of cerebral reactive hyperaemia after brief isc haemias. Adrenergic mechanisms might be of minor significance in this type of cerebral reactive hyperaemia.