Cerebrovascular volume and transmural pressure loads accompanying acute increases in cerebral blood flow are implicated in the pathogenesis of periventricular-intraventricular hemorrhage in preterm infants. An acute increase in cerebral blood flow would be expected during acute recovery from asphyxia. Therefore, cerebrovascular hemodynamics, including flow (microspheres), were studied during and after acute recovery from asphyxia in seven newborn dogs in order to study the determinants of these volume and pressure loads. During the acute recovery phase, cerebral hemispheric blood flow was 69.6 ± 10 ml/100 g/min (mean ± SEM) representing a 250% increase from baseline values of 19.9 ± 1.8 ml/100 g/min (p< 0.005), while combined cerebellar-brainstem flow was 204.3 ± 19.3 ml/100 g/min representing a 536% increase from baseline values of 32.0 ± 1.5 ml/100 g/min (p< 0.005). Blood flow to both areas had returned to baseline levels 20 min after the onset of recovery. Associated with this cerebral hyperemia was an acute increase in mean arterial pressure from 21.3 ± 4.5 mm Hg at end asphyxia to 69.5 ± 6.0 mm Hg at peak recovery (p< 0.01), and parallel acute increases in sagittal sinus pressure (from 4.0 ± 0.4 to 14.6 ± 1.9 mm Hg,p±.01) and cerebrospinal fluid pressure (from 3.8 ± 0.4 to 14.3 ± mm Hg,p<1). Central venous pressure fell from 4.3 ± 6 mm Hg at end asphyxia to 1.6 ± 0.5 mm Hg, and thus is not a determinant of the elevation in sagittal sinus pressure. AH of these pressure changes were attained within 20–30 s of the onset of recovery. Assuming that acute changes in cerebrospinal fluid pressure reflect acute changes in cerebrovascular volume via the cranial compliance (volume/pressure) relationship, then the acute (<30s) elevation of cerebrospinal fluid pressure reflects an acute cerebrovascular volume load. Also, the elevated cerebrospinal fluid pressure considerably modifies both the cerebral arterial and venous transmural pressures. The cranial compliance relationship thus plays a key role in determining both volume and transmural pressure loads. We propose that the combination of a high cranial compliance and frequent acute cerebral flow/volume loads may be involved in the pathogenesis of periventricular-intraventricular hemorrhage in premature newborn infants.