Hypoxia and hypotension are both common findings following traumatic brain injury occurring with a frequency of up to 46% according to data of the Traumatic Coma Data Bank. In the present study the influence of secondary injury on intracranial pressure and the cardiovascular response is investigated in developing rats. Differences from adult rats are determined. Diffuse brain injury was produced in intubated and ventilated 17-20 days old Sprague-Dawley rats (N = 16) using a modification of the Marmarou-model. Hypoxia was induced by reducing O2-concentration to 8% lasting for 15/30 min. Mean arterial blood pressure recordings and intracranial pressure recordings were performed continuously. Animals were divided into two groups, sustaining hypoxia alone (N = 9) and trauma/hypoxia (N = 7). The results were compared to readings in adult animals subjected to hypoxia (N = 5) and trauma/hypoxia (N = 5) (450 gm/150 cm). Immediately following the onset of hypoxia in the developing rat, MABP decreased from 76.5 +/- 13 mm Hg to 35.8 +/- 7 mm Hg. In the adult rat the decrease was more marked (from 93.3 +/- 8 mm Hg to 33.5 +/- 5.7 mm Hg) (p < 0.05). Mortality rate in developing rats with trauma/hypoxia was 43% with no significant change of ICP (from 13 +/- 5.2 to 22.3 +/- 11). All adult animals recovered following trauma/hypoxia with no relevant ICP-increase within one hour post-trauma. Hypoxia induces hypotension in adult and developing rats. However, developing rats appear to be more vulnerable to hypoxia associated with trauma.