Cocaine may cause stroke, seizures, and neurobehavioral abnormalities in fetuses(F), newborns(N), and adults(A). There may be developmental differences in the mechanisms for these cocaine-induced cerebral effects. Therefore, we compared the cerebrovascular response to a 2 mg/kg I.V. dose in unanesthetized F(n=8, direct fetal injection), N(n=6), and A(n=12) sheep. We measured cerebral blood flow(CBF), mean arterial blood pressure (MAP), arterial(CaO2), and venous O2 content, and calculated cerebral 02 consumption(CMRO2) and cerebral vascular resistance(CVR) at baseline, and at 0.5, 5, 15, and 60min after cocaine injection. Results(Mean±SEM) are shown in the table below.

Table 1 No caption available.

Conclusions:

Cocaine causes increased CMRO2, increased CBF and cerebral vasodilation (decreased CVR) at 5 minutes in F and N, but not until 15 minutes in A. Cocaine also causes an immediate increase in MAP, but this response was less in N compared to F and A. We observed a persistent decrease in CaO2 in F not seen in the N or A. Clinical differences in response to IV cocaine may be explained, in part, by these developmental differences in cerebrovascular and systemic oxygenation responses.