We compared the effects of the systemic hypotensive drugs prostaglandin E1 (PGE1) and nicardipine on the cerebral microcirculation and on the cerebrovascular reactivities to hypercapnia and hypoxia. In isoflurane-anesthetized rabbits (n = 48), we measured cerebral pial vessel diameters using a cranial-window preparation: (a) during IV PGE1- or nicardipine-induced mild or moderate hypotension (to 80% or 60% of initial mean arterial blood pressure), (b) after topical administration of these drugs, and (c) during hypercapnia or hypoxia induced during such mild or moderate hypotension. Pial arteriolar diameters were (a) unchanged when hypotension (mild or moderate) was induced by PGE1 but increased when it was induced by nicardipine and (b) increased dose-dependently by topical administration of nicardipine but not PGE1. Only small changes in cerebral venular diameter were observed in these experiments. The pial arteriolar dilator response to hypercapnia was potentiated during hypotension (mild or moderate) when it was induced by PGE1 but decreased when it was induced by nicardipine, whereas the response to hypoxia was maintained during PGE1-induced hypotension but decreased during nicardipine-induced hypotension. In conclusion, as a systemic hypotensive drug, PGE1 does not dilate cerebral arterioles and maintains cerebrovascular reactivities to hypercapnia and hypoxia, whereas nicardipine dilates such vessels and reduces these cerebrovascular reactivities.
Implications: When given systemically to produce mild or moderate hypotension, prostaglandin E1 does not induce cerebral vasodilation and maintains cerebrovascular reactivity to hypercapnia and hypoxia, whereas nicardipine dilates cerebral vessels and reduces both reactivities.