The effects of chronic two-fold dietary vitamin E supplementation on subarachnoid hemorrhage-induced brain hypoperfusion.

The effects of chronic dietary supplementation with D-alpha-tocopherol (vitamin E, 70 I.U./lb dry food for 16 weeks) were examined on the acute pathophysiology of experimental subarachnoid hemorrhage (SAH). The SAH was induced in alpha-chloralose-anesthetized cats by intracisternal injection of 0.5 ml/kg of unheparinized arterial blood after prior withdrawal of an equivalent cerebrospinal fluid (CSF) volume. Caudate nuclear blood flow (CBF) was measured via H2 clearance together with intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP), and caudate vascular resistance (CVR). In 6 non-supplemented cats (30 I.U. vitamin E/lb dry food), the SAH resulted in an initial 21.3 +/- 2.4% decrease in CBF by 5 min, followed by a slower secondary decline of 30.1% over the subsequent 3 h after SAH. Together with the fall in CBF, the ICP rose progressively by 18.5 mm Hg (P less than 0.004) and CPP decreased by 36.6 mm Hg (P less than 0.01) at 3 h post-SAH. Furthermore, the CVR increased by 42.9% over the course of the experiment. In comparison, in 6 vitamin E-pretreated cats, there was a complete inhibition of the acute decline in CBF and increase in CVR. In addition, the magnitude of the SAH-induced increase in ICP was significantly less than in the non-supplemented animals. However, the decrease in CPP was unaffected. The ability of intensive anti-oxidant treatment to antagonize post-hemorrhagic hypoperfusion suggests that cerebral microvascular lipid peroxidation may play a key role in its development.