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

The effects of chronic dietary supplementation with d-α-tocopherol (vitamin E, 70 I.U./lb dry food for 16 weeks) were examined on the acute pathophysiology of experimental subarachnoid hemorrage (SAH). TheSAH was induced in α-choralose-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 < 0.004) and CPP decreased by 36.6 mm Hg (P < 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.