Attenuation of cerebral vasospasm and secondary injury by testosterone following experimental subarachnoid hemorrhage in rabbit.

Background: The vasodilatator effects of testosterone have been widely studied and demonstrated. Based on previous studies of these vasodilatatory activities, we hypothesized that testosterone might have potential effects on subarachnoid hemorrhage-induced cerebral vasospasm.
Methods: Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits in each group: group 1 (control); group 2 (subarachnoid hemorrhage); group 3 (subarachnoid hemorrhage + vehicle); and group 4 (subarachnoid hemorrhage + testosterone). Testosterone (15 mg/kg, intraperitoneally) was administered 5 min after the intracisternal blood injection and continued for 72 h once per day in the same dose for group 4. Animals were killed 72 h after subarachnoid hemorrhage. Basilar artery cross-sectional areas, arterial wall thicknesses, and hippocampal degeneration scores were evaluated in all groups.
Results: Intraperitoneal administration of testosterone was found to attenuate cerebral vasospasm and provide neuroprotection after subarachnoid hemorrhage in rabbits. Testosterone treatment was determined to be effective at increasing the luminal area and reducing the wall thickness of the basilar artery.
Conclusions: Our findings show that testosterone has some preventive effects on SAH-induced vasospasm and secondary neuronal injury in rabbits. We propose that the vasodilatatory activity of testosterone is due to its effects on inhibiting calcium channels, activating potassium channels, augmenting nitric oxide synthesis, and inhibiting oxidant stress and inflammation.