The influence of anaesthesia in experimental stroke research is controversial. We addressed this problem using the model of endothelin-1-induced occlusion of the middle cerebral artery (eMCAO). This model provided the opportunity to compare the infarct volumes of rats which were under halothane anaesthesia during eMCAO induction with the lesions of rats which were without anaesthesia during eMCAO. All animals were implanted with guide cannulae which allowed the induction of ischaemia in freely moving animals. For comparison, one group of animals was exposed to halothane during the induction of ischaemia. Seven days after eMCAO, the average infarct volume of halothane-anaesthetised rats was significantly larger than the lesion in freely moving animals. This difference was mainly due to increased cortical damage, whereas the striatum was much less influenced. The cortical infarct volume 21 days after induction of eMCAO under anaesthesia was significantly reduced compared to the infarct volume 7 days after eMCAO under anaesthesia. Our results indicate that halothane anaesthesia during eMCAO can cause a transient cortical increase in ischaemic infarct volume. The influence of volatile anaesthetics on ischaemic pathophysiology should be taken into consideration when preclinically testing potential neuroprotective drugs for clinical applications.