However, the method also involves a sudden drop in blood supply, even though this is unilateral, and probably shorter than in VO.Once in position, the balloon is inflated and withdrawn some millimeters a few times to trigger endothelial damage.The balloon is then removed, and the external carotid artery is closed.This method causes intimal hyperplasia and arterial stenosis and is a commonly used model for clinical arterial reconstruction surgery. The cerebral hemodynamic, behavioral, and neuropathological consequences of balloon angioplasty in the rat are not known.Since the narrowing of the carotid arteries develops gradually in this model, a possible change in CBF and the development of neurodegenerative processes may be worth investigating.and, the degree of neuronal and retinal damage varies greatly, even within the same experiment, where the variables are kept at a minimum.The source of this heterogeneity is probably the cerebrovascular architecture or the ischemic tolerance of the nervous tissue of the individual animals, as is the case with humans.As an additional factor, the age of the animals at the time of VO surgery may also be responsible for the heterogeneity.The proportion of rats with severe brain damage after the onset of VO appears to be higher when the animals are young at the time of the surgery. Standardization of the experiments is a reasonable requirement as concerns reproducibility and interpretation.Since the VO model has been generally used for the investigation of chronic cerebral hypoperfusion, such standardization should be aimed at the selection of rats that do not suffer severe ischemic brain damage.Laboratories that use the VO model should agree on the selection criteria, though a number of variables complicate the development of such standards.For example, the heterogeneity of the survival times and the particular techniques used to collect data require different definitions for their standards.The observation and neurological evaluation of the motor dysfunction after VO surgery could be a rough approach, but VO animals do not display clear motor deficits like those observed in stroke models. As a consensus, brain slices containing the dorsal hippocampus could be stained with traditional dyes such as cresyl violet or hematoxylineosin, and the damage to the CA pyramidal cells could be graded for given survival times.Most investigators agree that the level of cerebral hypoperfusion in the model is moderate, and the resulting neuronal injury is relatively mild.However, the terms ischemia and oligemia are used inconsistently in the literature to describe the condition produced.In this terminology, oligemia means a range of cerebral hypoperfusion where the electrical function of the nervous tissue is not yet affected.Ischemia denotes a condition where the flow values are low enough to cause electrical failure and a massive K efflux into the extracellular space. The terms ischemia and oligemia in the VO model should therefore be used with care and selectively, with consideration to the time after occlusion of the vessels, and the brain region investigated.As regards the issue of acute and chronic neurodegeneration in the VO model, some researchers have expressed concern that the neuronal damage could primarily occur in the acute phase as opposed to the chronic phase of VO.