Hypoxia/ischemia may play an important role in the pathogenesis of sensorineural tinnitus due to the characteristics of the cochlear blood supply. In addition, hypoxia modulates molecular processes both in the acute and chronic forms of tinnitus. Transcription factor HIF-1 (hypoxia-inducible factor) may play a key role in the cells' adaptation to hypoxia and ischemia, while under hypoxic/ischemic conditions, HIF-1 induces changes in the gene expression which may contribute to the remodeling of particular structures within the cochlea. Disturbances in the cochlear blood supply may result in membrane changes, perineural edema, inflammation, disturbances in ion homeostasis and in the formation of reactive oxygen species. Thus, the pharmacotherapy of acute tinnitus may be aimed at the improvement of cochlear blood supply and the prevention of acute processes leading to cell damage. Pharmacotherapies with colloidal plasma substitutes, vasodilators, calcium antagonists, procaine, and cortisone have been described in the literature and are discussed here. Many of the pharmacological treatments have not been validated in double blind studies. Although it is impossible to deduce the cause of tinnitus from a drug's efficiency, there is some evidence that it can be effectively suppressed by improving blood supply, at least at certain stages. The aim is to achieve an improved pharmacotherapy by means of sophisticated diagnostic instruments for classifying particular types of tinnitus.