July 1988
Volume 29, Issue 7
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Articles  |   July 1988
An explanation of the "supernormal" b-wave in vitro.
Author Affiliations
  • S J Cringle
    Lions Eye Institute, University of Western Australia, Nedlands, Perth.
  • V A Alder
    Lions Eye Institute, University of Western Australia, Nedlands, Perth.
Investigative Ophthalmology & Visual Science July 1988, Vol.29, 1044-1049. doi:
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      S J Cringle, V A Alder; An explanation of the "supernormal" b-wave in vitro.. Invest. Ophthalmol. Vis. Sci. 1988;29(7):1044-1049.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

The isolated arterially perfused eye preparation has proven to be comparable to the in vivo model in many respects. However, the existence of "supernormal" b-wave amplitudes in the perfused eyes has remained an unexplained functional difference between the two preparations. The term "supernormal" reflected the observation that at high perfusate flow rates the amplitude of the b-wave from the perfused eyes was frequently larger than that recorded in vivo under the same stimulus and adaptation conditions. Recent investigations in this laboratory have demonstrated that the position of the scleral electrode on the isolated eye greatly influences the amplitude of the b-wave obtained. The simple comparison of b-wave amplitudes in vivo and in vitro was therefore not appropriate, due to the different electrode locations used in the two situations. In addition, the relationship between perfusate flow rate and b-wave amplitude at a fixed location has been reinvestigated. In our perfusion system the b-wave amplitude has been shown to saturate at moderate flow rates (1.5 ml/min), considerably lower than those required to maximize the b-wave amplitude in earlier studies. This difference is due to the higher oxygen tension of our perfusate at the entry point to the eye. It is concluded that b-wave stability with increasing perfusate flow can be achieved in vitro, and that the apparently supernormal b-wave amplitudes observed under these conditions can be explained in terms of the different electrode environment in the in vivo and in vitro preparations. The implications of these findings with regard to autoregulation of the retinal circulation are discussed.

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