Properties of the flash visual evoked potential recorded in the cat primary visual cortex.

The flash visual evoked potential (F-VEP), elicited by a 100 ms diffuse light flash presented at 2 Hz, was examined in the cat primary visual cortex (Area 17). Intracortical F-VEP depth profiles were recorded to characterize waveform changes with electrode depth. A positive surface component, with a latency of 200 ms, was the dominant waveform feature within the cortex, reversing in polarity and increasing in magnitude as the cortex was penetrated. Other prominent components with latencies of 30, 50, 100, and 125 ms were also observed. Changes in the waveform with stimulus duration and illumination were examined and revealed the sensitivity of prominent components to stimulus parameters.

Oxygenation of the cat primary visual cortex.

Tissue PO2 was measured in the primary visual cortex of anesthetized, artificially ventilated normovolemic cats to examine tissue oxygenation with respect to depth. The method utilized 1) a chamber designed to maintain cerebrospinal fluid pressure and prevent ambient PO2 from influencing the brain, 2) a microelectrode capable of recording electrical activity as well as local PO2, and 3) recordings primarily during electrode withdrawal from the cortex rather than during penetrations. Local peaks in the PO2 profiles were consistent with the presence of numerous vessels. Excluding the superficial 200 microm of the cortex, in which the ambient PO2 may have influenced tissue PO2, there was a slight decrease (4.9 Torr/mm cortex) in PO2 as a function of depth. After all depths and cats were weighted equally, the average PO2 in six cats was 12.8 Torr, with approximately one-half of the values being

Perfluorocarbon emulsion improves oxygenation of the cat primary visual cortex.

Tissue PO2 was measured in the primary visual cortex of anesthetized, artificially ventilated, normovolemic cats to evaluate the effect of small doses [1 g perfluorocarbon (PFC)/kg] of a PFC emulsion (1 g PFC/1.1 ml emulsion; Alliance Pharmaceutical, San Diego, CA) on brain oxygenation. The change in tissue PO2 (DeltaPO2), resulting from briefly changing the respiratory gas from room air to 100% oxygen, was measured before and after intravenous infusion of the emulsion. Before emulsion, DeltaPO2 was 51.1 +/- 45.6 Torr (n = 8 cats). Increases in DeltaPO2 of 34.0 +/- 26.1 (SD) % (n = 8) and 16. 3 +/- 8.4% (n = 6) were observed after the first and second emulsion infusions, respectively. The further increase in DeltaPO2 after the third dose (7.9 +/- 10.5%; n = 7) was not statistically significant. The observed increases in tissue oxygenation as a result of the PFC infusions appear to be the result of enhanced oxygen transport to the tissue.

Retinal hypoxia in long-term diabetic cats.

PURPOSE: To determine whether the retina is hypoxic in early stages of diabetic retinopathy in cats and to correlate intraretinal PO2 with fluorescein angiographic and histologic alterations. METHODS: Intraretinal PO2 was measured with microelectrodes in three cats with long-standing diabetes (>6 years) that had been followed with fluorescein angiographs every 6 months. Average PO2 in the inner vascularized half of the retina was compared with similar measurements in 21 control animals. Photoreceptor oxygen consumption was also compared. The retinal vascular endothelium of the diabetic animals was stained for ADPase activity in flatmounts, and transverse sections were used to visualize microscopic alterations in vascular structure. RESULTS: PO2 in the inner half of the retina was abnormally low in the diabetic cats, 7.7+/-5.2 mm Hg (35 penetrations in 3 cats) versus 16.4+/-9.3 mm Hg in normal cats (85 penetrations in 21 cats) (P << 0.001). Oxygenation was almost normal in some regions of the diabetic retinas, but little evidence of oxygen supply from the retinal circulation was observed in other regions. Inner retinal hypoxia was present in areas with no detectable capillary dropout in fluorescein angiograms or flatmounts. The worst changes histologically were microaneurysms, leukocyte and platelet plugging of aneurysms and venules, and degenerating endothelial cells in capillary walls. These histologic abnormalities were confined to small regions, some of which could be positively correlated with markedly abnormal PO2 profiles. Photoreceptor oxygen utilization was not affected in two diabetic cats, but was below normal in one animal in which choroidal PO2 was low. CONCLUSIONS: This is the first direct demonstration of retinal hypoxia in early diabetic retinopathy, before capillary dropout was evident clinically. Hypoxia was correlated with endothelial cell death, leukocyte plugging of vessels, and microaneurysms.