PURPOSE: The aim of the study was to investigate retrobulbar flow velocities during hypercapnia in patients with normal tension glaucoma (NTG) without systemic vasospasm and jn controls. METHODS: A total of 16 NTG patients (mean age 58 ± 14 years) and 16 control subjects (mean age 50 ± 13 years, p = 0.10) were enrolled in this study. Flow velocities, peak systolic velocity (PSV), end-diastolic velocity (EDV) and resistive indices (RI) of the ophthalmic (OA) and central retinal arteries (CRA) were assessed using color Doppler imaging. Blood flow velocities were measured under normocapnic and hypercapnic conditions (increasing the end-tidal pCO(2) by 15%). Blood pressure, ventilation rate and oxygen saturation were monitored simultaneously. RESULTS: During hypercapnia, velocity responses of the PSV (p = 0.044) and EDV (p = 0.037) of the CRA were significantly different in NTG patients and healthy controls, showing a greater increase of flow velocities in control subjects. Flow velocities of the OA increased significantly in both groups (PSV p = 0.039, EDV p = 0.003) during hypercapnia. Blood pressure, oxygen saturation and intraocular pressure changed similarly in both study groups with carbon dioxide provocation. CONCLUSIONS: Velocity response to hypercapnia was reduced in the CRA of NTG patients compared to controls. This may indicate a faulty vasodilatory response in NTG patients without vasospastic disease.
PURPOSE: The aim of the study was to investigate retrobulbar flow velocities during hypercapnia in patients with normal tension glaucoma (NTG) without systemic vasospasm and jn controls. METHODS: A total of 16 NTG patients (mean age 58 ± 14 years) and 16 control subjects (mean age 50 ± 13 years, p = 0.10) were enrolled in this study. Flow velocities, peak systolic velocity (PSV), end-diastolic velocity (EDV) and resistive indices (RI) of the ophthalmic (OA) and central retinal arteries (CRA) were assessed using color Doppler imaging. Blood flow velocities were measured under normocapnic and hypercapnic conditions (increasing the end-tidal pCO(2) by 15%). Blood pressure, ventilation rate and oxygen saturation were monitored simultaneously. RESULTS: During hypercapnia, velocity responses of the PSV (p = 0.044) and EDV (p = 0.037) of the CRA were significantly different in NTG patients and healthy controls, showing a greater increase of flow velocities in control subjects. Flow velocities of the OA increased significantly in both groups (PSV p = 0.039, EDV p = 0.003) during hypercapnia. Blood pressure, oxygen saturation and intraocular pressure changed similarly in both study groups with carbon dioxide provocation. CONCLUSIONS: Velocity response to hypercapnia was reduced in the CRA of NTG patients compared to controls. This may indicate a faulty vasodilatory response in NTG patients without vasospastic disease.