OBJECTIVE: Blood flow to the brain is extremely sensitive to changes in PCO2. While animal studies show a similar potent PCO2 dependence in retinal and choroidal vessels, the PCO2-retinal blood flow relationship has never been adequately studied in humans. METHODS: Video scanning laser ophthalmoscopy after fluorescein angiography was used to analyze retinal arterial and capillary blood velocity under conditions of mild hypercapnia and hypocapnia. Control conditions (end-tidal PCO2 = 38.3 +/- 0.4 mmHg) were contrasted with hyperventilation-induced hypocapnia (PCO2 = 34.0 +/- 0.4 mmHg) and hypercapnia (PCO2 = 42.3 +/- 0.5 mmHg) created by PCO2 addition to inspired gas. RESULTS: Both larger vessel and macular capillary blood velocity was dependent upon PCO2: arteriovenous passage time fell as PCO2 rose, and both mean arterial dye velocity and capillary blood velocity rose as PCO2 rose (all p < 0.05). These changes in flow velocity occurred despite unchanged heart rate, arterial systolic and diastolic blood pressure, intraocular pressure, and calculated ocular perfusion pressure. Contrast sensitivity was also unchanged by PCO2 variation. CONCLUSIONS: The human retinal circulation, like the whole cerebral circulation, may be strongly dependent upon PCO2 in a manner that is unrelated to perfusion pressure and apparently outside strict autoregulatory controls.
OBJECTIVE: Blood flow to the brain is extremely sensitive to changes in PCO2. While animal studies show a similar potent PCO2 dependence in retinal and choroidal vessels, the PCO2-retinal blood flow relationship has never been adequately studied in humans. METHODS: Video scanning laser ophthalmoscopy after fluorescein angiography was used to analyze retinal arterial and capillary blood velocity under conditions of mild hypercapnia and hypocapnia. Control conditions (end-tidal PCO2 = 38.3 +/- 0.4 mmHg) were contrasted with hyperventilation-induced hypocapnia (PCO2 = 34.0 +/- 0.4 mmHg) and hypercapnia (PCO2 = 42.3 +/- 0.5 mmHg) created by PCO2 addition to inspired gas. RESULTS: Both larger vessel and macular capillary blood velocity was dependent upon PCO2: arteriovenous passage time fell as PCO2 rose, and both mean arterial dye velocity and capillary blood velocity rose as PCO2 rose (all p < 0.05). These changes in flow velocity occurred despite unchanged heart rate, arterial systolic and diastolic blood pressure, intraocular pressure, and calculated ocular perfusion pressure. Contrast sensitivity was also unchanged by PCO2 variation. CONCLUSIONS: The human retinal circulation, like the whole cerebral circulation, may be strongly dependent upon PCO2 in a manner that is unrelated to perfusion pressure and apparently outside strict autoregulatory controls.