[The pathophysiology of retinal artery and vein thromboses (author's transl)].
The retinal blood flow is autoregulated. Retinal metabolic changes following PaCO2 and PaO2 variations, variably affect the arteriolar resistance to flow. It is postulated that PGE1 may play the role of mediator in the control of retinal blood flow. Retinal vascular obstruction leads to a circulatory disorder, but immediately physiopathological mechanisms (more or less efficient) tend to compensate again the circulatory disorder. For example, after arteriolar embolism the retrograde plasma flow starts immediately and the cells increase their anaerobic glycolytic activity to produce sufficient metabolic energy. In the case of vein thrombosis, the retrograde drainage develops collateral microvessels whose draining efficiency depends on their number and the surface of the thrombotic area.
D002245:Carbon Dioxide / Q000378:metabolism; D003097:Collateral Circulation; D006801:Humans; D010100:Oxygen / Q000378:metabolism; D010313:Partial Pressure; D012039:Regional Blood Flow; D012160:Retina / Q000378:metabolism; D012161:Retinal Artery / Q000503:physiopathology*; D012164:Retinal Diseases / Q000503:physiopathology; D012169:Retinal Vein / Q000503:physiopathology*; D013927:Thrombosis / Q000503:physiopathology*
D002245:Carbon Dioxide; D010100:Oxygen
Physiopathologie des thromboses artérielles et veineuses rétiniennes