Baseline calibers of selected arteriole and venule segments were recorded in measurement units.

Knowledge of pathological mechanisms underlying wider retinal venule may provide further insights concerning microvascular alterations in diabetes.

Relative dilations of selected arteriole and venule segments during flicker stimulation and resting diameters were measured automatically.

Here we discuss the idea that cerebral venule pathology could be an overlooked source for brain microinfarcts in humans.

Background: Damage to venules in multiple sclerosis was first described decades ago.

Further, OCTA is generally incapable of differentiating descending arterioles from ascending venules.

However, capillaries and venules were elongated and had increased diameters compared to normal.

Venules then pass to submucosal veins without receiving further capillary branches.

Antibodies to Fg and FN inhibited thrombosis in venules but not in arterioles.

The number of leukocytes sticking to submucosal venules was significantly increased at 30 min.

Both isoflurane and sevoflurane significantly dilated both arterioles and venules in a concentration-dependent manner.

These venules were collected into the large vein at the bottom of the tonsil.

The apparent permeability coefficient of albumin was measured in isolated and perfused coronary venules.

Antibody to vWF inhibited thrombosis in arterioles and venules.

Histopathology revealed disrupted epithelium, infiltration of both acute and chronic inflammatory cells, and high endothelial venules.

Shear rates increased approximately fivefold in arterioles and tenfold in venules during the formation of occlusive thrombi.