Experimental cerebral infarction in the dog: electron microscopic studies of the microvasculature.

Ultramicromorphological changes of the cerebral vessels were studied by observation of ultrathin section specimens under the transmission electron microscope, vascular cast specimens under the scanning electron microscope, and freeze-fracture replica specimens under the transmission electron microscope. Extensive infarction was found in areas supplied by the middle cerebral artery, but the disturbances in the microvasculature of the lesion are not simple. Bleeding came from arterioles in the basal ganglia, a perforating arterial terminal zone, and from venules in the corticomedullary border, a cortical arterial terminal zone. The number of pinocytotic vesicles was 3 times normal in the capillaries of ischemic cortex, and vesicle size increased 1.3 times. The tight junctions revealed discontinuity of strand-composing intramembranous particles, but no obvious disruption. It is concluded, therefore, that vesicular transport plays a major role in the increase of capillary permeability during experimental infarction.