✓ The authors describe investigations in cats to delineate a vasodilator system to the face, which they undertook after a previous study showed that radiofrequency coagulation of the trigeminal ganglion produced a pronounced flush in the skin of the corresponding division. Results demonstrate a vasodilator system emerging from the brain stem with the facial nerve which, by way of the greater superficial petrosal nerve, reaches the trigeminal ganglion. There the fibers are distributed to each of the divisions of the fifth nerve; in addition, a moderate number of vasodilator fibers also appear to leave the brain stem directly with the trigeminal nerve. Vasodilator effects were elicited by stereotaxic stimulation of the facial and trigeminal nuclei in the brain stem. There is, therefore, a dual vasomotor control of the facial cutaneous vascular bed; the classical sympathetic vasoconstrictor system of the face is complemented by a vasodilator system capable of producing changes of equal but opposite amplitude in vessel caliber.
Guillermo Gonzalez, Burton M. Onofrio and Frederick W. L. Kerr
An experimental study in monkeys
John R. Little, Thoralf M. Sundt Jr. and Frederick W. L. Kerr
✓ The sequential neuronal alterations that occur during the early phase of developing cortical infarction in the squirrel monkey were studied by light and electron microscopy. A technique used to select ischemic tissue based on spectrophotometry is described. Neuronal shrinkage, characterized by angularity, cytoplasmic eosinophilia, and nuclear pyknosis on light microscopy and by an increase in electron density of the cytoplasmic and nucleoplasmic matrix on electron microscopy, was the predominant reaction. The increased electron density of the cytoplasm and nucleoplasm suggested a diffuse alteration at the molecular level and the appearance of this abnormality between 3 and 6 hours corresponded with the development of an irreversible neurological deficit. In contrast, approximately 10% of the neurons became very swollen and pale. The pattern of perineuronal astrocytic alterations suggested that some form of interaction involving fluid transfer may exist between astrocyte and neuron and that shrinkage or swelling of neurons may depend in part upon the presence or absence of direct fluid exchange with astrocytes. Most terminal boutons became progressively shrunken and dense resembling the changes which occur in anterograde axonal degeneration. Swelling and fragmentation of large lysosomes occurred at 12 hours. Disruption of neural membranes was widespread by 24 hours and was more severe in swollen neurons.