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The morphology and permeability to horseradish peroxidase (HRP) of the ciliary muscle capillaries of squirrel monkeys were studied. The endothelial cells of the capillaries were of the continuous type and the interendothelial clefts were closed by a zonula occludens. Many vesicles were present in the cytoplasm of the endothelial cells. In addition to these vesicles, large vacuole-like structures, 100-500 nm in diameter, were observed in the cytoplasm of capillary endothelium, especially in the circular and radial ciliary muscles. When HRP was perfused into the anterior chamber, the 3,3'-diaminobenzidine reaction product was observed in the lumen of the ciliary muscle vessels after 30 minutes. When HRP was administered intravenously, the reaction product was observed among the muscle fiber bundles after 15 minutes. In both cases, the reaction products were also present in the cytoplasmic vesicles and vacuole-like structures, suggesting that these structures are involved in the bidirectional transport of HRP between interstitium and blood.

It is well recognized that extravasation of circulating proteins is contributed to the formation of vasogenic brain edema after traumatic brain injury. However, clearance of the extravasated proteins from brain tissue remains unclear. In the present study we therefore identified the clearance procedure by evaluating extravascular localization of endogenous serum albumin and exogenous protein tracer, horseradish peroxidase (HRP), after experimental brain injury in rats. Adult male Wistar rats were subjected to a lateral fluid percussive injury. In study 1, HRP was given intravenously 10 minutes before sacrifice. Animals were sacrificed at 1, 2, 24, 72 hours and 7 days after injury in order to determine re-establishment of the blood-brain barrier. In study 2 extravascular accumulation of serum albumin and HRP given before impact was examined at 1, 6, 24, 72 hours and 7 days after injury to evaluate the clearance of these extravasated proteins. Localization of each protein was assessed in injured brain sections at the microscopic level. In study 1, breakdown of the blood-brain barrier was noted in various regions of the injured brain at 1 hour. This barrier disruption was restored in almost regions by 2 hours. Impact site, however, remained permeable upto 72 hours. In study 2, the distribution of extravasated proteins was similar between albumin and HRP at 1 hour post-injury. Pronounced extravasation of both proteins occurred in discrete regions through the injured brain. After 6 hours post-injury a differential accumulation was noted between albumin and HRP. The diffuse extracellular accumulation of albumin was most widespread at 24 hours and less intense at 72 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

We developed a method for a determination of the amount of retrogradely transported HRP in the rat masseteric motoneuron using a modification of Mesulam's HRP histochemical protocol and an image processing system combined with a light microscope and a television camera. To test the validity and reproducibility of the new method, a quantitative comparison of the amount of dark blue granules of HRP-product in the cell body of masseteric motor neurons was performed between the right and left trigeminal motor nuclei of 70 rats, which resulted in no significant difference. An additional study used the method was made of the effects of administration of five dopamine receptor antagonists with different biochemical and pharmacologic properties on retrograde transport of HRP in the rat masseteric motoneuron. As a result, chlorpromazine, haloperidol, SCH 23390, and sulpiride significantly enhanced retrograde transport of HRP as against domperidone which showed no significant change in the transport. A possible regulatory system for retrograde transport of HRP in the masseteric motoneuron was discussed in relation to the action of the dopamine receptor.

Small cerebral blood vessels are provided with slender phagocytic cells which were designated as FGP (fluorescent granular perithelial) cells from their localization and property. They were derived from pial cells and became potent in the uptake capacity for exogenous substance about at one week after birth. The present study aims to confirm the role of FGP cells and to clarify morphological changes of them in cerebral edema. Cerebral cortices of Wistar rats received head injury (caused with dry ice) were studied electron microscopically at 0.5, 2, 5, 10, 16, 30, 48 and 72 hours after the injury. At the same interval, HRP (horseradish peroxidase) was injected intravenously for the demonstration of uptake capacity of FGP cells. The authors' attention focused on the change of ultrastructure of vascular wall including perivascular phagocytic FGP cell around small blood vessels and on the uptake capacity of FGP cells at each time. From 2 to 5 hours after the cold injury, pinocytotic vesicles often appeared in endothelium and smooth muscle cells, and blood plasma infiltrated into the perivascular space and was taken in the FGP cells. The FGP cells in control were provided with intense round inclusion bodies and looked moderately intense. However, the FGP cells in the experimental animals after the injury became swollen and vacuolized following the fusion of inclusion bodies and breakdown of their limiting membrane and looked pale owing to presence of vacuoles. Under this condition, the uptake capacity of FGP cells for HRP decreased remarkably, and ACPase which was confined to the inclusion bodies in controls spread diffusely into cytoplasm.(ABSTRACT TRUNCATED AT 250 WORDS)