Experimental brain stem infarction in the dog. Observation of the course (author's transl)

Abstract

The authors reported previously on a method of producing brain stem infarction in the dog by segmental embolization of the basilar artery using a silicone rubber cylinder. In the present study the course of infarction in the brain stem was followed and the pathogenesis of hemorrhagic infarction was also explored. A total of 28 adult mongrel dogs were used in this study. Five of them belonged to the control group and the others belonged to the embolized group. The dogs were anesthetized by intravenous injection of sodium pentbarbital and ventilated mechanically through an endotracheal tube. A silicone rubber cylinder was injected into the unilateral cervical vertebral artery to embolize the basilar artery segmentally. In the control group animals, only saline solution was injected into the right cervical vertebral artery and they were sacrificed after observation for 6 hours. The embolized group animals were sacrificed 1 hour, 6 hours, 3 days, or 1 week after embolization. Before sacrificing the animals, final vertebral angiograms were obtained to determine the distal migration of the embolus, and 1% trypan blue was administered, except in the animals sacrificed 1 week after embolization, to examine the blood-brain barrier status. Thereafter, the brain was perfused with 50% microbarium containing 5% gelatin in order to evaluate the microcirculation in the brain stem. The brain was fixed in 10% formalin for one to three weeks and then embedded in paraffin. The histological specimens were stained with hematoxylin eosin and in some cases with luxol fast blue. One hour after embolization, the lesions could not be observed macroscopically, but there was a slight extravasation of dye. Microangiograms revealed interruption and disappearance of perforating arteries and avascular areas. Histologically, some small vessels were not perfused with microbarium. Six hours after embolization these lesions could be easily observed macroscopically and some of them were hemorrhagic. Diapedesis and edema could be observed histologically at this stage. On the third day extravasation of dye was slight. Microangiogram revealed extravasation of microbarium in addition to the earlier findings. The major histological findings were microangionecrosis and hemorrhage due to rupture of the necrotic vessels. The additional findings were fine vasculature around the avascular area and tortuosity of the perforating arteries on the microangiogram 1 week after embolization. Newly developed blood vessels and many gitter cells were observed histologically. Distal migration of the embolus could not be observed on the vertebral angiogram at any time. When the basilar artery was embolized segmentally and the brain stem was infarcted, diapedesis developed in the brain stem 6 hours after embolization, which was attributable to increased permeability of small vessels, and hemorrhage occured in the infarction area due to rupture of the necrotic vessels on the third day.