Vascular occlusion of the retina: an experimental model. I. Leukocyte aggregates.

A new technique was developed to study the pathogenesis of retinal arteriolar occlusion in the pig. Using a catheter with its tip in front of the exit of the ophthalmic artery, autologous microparticles could be injected directly into the retinal arterial system. These microparticles were C5a-des-Arg stimulated leukocytes, which were aggregated to pellets of different sizes ranging from 0.26 to 1.0 mm. For better adhesion of the aggregates to the endothelium, endothelial damage was induced by the injection of additional substances, including methomidate and endothelial antibodies. In a further series of experiments systemic hypoxemic conditions were created over several hours prior to injection of the leukocyte aggregates. This resulted in cotton-wool spots and arterial branch occlusions with retinal edema. Furthermore, retinal hemorrhages occurred. This experimental model seems to be appropriate for mimicking retinal arteriolar occlusion syndromes.

Vascular occlusion of the retina--an experimental model. II. Platelet aggregates.

Using a new technique to mimic arteriolar occlusion syndromes, different microparticles were injected into the ophthalmic artery of pigs. These microparticles were platelet aggregates of various sizes ranging from 0.15 mm to more than 0.8 mm. Aggregation was induced using adenosine diphosphate and thrombin. In some experiments, acetylsalicylic acid and histamine were also applied. In a further series of experiments, mixed aggregates containing platelets and leukocytes were injected. The results were observed by indirect ophthalmoscopy and consisted of superficial and deep retinal infarction. Large platelet aggregates resulted in arterial branch occlusion, whereas mixed and small platelet aggregates produced occlusion of small arterioles. This technique seems to be valuable in studying retinal arteriolar occlusion syndromes.

Pathogenesis of Purtscher's retinopathy. An experimental study.

Laboratory and clinical observations have implicated microparticles in the pathogenesis of Purtscher's retinopathy, which leads to the occlusion of small arterioles. These microparticles may be caused by aggregated leukocyte platelets or fibrin clots. The phenomenon of intravascular coagulation is well known following trauma or acute pancreatitis. Purtscher's retinopathy is linked with both diseases. To support this presumed pathogenesis of Purtscher's retinopathy, fibrin clots ranging in size from 0.15 to 1.0 mm were injected into the ophthalmic artery of the pig. They resulted in superficial and deep retinal infarctions. In addition, flame-shaped and spotted hemorrhages occurred. These retinal changes are characteristic of Purtscher's retinopathy.

[Purtscher disease. Range of variation of clinical manifestations in 11 patients and pathogenetic considerations]. / Morbus Purtscher. Variationsbreite der klinischen Manifestationen bei 11 Patienten und Uberlegungen zur Pathogenese.

Eleven patients with M. Purtscher are presented with different manifestations of the retinopathy. The main characteristics are (1) yellowish-white "Purtscher-Flecken", which have a polygonal margin and are lying in the inner nuclear layer between the arterioles, (2) white typical cotton-wool-spots located in the nerve-fiber-layer covering the vessels and hemorrhages, which are (3) spot-like or (4) flame-shaped due to their location in the different retinal layers. All of these four manifestations may be isolated or combined, as we have observed in bilateral cases. Ten cases were caused by trauma of the thorax or the skull and one by pancreatitis. The pathogenesis of M. Purtscher can be explained by microembolization. An intravasal coagulation and/or aggregation of leukocytes resp. thrombocytes may develop after trauma as well as in pancreatitis. This may lead to microinfarcts and hemorrhages. The "microinfarct-hypothesis" has been experimentally proved and is able to explain the rarity of M. Purtscher, the range of variation, the monolateral and bilateral manifestation and identical ophthalmoscopic pictures despite different etiology.

[Ablation of the trabecular meshwork]. / Die Ablation des Trabekelwerks.

In an experimental investigation we examined the possibility to create an open pathway between the anterior chamber and Schlemm's canal by excimer laser ablation of the trabecualr meshwork (AT) in enucleated eyes. A quartzfiber was directed through the anterior chamber to the opposite chamber angle. With an energy of 0.3-1.5 mJ and wavelengths of 248 and 308 nm pores were easily made into the trabecular meshwork leading to a direct connection between the anterior chamber and Schlemm's canal. This result was confirmed by histologic examination of the globes. The trabecular meshwork has disappeared completely. The surrounding tissue reveals only minimal thermal effects due to the laser burns. With the same method cyclodialysis and basal iridectomy may be performed. The operation is simple and effects can be placed with great accuracy.