PURPOSE: Using a pig model: (1) to evaluate the vascular distribution pattern, including the homogeneity and completeness of the intra-arterial microsphere distribution, of 40-120-microm trisacryl-gelatin microspheres (Embospheres) in acute whole-kidney embolization; (2) to evaluate the durability and biocompatibility of 40-120-microm trisacryl-gelatin microspheres (Embospheres) in chronic partial kidney embolization. METHODS: Twenty-two animals were divided into four groups: group 1 (n = 4) underwent total arterial renal occlusion with immediate euthanasia. Groups 2-4 had chronic superselective and partial renal embolization with increasing follow-up times: group 2 (n = 2), 1 week; group 3 (n = 7), 4 weeks; and group 4 (n = 9), 14 weeks. Key endpoints in group 1 were homogeneity and completeness of acute embolizations. In groups 2-4 the key endpoints were durability of embolization and particle-related inflammation in chronic partial embolizations as assessed by quantitative angiography or histomorphometry. A numerical angiographic occlusion score (0.0 to 4.0, where 3.0 is optimal) was developed to assess and quantify the angiographic durability of superselective embolizations (groups 2-4). RESULTS: In group 1, a relatively homogeneous distribution of the particles from segmental arteries to the precapillary level was shown by histomorphometry. Some particles reached the glomerular vas afferens (10 microm diameter). In groups 2-4, a mild recanalization appeared during follow-up. The immediate average postembolization occlusion score of 3.18 +/- 0.73 was reduced to 1.44 +/- 0.73 (statistically significant). Microscopy revealed subtotal necrosis but no foreign body granuloma formation. The intra-arterial appearance of giant cells closely attaching to the surface of the embolic spheres inside the vessel lumen was noted. Vessel walls showed major ischemic reactions. CONCLUSION: Microspheres 40-120 microm in diameter might achieve total occlusion of the arterial kidney vasculature when injected centrally as a result of their fairly homogeneous distribution. Segmental renal infarction occurs after chronic partial embolization despite recanalizations during follow-up. Only mild specific intra-arterial foreign body reactions were found.

Acrylic Resins↗

PubMedDate not supplied

In vivo inhibitory effect of lanreotide (BIM 23014), a new somatostatin analog, on prostaglandin- and cholera toxin-stimulated intestinal fluid in the rat.

The antisecretory action of subcutaneously (SC) administered somatostatin(1-14), octreotide, and lanreotide on jejunal net flux of water under basal, prostaglandin E1 (PGE1)- and cholera toxin (CT)-stimulated secretory conditions was determined in vivo on isolated intestinal loop in anesthetized rats. Both PGE1 and CT induced intestinal hypersecretion in the rats. This secretory effect was not affected by SC administration of saline. Lanreotide (1, 10, and 100 micrograms/kg) reduced the maximal PGE1-induced secretion, while 200 micrograms/kg had no effect. Similarly, octreotide (1 and 10 micrograms/kg) and somatostatin (1-14) (0.1 and 1 microgram/kg) reduced the increase of net water flux induced by PGE1. However, higher doses of octreotide (100 and 200 micrograms/kg) and somatostatin(1-14) (10 and 100 micrograms/kg) had no effect on PGE1-induced secretion. Lanreotide, octreotide, and somatostatin(1-14) (1 and 10 micrograms/kg) abolished the maximal secretion induced by cholera toxin. However, 100 micrograms/kg of lanreotide, octreotide, and somatostatin(1-14) had no effect on cholera toxin-induced secretion. The present study shows that lanreotide, octreotide, and somatostatin(1-14) reduce the secretion induced by PGE1 and abolish that induced by CT. These effects were obtained with doses of less than 100 micrograms/kg of the products, higher doses being ineffective. The higher efficacy against CT-induced hypersecretion as compared to PGE1-induced hypersecretion suggests a direct antisecretory effect at the enterocyte level and indicates the usefulness of these products as antidiarrheal agents in nonhormonally mediated diarrhea.

Alprostadil↗

PubMedDate not supplied