Spontaneous rupture of a left gastroepiploic artery aneurysm in a patient with autosomal-dominant polycystic kidney disease.

Autosomal-dominant polycystic kidney disease (ADPKD) has been known to be associated with a variety of vascular diseases. We present a hemodialysis patient with ADPKD who died of a massive intraperitoneal hemorrhage caused by the spontaneous rupture of a left gastroepiploic artery aneurysm. A 64-year-old male was admitted to our hospital with acute upper abdominal pain and hemorrhagic shock. An abdominal angiography showed three aneurysms and the source of hemorrhage was assumed to be the left gastroepiploic artery aneurysm. The patient died of severe metabolic acidosis and disseminated intravascular coagulation (DIC) on the second hospital day. At autopsy, there was massive bleeding into the abdominal cavity, and pathological examination of the left gastroepiploic artery aneurysm revealed a dissecting aneurysm. This is the first case describing a rupture of a gastroepiploic aneurysm in a patient with ADPKD.

Mechanism for the antihypertensive effect of a polysaccharide-glycopeptide complex from Lactobacillus casei in spontaneously hypertensive rats (SHR).

Pharmacological studies on the antihypertensive effect of a polysaccharide-glycopeptide complex (SG-1) isolated from Lactobacillus casei were carried out by using spontaneously hypertensive rats (SHR). An antihypertensive effect of SG-1 was observed by oral, but not by intravenous or intraperitoneal administration, and the effect was attenuated by orally pre-treating with indomethacin. A single oral administration of SG-1 (20 mg/kg) decreased the peripheral vascular resistance (PR). The daily oral administration of SG-1 (10 mg/kg) for 14 days had no effect on either the urine volume or urinary electrolytes (Na+, K+, and Cl-), but it did increase the excretion of 6-keto-PGF1 alpha, a metabolite of PGI2, in the urine. Moreover, a single oral administration of SG-1 (20 mg/kg) also increased the biliary 6-keto-PGF1 alpha excretion. These results suggest that the antihypertensive effect of orally administered SG-1 resulted from an enhancement of PGI2 biosynthesis and the subsequent decrease in PR.