Biomedical subjects

L Bartula

Publications and source records attributed to L Bartula.

22 records · Page 2Linked to original sources

PubMed1992

Human cholecystitis is associated with increased gallbladder prostaglandin I2 and prostaglandin E2 synthesis.

Microsomal prostanoid synthesis was compared in normal gallbladders removed during organ donation and inflamed gallbladders removed at cholecystectomy. Normal human gallbladder microsomes demonstrated low rates of conversion of [14C]arachidonic acid to total labeled prostanoids, which increased during 1 to 30 min of incubation. Normal human gallbladder microsomes converted labeled substrate to all primary prostaglandins without demonstration of a major product. Inflamed human gallbladder microsomes increased the rate of conversion of [14C]arachidonic acid to total labeled prostanoids two or three times over the levels demonstrated by normal gallbladder microsomes at all times of incubation (p < 0.01). The main prostanoids synthesized by the inflamed human gallbladder microsomes were prostaglandin E2 and 6-keto-prostaglandin F1 alpha, which were increased four times over the levels demonstrated by normal gallbladder microsomes (p < 0.01). These data showed that inflammation of the human gallbladder was associated with increased synthesis of gallbladder 6-keto-prostaglandin F1 alpha and prostaglandin E2.

6-Ketoprostaglandin F1 alpha↗

PubMed1991

Long-term cholesterol feeding stimulates increased bile phospholipids and gallbladder prostanoid synthesis.

The effect of long-term cholesterol feeding on male rabbit gallbladder prostanoid synthesis and bile phospholipid and bile acid levels was examined. In rabbits fed a 2% cholesterol diet for 2, 5, 7, 9, 12, 15, 18, and 21 weeks, serum cholesterol levels increased 12-fold or higher (68-fold at 21 weeks) when compared to the control levels. Total prostanoid synthesis was significantly increased at 7 weeks or more of cholesterol feeding with 6-keto PGF1 alpha (PGI2 metabolite) and PGE2 as the major products. By 21 weeks of cholesterol feeding, 6-keto PGF1 alpha and PGE2 levels were increased 15-fold and 11-fold higher, respectively, compared to the control. Total bile phospholipid levels were significantly increased at 12 weeks or more of cholesterol feeding, and total bile acids significantly increased only from 5 through 12 weeks of cholesterol feeding. These data show that long-term feeding male rabbits with a 2% cholesterol diet increased endogenous gallbladder prostanoid synthesis, which was associated with an increase in bile phospholipid levels. Increased rabbit gallbladder bile phospholipids may represent a compensation of the animal for toxic levels of tissue and bile cholesterol. Increased phospholipid levels in the bile or tissue could serve as a source of increased availability of arachidonic acid leading to a nonspecific increase in gallbladder prostanoid synthesis.

Analysis of Variance↗

PubMed1991

Hypoxia inhibits renal thromboxane and not prostacyclin release.

The effect of hypoxia on renal prostanoid synthesis and renal function was studied. The kidneys of male Sprague-Dawley rats were cannulated and perfused in vitro with Krebs-Henseleit buffer with a pO2 of 460 (control) or 60 mm torr (hypoxia). The rate of perfusion was adjusted to maintain perfusion pressure at 100 mm Hg. The renal venous effluent was collected at 15, 30, 60, 120, 150, and 180 min and assayed for basal release of 6-keto-PGF1 alpha, PGE2, and thromboxane B2 by radioimmunoassay and inulin and sodium clearance. Prostanoid release was high at 15 min, decreased to a lower level up to 120 min, and then progressively increased after 150 min of perfusion. Hypoxia significantly decreased TxB2 release at 30, 60, 150, and at 180 min but not PGE2 or 6-keto-PGF1 alpha release. Hypoxia proportionally decreased both sodium and inulin clearances suggesting that the decrease in renal function was from decreased renal flow. The kidney responded to the altered renal function by increasing the ratio of vasodilator to vasoconstrictor prostanoids by inhibition of TxB2 release.

6-Ketoprostaglandin F1 alpha↗

PubMed1990

The effect of diabetes mellitus on aortic prostanoid synthesis and serum cholesterol levels in the rat fed a high cholesterol diet.

The effect of diabetes mellitus on serum cholesterol and aortic microsomal prostanoid synthesis was studied in cholesterol fed male Lewis rats. Normal, diabetic and diabetic rats treated with pancreatic islets were divided into three diet subgroups, control diet, control +2% cholesterol for 8 weeks and control +2% cholesterol diet for 16 weeks. Serum glucose levels were elevated three-fold in the diabetic group compared to normal. Treatment with islets restored serum glucose to normal levels in diabetic rats. The 2% cholesterol diet did not significantly alter serum glucose levels in any of the groups. Body weights in the diabetic group were significantly lower than normal or diabetic rats treated with islets. Feeding 2% cholesterol for 16 weeks significantly increased weight in normal and islet treated diabetic rats but not in the diabetic group. Aortic microsomal prostanoid synthesis was similar in all experimental groups with 6-keto-PGF1 alpha (PGI2 metabolite) being the major product synthesized in all groups. Aortic microsomal prostanoid levels were not altered by the 2% cholesterol diet. Serum cholesterol levels increased 14-fold in the diabetic group which returned to the normal level in the diabetic animals treated with islets. These data show that diabetes does not alter aortic microsomal prostanoid levels in the rat. However, diabetes significantly increased serum cholesterol levels which were reversed by islet transplantation.

Analysis of Variance↗