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Biomedical subjects

B M Taylor

Publications and source records attributed to B M Taylor.

65 records · Page 4Linked to original sources

Metabolism of prostacyclin. III. Urinary metabolite profile of 6-keto PGF1 alpha in rat.

The in vivo metabolism of 6-keto PGF1 alpha was investigated in rats. Following continuous intravenous infusion for 14 days the urinary metabolites were isolated and identified. A substantial amount of unchanged 6-keto PGF1 alpha was recovered in the urine. The metabolic pattern very closely resembles that of PGI2 in rats. Metabolites were found which represented 15-dehydrogenation, beta-oxidation, omega and omega-1-hydroxylation and oxidation. Previous work showed that 6-keto PGF1 alpha is very poorly oxidized by 15-PGDH. We administered 15-[H3]-PGI2 and 15-[H3]-6-keto PGF1 alpha to rats and measured urinary tritiated water as an index for in vivo 15-PGDH activity. The results showed that PGI2 and 6-keto PGF1 alpha were both oxidized to the 15-keto product, although the rate of oxidation of PGI2 was greater than that of 6-keto PGF1 alpha. We concluded that the administered PGI2 was oxidized by 15-PGDH before hydrolysis to 6-keto PGF1 alpha. A portion of the dose is probably hydrolzyed before 15-dehydrogenation.

Animals↗

The significance of urine phosphate measurements in the early diagnosis of intestinal infarction.

This study has confirmed previous experiments which indicated that inorganic phosphate concentrations rise in body fluids after intestinal infarction. The phosphate clearance ratio is elevated in dogs after occlusion of the superior mesenteric artery, but is not as sensitive as indicator of the presence of a necrotic intestine as the serum or peritoneal fluid phosphate levels. The rise and fall of phosphate levels occur within the first 24 hours after infarction, similar to amylase levels in acute pancreatitis. The renal failure observed in dogs after ligation of the superior mesenteric vein is likely on the basis of hypovolemia and does not seem to result from hyperphosphatemia. Intestinal infarction should be suspected with laboratory evidence of hemo-concentration, marked leukocytosis, an inappropriate metabolic acidosis and elevated serum and peritoneal fluid phosphate levels. In dogs with normal renal function, an elevated urinary phosphate clearance ratio of greater than 0.20, as measured on a spot sample of urine and serum, is also highly suggestive of the presence of this condition, but its absence, by no means, excludes the diagnosis. With these simple laboratory tests, possibly an earlier diagnosis can be made, and timely operation can be an entirely intestine-saving procedure.

Acute Kidney Injury↗

Preinfarction diagnosis of acute mesenteric ischemia by simple measurement of inorganic phosphate in body fluids.

Acute mesenteric ischemia is extremely difficult to diagnose because peritoneal signs are absent until the bowel becomes necrotic and irretrievably damaged. So far the only reliable diagnostic procedure has been mesenteric angiography. The present study verifies that significant elevations of serum inorganic phosphate concentrations occur in dogs after mesenteric occlusion; the authors' initial clinical studies in humans support these experimental findings. Detailed analysis of body fluid and soft tissue phosphate content shows that the high phosphate load originates in the sloughing intestinal mucosa; if this phosphate escapes filtration by the liver it enters the systemic circulation. Simple measurement of the inorganic phosphate concentrations of the serum and peritoneal fluid may lead to earlier diagnosis of acute intestinal ischemia and a successful revascularization procedure to prevent its progression to infarction.

Acute Disease↗

Metabolism of prostacyclin in rat.

Following a single intravenous administration of [11-3H]prostacyclin in rat, 77% of the administered dose was excreted within 3 days with 33% in urine and 44% in feces. Urinary metabolites were accumulated by chronic intravenous infusions of [11-3H]prostacyclin for 14 days. The drug was extensively metabolized and the structures of seven metabolites were elucidated by combined gas chromatography and mass spectrometry. The urinary products include the dinor and 19-hydroxy dinor derivatives of 6-keto-PGF1alpha and 13,14-dihydro-6,15-diketo-PGF1alpha, omega-hydroxy and omega-carboxyl dinor derivates of dihydro-6,15-diketo-PGF1alpha, and a dihydrodiketotetranordicarboxylic acid. The metabolic pathways of PGI2 in rat are similar to that of PGF2alpha.

Animals↗