PubMed Health⌕ Search

Biomedical subjects

R E Clement

Publications and source records attributed to R E Clement.

9 recordsLinked to original sources
PubMed1990

A paraprosthetic-enteric fistula associated with a duodenal tumor.

An unusual etiology and presentation of a paraprosthetic-enteric fistula is reported involving a duodenal tumor. Review of the possible mechanisms of graft-enteric fistula formation and diagnostic evaluation is presented. Initial insertion of an extraanatomic bypass followed by graft excision was performed in the present case and is encouraged in hemodynamically stable patients. Additionally, resection of the eroded duodenum with end-to-end anastomosis was performed in order to restore intestinal continuity.

Aged↗
PubMed1988

Gas chromatography.

Explore the source record for details and available documents.

Chromatography, Gas↗
PubMed1988

Systemic and regional hemodynamic effects of cyclo-oxygenase and thromboxane synthetase inhibition in normal and hyperdynamic endotoxemic rabbits.

We tested the hypothesis that prostaglandins (PGs) and thromboxane (Tx) A2 are important mediators of the hemodynamic derangements occurring in a rabbit model of hyperdynamic endotoxicosis. Rabbits were injected with either normal saline (NS) or Escherichia coli lipopolysaccharide (LPS; 1-3 micrograms/kg) and studied 6 hr later. Cardiac index (CI) and regional blood flow were determined using thermodilution and radioactive microspheres, respectively. Systemic and regional hemodynamics were determined before and 40 min after administering indomethacin (cyclo-oxygenase inhibitor; 5 mg/kg), UK38485 (Tx synthetase inhibitor; 10 mg/kg), or NS. LPS increased CI (P = .0024) and decreased mean arterial pressure (P = .0031) and systemic vascular resistance index (P = .0001). LPS increased flow to the heart and small intestine and decreased flow to the hepatic artery and pancreas. The systemic and regional hemodynamic effects of indomethacin were similar in NS- and LPS-treated rabbits. UK38485 decreased perfusion of skeletal muscle and diaphragm in both endotoxemic and control animals. This agent increased splenic perfusion only in NS-treated rabbits. Plasma levels of 6-keto PGF1 alpha (PGI2 metabolite) were typically undetectable in both NS- and LPS-treated rabbits. These data do not support the hypothesis that PG's or TxA2 are major determinants of the hemodynamic perturbations that occur in this endotoxicosis model.

6-Ketoprostaglandin F1 alpha↗