Search PubMed⌕ Search

Biomedical subjects

C E Jones

Publications and source records attributed to C E Jones.

188 records · Page 11Linked to original sources

Reduced resistances of septal artery collateral channels after cardiac sympathectomy.

We have shown that chronic cardiac sympathectomy reduces coronary collateral resistances. The present experiments in isolated dog hearts delineated the role of intramyocardial collateral channels from the septal (SEP) to the circumflex (CIRC), left anterior descending (LAD), and right (RT) coronary arteries in this phenomenon. In 11 controls and 8 2-wk sympathectomized hearts, a retrograde flow technique was used to determine collateral resistances between the epicardial arteries (CIRC, LAD, RT). Collateral resistances between the CIRC and LAD and between the LAD and RT were 42-68% less in sympathectomized hearts (P less than 0.05). Collateral resistances from the SEP to each epicardial artery were determined from retrograde flows simultaneously collected on each epicardial artery when the SEP was the only vessel perfused. Collateral resistances from the SEP to the CIRC and LAD were 51-59% less in the sympathectomized hearts (P less than 0.05). Thus, intramyocardial channels from the SEP to the left coronary arteries show reduced resistances after sympathectomy and can provide a substantial portion of the increased collateral flow to these vessels.

Animals↗

Relaxation of the isolated coronary artery by inosine: noninvolvement of the adenosine receptor.

The relaxation responses to adenosine and its analog inosine were compared in isolated canine coronary arterial rings (1-2 mm o.d.). The rings were contracted with prostaglandin F2 alpha (PGF2 alpha) and relaxed by progressively increasing the nucleoside concentration in the bathing medium. The maximal relaxation (Rmax) was expressed as a percentage of the increase in isometric tension caused by PGF2 alpha. All 15 rings responded to inosine, but only 10 responded to adenosine. In the 10 rings responding to both nucleosides, the ED50 (geometric mean with 95% confidence limits) for adenosine and inosine was 0.89 (0.76-1.26) and 224 (166-302) microM, respectively (p less than 0.001). However, in these 10 rings, the Rmax for adenosine was much less than that for inosine (p less than 0.05); thus, the mean ratio of adenosine Rmax/inosine Rmax was only 0.56 +/- 0.15 (SE). In further experiments, the methylxanthine aminophylline completely abolished the relaxation response to adenosine but did not affect the response to inosine. These results suggested that inosine relaxes the coronary artery by stimulation of a site distinct from the vascular adenosine receptor.

Adenosine↗

Identification of the metabolites of erythro-9-(2-hydroxy-3-nonyl)hypoxanthine from laboratory animals.

After administration of erythro-9-(2-hydroxy-3-nonyl)hypoxanthine, eight compounds were isolated from the urine of rats, dogs, and monkeys. All of the drug metabolites were modified on the nonyl side chain. The oxidatively degraded metabolites included an alcohol (9-(2,8-dihydroxy-3-nonyl)hypoxanthine), the corresponding ketone (erythro-9-(2-hydroxy-8-keto-3-nonyl)hypoxanthine), and three carboxylic acids [erythro-6-hydroxy-5-(9- hypoxanthyl ) hepanoic acid, erythro-7-hydroxy-6-(9- hypoxanthyl )octanoic acid, and erythro-8-hydroxy-7-(9- hypoxanthyl )nonanoic acid]. Glucuronide conjugates of the unchanged drug and the alcohol metabolite were also found. The alcohol, ketone, and nonanoic acid metabolites were produced by all three species. Only the rat produced the shorter chain acid derivatives and no glucuronides. The monkey excreted both glucuronides, while dogs formed one glucuronide conjugate, that of the parent drug.

Adjuvants, Immunologic↗

The comparative toxicity of operational Air Force hydraulic fluids.

The subchronic (26 day) oral toxicities of two AF hydraulic fluids (MIL-H-5606 [H5], MIL-H-83282 [H8]), a commercial phosphate ester (PE), and two candidate hydraulic fluids (low temperature version of MIL-H-83282 [LT] and chlorotrifluorethylene oligomers [polyCTFE]) were compared in male F-344 rats. Oral dosing was used in order to quickly compare these fluids to PolyCTFE, the only fluid at the time to have been tested in a 90-day inhalation study. Rats were initially dosed with 1.0 g/kg/day of each fluid. H8 increased alkaline phosphatase (ALKP) while LT produced an anemia and leukocytosis. Exposure to H5 fluid resulted in lymphocytopenia and persistent diuresis. Due to their greater toxicity, resulting in lethality in the first dosing study, only 0.5 g/kg/day of PE and PolyCTFE were administered in the second study. Exposure to PE (0.5 g/kg) resulted in an anemia and decreases in BW (day 10 until day 25), spleen/BW ratio, blood urea nitrogen (BUN), and creatinine (CREAT). PolyCREAT (0.5 g/kg) decreased BW (day 11 to the end of the study) and testicular weight. PolyCTFE (0.5 g/kg) increased relative spleen weights, various clinical chemistry parameters, and triggered a reversible diuresis. PolyCTFE (0.5 g/kg), PE (0.5 g/kg), and H5 produced an increase in absolute and relative liver weights compared to control livers. Peroxisomal beta oxidation, an indicator of peroxisomal proliferation, was significantly increased above control levels in the livers of all rats except the PE (0.5 g/kg) group, where the increase was not significant. Hydrocarbon nephropathy, indicated by increased levels of hyaline droplets in kidney tubules, was severe in H5, mild in H8, LT, and PolyCTFE (0.5 g/kg), and minimal in PE (0.5 g/kg). The MIL-H-83282 fluids (H8 and LT) were the least toxic hydraulic fluids. PolyCTFE and PE were the most toxic, with H5 intermediate.

Administration, Oral↗

Pancreatic trauma.

Explore the source record for details and available documents.

Humans↗