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Biomedical subjects

K Rodgers

Publications and source records attributed to K Rodgers.

45 records · Page 3Linked to original sources
PubMed1982

Chelation of cadmium from metallothionein in vivo and its excretion in rats repeatedly injected with cadmium chloride.

Chelation and removal of cadmium from rats which were exposed to cadmium by multiple injections were studied in vivo after injection of two different compounds, 2,3-dimercaptopropanol (BAL) and diethylenetriamine pentaacetic acid (DTPA). Rats were injected i.p. with 1 mg of Cd/kg as 109CdCl2 daily for 4 days and 3 days after the last injection, they were treated with the chelating agents alone or in combination 5 days in a week for 2 weeks. BAL (50 mg/kg) alone or in combination with DTPA (50 mg/kg) was effective in removing cadmium from the body without increasing the level of cadmium in the kidney, the critical organ in cadmium toxicity. After treatment with BAL alone and BAL-DTPA, cadmium was excreted mainly in the feces with marked decrease in hepatic and renal concentrations of both cadmium and metallothionein. Injection of DTPA alone increased the urinary excretion of cadmium without any significant change in tissue cadmium. Although the urinary excretion of zinc was increased after injection of DTPA and also BAL-DTPA, there was no change in the tissue levels of zinc and copper. The results of this study suggest the potential use of BAL or BAL-DTPA combination as a mode of chelation of cadmium from the body under proper experimental conditions in chronic cadmium poisoning. It may be possible to prevent tubular damage in the kidney, the critical organ in cadmium toxicity by this treatment.

Animals↗
PubMed1980

Extraction, cleanup, and quantitative determination of aflatoxins in corn.

A method is proposed for extraction and cleanup of corn samples for the quantitation of 4 aflatoxins by high pressure liquid chromatography (HPLC). After aqueous methanol extraction, ammonium sulfate treatment, and partition of aflatoxins into chloroform, sample extracts are partially purified on Sep-Pak cartridges or small columns packed with HPLC grade silica; cleanup requires only 13 mL solvent/sample. Aflatoxins B1, B2, G1, and G2 in the purified extract are resolved in ca 10 min by normal phase HPLC on a microparticulate (5 mum) silica gel column with a 50% water-saturated chloroform-cyclohexane-acetonitrile-ethanol solvent, and are measured by ultraviolet fluorescence in a silica gel-packed flowcell. Recoveries of added aflatoxins B1, B2, G1, and G2 were 84-118% at levels of 1.5-125 micrograms/kg.

Aflatoxins↗
PubMedDate not supplied

Acceleration of dermal tissue repair by angiotensin II.

Angiotensin II is a naturally occurring peptide which has been shown to possess angiogenic properties. In the studies reported here, angiotensin II was shown to increase the proliferation of cultured bovine aortic arch endothelial cells in a concentration-dependent manner. Acute administration of angiotensin II in Hydron accelerated the repair of dermal injuries in a full-thickness excisional rat model. Additional studies were done to determine the best vehicle for delivery of angiotensin II to a dermal injury. Several vehicles, including 10% low-viscosity carboxymethyl cellulose, 4% medium-viscosity carboxymethyl cellulose, and 3% high-viscosity carboxymethyl cellulose, were found to be effective in this regard. Daily administration of angiotensin II for days 0 to 4 after injury (day 0 being the time of surgery) was determined to provide the optimal dosage for acceleration of wound repair by angiotensin II. In addition, dose-response studies indicated that angiotensin II accelerated wound repair in a dose-dependent fashion with 0.03 and 0.01 microg/rat/day of angiotensin II administered on days 0 to 4 being the minimally effective and no-effect doses, respectively. Administration of 100 microg/day of angiotensin II in 10% carboxymethyl cellulose for 5 days after injury to animals with impaired healing (steroid- and adriamycin-treated rats and diabetic mice) was also found to accelerate the rate of repair. In conclusion, angiotensin II accelerated the closure of full-thickness skin injuries in a dose-dependent manner in normal and impaired animal models.

Journal Article↗
PubMedDate not supplied

Development of angiotensin (1-7) as an agent to accelerate dermal repair.

Angiotensin II has been shown to be a potent agent in the acceleration of wound repair. Angiotensin (1-7), a fragment of angiotensin II that is not hypertensive, was found to be comparable to angiotensin II in accelerating dermal healing. This activity was evaluated in four models: rat and diabetic mouse full-thickness excisional wounds; rat random flap; and guinea pig partial thickness thermal injury. In all models, angiotensin (1-7) was comparable to angiotensin II. Angiotensin (1-7) accelerated the closure of wounds in diabetic mice and rats. In diabetic mice the resultant tissue at day 25 after injury was more comparable to normal tissue than the fibrotic scar observed in placebo-treated wounds. In the random flap model, angiotensin (1-7) was comparable to angiotensin II in maintaining flap viability (approximately 82%) and flap survival (40%). Finally, angiotensin (1-7) increased proliferation in the hair follicles at the edge of the wound and site of thermal injury, and the number of patent blood vessels on day 7 after partial thickness thermal injury. These data may be partially explained by the effect of angiotensin II and angiotensin (1-7) on keratinocyte proliferation. While platelet-derived growth factor had no effect on keratinocyte proliferation, angiotensin II and angiotensin (1-7) significantly increased keratinocyte proliferation. These data show that angiotensin(1-7) is comparable to angiotensin II in accelerating skin repair. Furthermore, the hypertensive and wound healing effects can be separated within the family of angiotensin peptides.

Angiotensin I↗
PubMedDate not supplied

Intraperitoneal tolmetin prevents postsurgical adhesion formation in rabbits.

Previous studies showed that drugs that suppress prostaglandin synthesis were able to prevent adhesion formation following surgical trauma to the peritoneum. In our study, this premise was extended to examine the effects of various delivery systems on the ability of a nonsteriodal antiinflammatory drug, tolmetin, to prevent intraperitoneal adhesion formation after a standardized injury to the peritoneum. Continuous delivery of small amounts of tolmetin directly to the injury site following parietal peritoneal injury led to a significant reduction in the number and severity of adhesions formed. A single intraperitoneal injection of tolmetin in 5% Tween, however, required a relatively higher concentration of drugs to prevent adhesion formation. In a follow-up study of abrasion and devascularization of both uterine horns, the acid form of tolmetin was shown to be more potent than the sodium salt for the prevention of adhesion formation.

Animals↗
PubMedDate not supplied

Inhibition of postsurgical adhesions by liposomes containing nonsteroidal antiinflammatory drugs.

Intraperitoneal administration of liposomes containing the nonsteroidal antiinflammatory drugs (NSAID) ibuprofen or tolmetin was tested for their efficacy in the prevention of adhesion formation. Both NSAIDs were able to reduce adhesions in an animal model for moderate adhesion formation. However, tolmetin-containing liposomes were more efficacious than ibuprofen-containing liposomes in the reduction of adhesion formation following bilateral uterine abrasion and devascularization surgery.

Animals↗