ABSTRACT
The effect of anodization on passive dissolution of titanium was studied by measuring titanium levels in peritoneal leukocytes and tissues of laboratory animals with titanium plates implanted into the peritoneal cavity. Fifteen Sprague-Dawley rats were assigned randomly to three treatment groups of five animals. One group served as controls, the other two groups had an anodized or an unanodized implant placed in the left paracolic gutter. Peritoneal lavage samples and blood samples, organ tissues and tissue surrounding the implants, were removed for histologic examination and titanium levels. Titanium was not detected in any distant organs or in the peritoneal lavage fluid. The capsular tissues surrounding the implants contained titanium at levels ranging from 2610 to 16786 ng/g for unanodized plates, and 888-5933 ng/g for anodized plates. The titanium levels within the peritoneal leukocytes of animals with unanodized implants were significantly elevated (P = 0.01) over time, as compared with controls. The level of titanium in the peritoneal leukocytes of animals with anodized implants was not significantly elevated when compared with controls. Titanium levels in the trace range, as measured in the capsular tissues, are likely a result of corrosion. Surface treatment of titanium by anodization reduces passive dissolution.
Subject(s)
Bone Plates , Facial Bones , Implants, Experimental , Leukocytes/metabolism , Titanium/pharmacokinetics , Animals , Cell Count , Eosinophils/cytology , Leukocytes/cytology , Macrophages, Peritoneal/cytology , Male , Mast Cells/cytology , Peritoneal Cavity/cytology , Peritoneal Cavity/physiology , Proteins/metabolism , Rats , Rats, Sprague-Dawley , Spectrophotometry, Atomic/methods , Tissue DistributionABSTRACT
PURPOSE: A swine model of penetrating ocular trauma was used to determine the delivery of systemically administered cefazolin to the vitreous cavity of traumatized and nontraumatized eyes. METHODS: Thirty-one pigs received a scleral laceration to the right eye under anesthesia and then were given intravenous cefazolin every 8 hours. Seven pigs received nine doses at 17 mg/kg. Seven animals received three doses of 36 mg/kg, and six others received nine doses of this regimen. Six pigs received three doses of 79 mg/kg and five others received three doses of 190 mg/kg. RESULTS: Vitreous levels of cefazolin averaged 15.6 micrograms/mL in traumatized eyes but were less than 1 microgram/mL in control eyes of animals receiving three doses at 190 mg/kg (P < or = 0.025). Mean serum concentration in these animals was 49.3 micrograms/mL. Vitreous levels were less than 1 microgram/mL in traumatized and control eyes in animals given lower doses of cefazolin (range, 17-79 mg/kg) despite multiple treatments over 2 and 3 days. CONCLUSIONS: These data demonstrate that systemically delivered cefazolin achieves levels ten times the minimum inhibitory concentration for Staphylococcus epidermidis in injured eyes. Therapeutic intraocular levels can be obtained through intravenous dosing, provided that therapeutic serum concentrations are achieved.
