The abdomen, thigh, and arm as sites for subcutaneous sodium heparin injections.

The purpose of this study was to evaluate three subcutaneous injection sites for low-dose heparin therapy (5,000 units). One hundred and one subjects were randomly placed in one of three groups. Group A received injections in the abdomen, Group B, in the thigh, and Group C in the arm. Each subject received three injections at the one site. Activated partial thromboplastin time (APTT) was measured prior to initiation of heparin and again four hours after the first injection. Bruising was measured at 48, 60, and 72 hours postinjection. There were no statistically significant differences among groups for either changes in APTT or bruising at 60 and 72 hours postinjection. Thus the clinical practice of utilizing the abdomen as the only or preferred site for subcutaneous heparin injections was not supported.     

Therapeutic considerations in childhood idiopathic thrombocytopenic purpura

This monograph reviews the literature regarding therapy for childhood idiopathic thrombocytopenic purpura (ITP). The role and mechanism of action are discussed for corticosteroids, splenectomy, and intravenous gamma globulin. Alternative therapies with potent immunosuppressive agents are also mentioned. Guidelines for the management of children with ITP are presented.     

Clinical response of hard tissue replacement (HTR) polymer as an implant material in oral surgery patients.

This study evaluated the performance of a synthetic implant material, Hard Tissue Replacement Polymer, for: (1) ease of handling, (2) compatibility with bone and soft tissue, (3) stability of augmentation over time, and (4) development of untoward effects. HTR (a registered trademark of HTR Sciences, a division of United States Surgical Corporation, Norwalk, CT 06856) was implanted into 34 patients by means of five different surgical procedures. The material was found to be easy to manipulate during surgery. Tissue and bone compatibility, defined as absence of inflammation, was present in 32/34 surgical sites (94%). In extraction sites during the 18-month follow-up, no measurable decrease in bone height or width was seen. One patient with a large periodontal endodontic defect developed a post-operative infection necessitating extraction of the tooth. No induction of bone was seen in response to placement of HTR material.     

Comparative testicular toxicity of bis(2-methoxyethyl) ether and 2-methoxyethanol in rats

Male rats were exposed to 0, 110, 370, or 1100 ppm bis(2-methoxyethyl)ether (diglyme) 6 h/day, 5 days/week for 2 weeks. One group of male rats was exposed to 300 ppm 2-methoxyethanol (2-ME) for 2 weeks as a positive control. Exposed rats were killed after 10 days of exposure and 14, 42, or 84 days post-exposure (PE), respectively. At 110 ppm diglyme, spermatocytes in pachytene and meiotic division at spermatogenic stages XII-XIV were mainly affected. At 370 ppm diglyme, affected germ cells were similar to those seen at 110 ppm diglyme, but round spermatids at spermatogenic stages I-VII were also affected. The testes regained normal spermatogenesis by 84 days PE. At 1100 ppm diglyme or 300 ppm 2-ME, marked testicular atrophy was found affecting all spermatogenic stages. Damaged seminiferous tubules were lined with regenerating pachytene spermatocytes at 14 days PE and with spermatocytes and round spermatids after 42 days PE. Most but not all testes in rats exposed to 300 ppm 2-ME or 1100 ppm diglyme had normal morphology after 84 days PE. Based on the observation of germ cell damage, spermatozoa population in the epidymal tubules, reversibility of spermatogenesis after various PE periods, testicular toxicity induced by 300 ppm 2-ME was more severe than that seen at 370 ppm diglyme but was slightly less remarkable than that of 1100 ppm diglyme.     

Nimodipine reduces the toxicity of intravenous bupivacaine in rats.

We examined nimodipine modification of bupivacaine toxicity in anesthetized male rats. Three minutes after pretreatment, group 1 (n = 11), group 3 (n = 10), and their respective control groups (n = 11 and n = 9) received intravenous bupivacaine LD50 (median lethal dose). After pretreatment, group 2 (n = 10), group 4 (n = 8), and their respective control groups (n = 10 and n = 8) received intravenous bupivacaine LD90 (90% lethal dose). Pretreatment was 200 micrograms/kg intravenous nimodipine in groups 1 and 2 and 500 micrograms/kg in groups 3 and 4. Control animals were pretreated with intravenous saline solution. Data were analyzed by chi 2-analysis and analysis of variance. Survival increased after 200 micrograms/kg nimodipine (P less than 0.05). In group 1, 9 (81%) of 11 survived compared with control animals (4 [36%] of 11). In group 2, 8 (80%) of 10 survived compared with control animals (2 [20%] of 10). Survival was not increased after 500-micrograms/kg nimodipine pretreatment. In group 3, 2 (22%) of 9 survived compared with control animals (4 [40%] of 10). In group 4, 4 (50%) of 8 survived compared with control animals (2 [25%] of 8). We conclude that nimodipine pretreatment with 200 micrograms/kg protects against fatal toxicity from LD50 and LD90 bupivacaine, but 500 micrograms/kg does not.