Gunshot wounds to the spine associated with a perforated viscus

The cases of 42 patients with low-velocity gunshot wounds to the spine with an associated perforated viscus were reviewed. All viscus perforations occurred prior to the spinal injury. There were a total of 51 perforations, including 14 of the colon, 15 of the small bowel, 15 of the stomach, five of the esophagus, and two of the pharynx. All patients had significant neurologic deficits, with 23 patients suffering a complete neurologic injury. Average clinical follow-up was 18 months (range: 4-64 months). Only three patients developed documented spinal or paraspinal infections. One case of acute meningitis occurred after an isolated stomach perforation, while two other patients developed psoas abscesses after colon injuries. The roles of initial antibiotic therapy and of early bullet removal were evaluated in regard to infection. An extended course of broad spectrum antibiotics combined with bedrest appeared to significantly reduce the risk of spinal or paraspinal infection as compared with a previous study. Early bullet removal did not appear to be a significant factor in the prevention of infection. Prospective studies are needed to accurately delineate the role of initial antibiotic therapy for the prevention of spinal infection in these injuries.     

The effect of the halovest and body position on pulmonary function in quadriplegia

Pulmonary function (vital capacity) was measured in ten quadriplegics and ten normal subjects in the following situations: supine, sitting, supine with a halovest, and sitting with a halovest. When changing from the supine to sitting positions, vital capacity decreased in the quadriplegics and increased in normal subjects. The halovest significantly reduced the vital capacity in normal subjects, but had much less of a detrimental effect in quadriplegics. As a result of this prospective, controlled study, we conclude the following: (a) the compromised state of pulmonary function in quadriplegics is not a contraindication for the use of a halovest, (b) the halovest causes a significant (p less than 0.01) restriction in vital capacity in able bodied subjects, and (c) when tenuous pulmonary function exists in a quadriplegic, pulmonary mechanics are better in the supine position.     

Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate

We observed that pretreatment of male F344 rats with benzyl selenocyanate, a versatile organoselenium chemopreventive agent in several animal model systems, decreases the levels of DNA and RNA modifications produced in the liver by the hepatocarcinogen 2- nitropropane. To clarify the mechanisms involved, we pretreated male F344 rats with either benzyl selenocyanate, its sulfur analog benzyl thiocyanate, phenobarbital or cobalt protoporphyrin IX; the latter is a depletor of P450. We then determined (1) the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on 2-nitropropane- induced liver DNA and RNA modifications and (3) amount of nitrate excreted in rat urine following administration of the carcinogen. Pretreatment with benzyl selenocyanate or phenobarbital increased the denitrification activity of liver microsomes by 217 and 765%, respectively, increased liver P4502B1 by 31- and 435-fold, respectively, decreased the levels of 2-nitropropane-induced modifications in liver DNA (29-70% and 17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and increased the 24-h urinary excretion of nitrate by 157 and 209%, respectively. Pretreatment with benzyl thiocyanate had no significant effect on any of these parameters. Pretreatment with cobalt protoporphyrin IX decreased liver P4502B 1 by 87%, decreased the denitrification activity of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic acid modifications by 17-67%. These results indicate that the metabolic sequence from 2-nitropropane to the reactive species causing DNA and RNA modifications does not involve the removal of the nitro group. Moreover, they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic acid modifications in part by increasing its detoxication through induction of denitrification, although it is evident that other mechanisms must also be involved.      

Pigmentary changes in rat oral mucosa following antimalarial therapy

Pharmacogenic pigmentation of the oral mucosa has been reported following the use of a number of anti-malarial drugs. The nature and distribution of the pigment is inconclusive in the literature. The aim of the present study was to document pigment deposition within the oral mucosa of DA rats following prolonged chloroquine and pyrimethamine administration. The drugs were given as a combined dosage and separately to different groups via stomach gavage tube. After 12 weekly administrations the palatal mucosa was examined histochemically and ultrastructurally for changes in numbers and size of active melanocytes using the dopa-oxidase technique. The serum was analysed for changes in ACTH and testosterone levels. Morphometric analysis of cells incubated for dopa-oxidase showed a significant increase in the size of dopa positive cells with both drugs but an increase in the number of active melanocytes with chloroquine only. Serum levels of ACTH remained unchanged with both drugs but pyrimethamine caused an elevation in testosterone.