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Biomedical subjects

R L Harris

Publications and source records attributed to R L Harris.

At least 109 records · Page 6Linked to original sources
PubMed1972

The effects of acute and chronic morphine treatment and of morphine withdrawal on rat brain in vivo.

1. The effects of morphine, nalorphine, acetazolamide, and 10% CO(2) on brain metabolite concentrations of 24h-starved rats were studied. 2. A single dose of morphine (20mg/kg body wt.) caused an increase in brain glucose concentration (42%) and decreased concentrations of lactate (24%), pyruvate (29%), citrate (20%), alpha-oxoglutarate (16%), malate (14%) and creatine phosphate (10%) after 30min. No changes were found in adenine nucleotide concentrations. 3. The same dose of morphine increased arterial CO(2) from 5.07 to 7.60 kN/m(2) (38 to 57 Torr), decreased the pH from 7.41 to 7.31 and decreased O(2) from 14.1 to 10.8kN/m(2) (106 to 81 Torr) at 30min. 4. Rats injected with morphine three times daily (20mg/kg body wt.) for 2 weeks had no changes in brain metabolite concentrations or in blood gases 30min after their last injection. 5. Nalorphine (an antagonist of morphine) caused essentially no changes in brain metabolite concentrations in normal rats. When nalorphine (20mg/kg) was administered to rats previously treated with morphine three times daily for 2 weeks, there was an increase in brain glucose (100%), lactate (23%), pyruvate (18%) and citrate (10%) concentrations. 6. Acetazolamide (an inhibitor of carbonic anhydrase) and 10% CO(2) increased the arterial CO(2) from 4.79 to 6.78kN/m(2) (36 to 51 Torr) and from 5.32 to 10.8kN/m(2) (40 to 81 Torr) respectively. 7. Both acetazolamide and 10% CO(2) caused changes in brain metabolite concentrations similar to those for acutely administered morphine. Thus 10% CO(2) caused increased brain glucose concentration (123%) and decreased brain lactate (46%), pyruvate (34%), citrate (26%), alpha-oxoglutarate (33%), malate (45%) and creatine phosphate (7%) concentrations. No changes in adenine nucleotide concentrations were found. 8. The results indicate that the effect of morphine on brain metabolite concentrations may be accounted for by the increased [CO(2)]. 9. These findings constitute a consistent pattern of metabolic changes after acute morphine administration, morphine addiction, and withdrawal from morphine addiction.

Acetazolamide↗
PubMedDate not supplied

Periprosthetic candidal infections following arthroplasty.

Candidal infection after prosthetic arthroplasty has been reported in six previous cases, to which four cases are now added. Candida albicans was the offending organism in four patients, Candida parapsilosis in three, Candida tropicalis in two, and Candida (Torulopsis) glabrata in one. None of the 10 patients had evidence of disseminated candidiasis, and, except for the uniform presence of a prosthesis, other underlying factors that are generally associated with candidal infections were present in only three. Clinical features that distinguished periprosthetic from natural bone and joint infection included an older patient population, the usual lack of predisposing factors other than the prosthesis, and the absence of evidence of disseminated candidiasis. All patients were treated with removal of the prosthesis and antifungal therapy, consisting of amphotericin B alone (six patients) or combined with 5-fluorocytosine (three patients) or ketoconazole (one patient). Infection appeared to be cured in nine of the 10 patients, but the follow-up was less than 1 year in five cases. Replacement with a new prosthetic joint was attempted in only two cases and successful in only one. Direct inoculation of organisms during surgery or transient unrecognized candidemia may initiate periprosthetic infection, which might then be promoted by favorable local factors, both mechanical and molecular. The role of prosthetic materials, candidal adhesins, and human factors such as fibronectin in initiating these infections has yet to be characterized.

Adult↗