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L P Parmer

Publications and source records attributed to L P Parmer.

4 recordsLinked to original sources
PubMed1987

A peroxide-induced inflammation model for drug testing.

Peroxide-induced cellular injury is an important mediator of inflammation. Whether the injection of glucose oxidase (GO) with its generation of H2O2 may be utilized as an inflammatory model was studied. Anesthesized mice were injected in the right hind foot with either water or an equal volume of 10 or 100 units/ml GO. The animals were sacrificed at 1.5 or 24 hours post injection and both hind feet amputated and each foot weighed. Difference in weights for each animal's feet was called edema index (EI). GO produced significant increases in weight. The use of GO to produce inflammation may be useful in testing potential peroxide quenching agents.

Animals↗
PubMed1980

Protective effect of a splenic factor in mice with burns.

We have previously described the protective effect of a lipoidal splenic factor (SF) against lethal endotoxemia in mice. Since this protective effect is also accompanied by significant antithrombotic changes, and since burn injury causes thrombosis and consumptive coagulopathy, it was postulated that SF decreased the severity of the burn wound. Swiss white mice were anesthetized with pentobarbital sodium and then burned on a depilated area of the lower back with a 2-cm diameter stainless steel weight at 95 degrees for 10 sec. SF (10 mg/kg) (n = 20) or an equal volume of saline (controls) (n = 13) was administered within 1 hour after thermal injury. Severity of burn injury was assessed by examination of hematoxylin and eosin-stained biopsies obtained 24 hours postburn by a grading scale of 0 (normal) to 4 (severe) depending on the degree of epidermal loss, coagulation necrosis, and inflammatory cell infiltrate. Average degree of burn severity was 1.10 +/- 0.20 for SF recipients and 2.85 +/- 0.27 for the controls (p less than 0.001).

Animals↗
PubMed1980

Protective effect of a splenic extract in mice with endotoxemia.

We have previously described the isolation of a lipoidal splenic extract (LSE) that demonstrated a variety of hematologic effects including inhibition of platelet aggregation both in vivo and in vitro. Since endotoxin causes platelet aggregation and microembolism the protective effect of LSE in endotoxemia was examined in the present study. Both young and elderly Swiss mice given LSE 2--3 hours before endotoxin challenge showed a statistically significant increase in survival compared with saline-treated controls. However, no significant improvement in survival was noted when LSE was administered at the same time as endotoxin. These results add further support to the role of the spleen in the control of infection.

Animals↗