Due to the physiologic effects of arsenic on all body systems, the chronic arsenic-poisoned patient is a major nursing challenge. The critical care nurse provides valuable assessment and interventions that prevent major multisystem complications from arsenic toxicity.

Adult↗

PubMedDate not supplied

Assessment of clinical decision-making ability of critical care nurses.

What are nurse administrators to do when their institution is in need of competent nurses to staff the ICU and the majority of applicants are either inexperienced or new graduates? Nurses from one institution grappled with this question. They decided that it was their job to teach novice nurses to make sound clinical judgments in life-threatening situations. As part of this process, they developed a Clinical Decision-Making Assessment (CDMA) tool. This article describes the CDMA and provides suggestions for classroom and clinical teaching.

Adult↗

PubMedDate not supplied

Effects of antioxidants apocynin and the natural water-soluble antioxidant from spinach on cellular damage induced by lipopolysaccaride in the rat.

Oxidative damage plays a key role in septic shock induced by the endotoxin lipopolysaccaride (LPS) by enhancing the formation of reactive oxygen species such as superoxide anion radicals, peroxides, and their secondary product, malondialdehyde, especially in the liver. In this study, histopathologic changes in several organs were compared among groups of male Wistar rats that had been injected with LPS following prophylactic pretreatment with either of 2 antioxidants, a group that had been injected with LPS without pretreatment with antioxidants, an untreated control group, and groups that had been injected with either of the 2 antioxidants only. The antioxidants used were a water-soluble natural antioxidant from spinach (NAO) and the NADPH oxidase inhibitor apocynin. Hematoxylin-and-eosin-stained slides were prepared, and lesions were semiquantitatively scored. Exposure to LPS alone was associated with multifocal hepatocellular necrosis and acute inflammation, thymic and splenic lymphoid necrosis, ocular retinal hemorrhage and acute endophthalmitis, adrenal medullary vacuolation and necrosis and acute inflammation, and decreased adrenal cortical cytoplasmic vacuolation (consistent with depletion of steroidal hormone contents). Results indicated that pretreatment with both antioxidants for 8 days reduced, in some organs, the necrotic and inflammatory changes associated with the LPS challenge. These findings suggest a potential therapeutic application for these antioxidants in clinical sepsis.

Acetophenones↗

PubMedDate not supplied

The prophylactic effects of natural water-soluble antioxidant from spinach and apocynin in a rabbit model of lipopolysaccharide-induced endotoxemia.

Radical-scavenging antioxidants, as part of the cellular defense system, function to inhibit the formation and propagation of free radicals and active oxygen species formation. In previous studies we demonstrated that endotoxin lipopolysaccharide (LPS) promotes oxidative stress and associated pathological changes in a rat model and that use of selected antioxidants was effective in reducing LPS-related lipid peroxidation product formation in the liver, as well as LPS-related pathological changes in different organs. In this study, several toxicological parameters (ie, clinical signs, blood chemistry, and histopathological changes) were compared among groups of male New Zealand rabbits injected with LPS following prophylactic pretreatment with either of 2 antioxidants, a group injected with LPS without pretreatment with antioxidants, groups injected with either of the 2 antioxidants only, and an untreated control group. The antioxidants used were a water-soluble natural antioxidant (NAO) from spinach and the NADPH oxidase inhibitor, apocynin. Exposure to LPS alone was associated clinically with depression, tachypnea, outer ear vasodilation, and iris congestion; biochemically with a significant increase in blood total bilirubin, transaminase activity, and glucose, total cholesterol, and triglyceride levels; macroscopically with multiple whitish areas in the liver; and histologically with hepatocellular focal necrosis and acute inflammation, thymic and splenic lymphoid necrosis and depletion, acute uveitis and hemorrhages in the ciliary processes, and decreased adrenal cortical cytoplasmic vacuolation considered consistent with depletion of steroidal hormone contents. The NAO had more effective prophylactic capacities than the apocynin. The protective effects were obvious in all investigated parameters. The results indicate the possible therapeutic efficacy of NAO in the treatment of clinical endotoxemia associated with gram-negative bacterial sepsis that is known to be associated with oxidative stress.

Acetophenones↗

PubMedDate not supplied

Evidence against oxidant injury and endotoxin underlying glycerol-induced fatal rhabdomyolysis in rats.

Rhabdomyolysis in experimental animals and in man may be fatal. The mechanism of action causing death in man and in the experimental model of laboratory animals injected with glycerol in a dose causing fatal rhabdomyolysis is unknown. The aim of this study was to examine two possible causes of death following glycerol injection (0.5-2 ml/100 g) to the leg muscle of rats following a period of water deprivation (24-72 h). The first factor examined was free radical formation, via the administration of various antioxidants such as natural antioxidant (NAO - 5 mg/100 g), vitamin E (0.2 mg/100 g each day for 7 days), dimethylthiourea (DMTU - 50 mg/100 g) and superoxide dismutase (SOD - 0.8 mg/100 g). The second factor was a high blood endotoxin level due to the glycerol injection. This possibility was examined by glycerol injection to rats that had developed endotoxin tolerance. The low survival rate (0-30%) of rats receiving a glycerol injection following preventive treatment with antioxidants as well as rats which had developed endotoxin tolerance (0-40%), excludes the possibility that the cause of death in the glycerol model resulting in fatal rhabdomyolysis is due to free radical formation or to a high and unneutralized blood level of endotoxin.

Animals↗