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Biomedical subjects

Timothy W Evans

Publications and source records attributed to Timothy W Evans.

25 records · Page 2Linked to original sources
PubMed2003

Nutritional support in critical care.

Despite the key role of nutrition in health and the almost universal use of supplemental feeding in the ICU, there is a lack of high-quality evidence to guide clinical practice. Enteral nutrition is superior to TPN in almost all circumstances and most patients in the ICU can be fed successfully by this route. There is little evidence to support the use of special feeds and the role of immunonutrients remains unproven. Nutritional support cannot completely prevent the adverse effects of catabolic illness and overfeeding should be avoided.

Basal Metabolism↗
PubMed2003

Terminal diffuse alveolar damage in relation to interstitial pneumonias. An autopsy study.

Acute exacerbations of idiopathic pulmonary fibrosis/cryptogenic fibrosing alveolitis (IPF/CFA) are rare and typically terminal events, but their relationship to underlying patterns of idiopathic interstitial pneumonias is unknown. We reviewed autopsy material from patients who died of diffuse alveolar damage in the clinical setting of pulmonary fibrosis, both idiopathic and with background fibrosing alveolitis with connective tissue disorders (FA-CTDs), and compared them with cases of acute interstitial pneumonia. Of 15 patients with acute exacerbations of IPF/CFA (n = 12) or FA-CTD (n = 3), 12 had a background pattern of usual interstitial pneumonia and 3 had fibrotic nonspecific interstitial pneumonia. All cases of fibrotic nonspecific interstitial pneumonia were seen in association with FA-CTD. The cause of acute exacerbations is unknown, but our data suggest that toxic effects of oxygen and triggering infection are unlikely causes. In patients with CTDs, it remains uncertain whether the acute exacerbation is related to the fibrosis, the associated CTD, or a combination of these factors. Acute exacerbations of IPF/CFA may be a more common terminal event than previously thought.

Aged↗
PubMed2002

Nitric oxide supports atrial function in sepsis: relevance to side effects of inhibitors in shock.

The mechanisms underlying myocardial dysfunction in sepsis remain poorly understood. The theoretical benefits of nitric oxide synthase (NOS) inhibition in reversing the haemodynamic changes that characterise septic shock have not been supported by clinical trials, some of which have demonstrated detrimental myocardial effects. We have therefore assessed the effects of endotoxaemia on NOS enzyme expression as well as a number of functional responses of myocardial tissue from rats. Atrial tissue expressed high levels of mRNA for inducible (i) NOS and released increased levels of nitrite after animals were treated with endotoxin. In parallel, the inotropic response stimulated by isoprenaline was reduced in atria from endotoxin-treated animals, an effect that was reversed when endogenous release of NO was maximised. Our results suggest that myocardial contractility is maintained by NO production and that inhibitors may compromise cardiac output; this may explain the deleterious effects of NOS inhibition on cardiac function in clinical trials.

Animals↗
PubMed2002

Pulmonary versus extrapulmonary acute respiratory distress syndrome: different diseases or just a useful concept?

The acute respiratory distress syndrome may complicate both pulmonary and extrapulmonary conditions. There is a growing belief that the predisposition to, and clinical course of, the syndrome may be influenced by the extent to which the lung is directly involved in the precipitating pathologic changes. Several studies have highlighted differences in morphology and respiratory physiology between the two subgroups in the early stages of acute respiratory distress syndrome. Further, preliminary reports have suggested that the effects of therapeutic interventions such as alterations in positive end-expiratory pressure, prone ventilation, and the use of inhaled vasoactive agents may differ between pulmonary and extrapulmonary acute respiratory distress syndrome. There are, however, inconsistencies between various studies addressing these issues, which may relate in part to differences in etiologic case mix. There are also practical difficulties in assigning certain cases to one of these two groups. Finally, there are as yet no outcome data to support any modification of clinical management on the basis of this distinction.

Acute Disease↗
PubMed2002

Cyclooxygenase-2 acts as an endogenous brake on endothelin-1 release by human pulmonary artery smooth muscle cells: implications for pulmonary hypertension.

Endothelin-1 is a potent vasoconstrictor and comitogen for vascular smooth muscle. As such, it has been implicated in pulmonary vascular remodeling and in the development of pulmonary hypertension. Prostacyclin has been shown to be an effective therapy for human pulmonary hypertension, reducing morbidity and mortality, although the mechanism of its action is unknown. Here, we show that the combination of TNF-alpha and IFN-gamma induces the release of endothelin-1 from human pulmonary artery smooth muscle cells via increased transcription of prepro endothelin-1. The release of endothelin-1 and the transcription of prepro endothelin-1 mRNA were inhibited by the activity of coinduced cyclooxygenase-2. Endothelin-1 release was also inhibited by a prostacyclin-mimetic (cicaprost). Thus, under inflammatory conditions, in which vascular smooth muscle is an important source of endothelin-1, the induction of cyclooxygenase-2 represents an endogenous "braking" mechanism. In addition, the beneficial effects of prostacyclin in the treatment of pulmonary hypertension may be caused, at least in part, by the inhibition of endothelin-1 release. Finally, we suggest that these observations may help to explain why patients with pulmonary hypertension experience exacerbations after taking indomethacin and that the newly introduced selective cyclooxygenase-2 inhibitors may increase endothelin-1 production in susceptible patients, leading to vascular remodeling and the development of pulmonary hypertension.

Cyclic AMP↗