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PubMed · 11242740

Altered cardiac function.

Abstract

An understanding of the normal functioning of the heart and how it fails is important since it allows rational treatment. Pre-existing cardiac disease and myocardial dysfunction is common in the surgical patient. Moreover, the stress response of surgery and the alterations in body physiology seen in the post-operative period may further aggrivate any cardiac compromise. The end result may be a patient who has cold peripheries due to vasoconstriction and hypoperfusion with dyspnoea due to congested lungs and a heart that cannot function adequately. The postoperative patient is at risk of these changes because of the stress response, analgesic therapy, inappropriate fluid management, hypoxia and previous cardiac compromise. The patient with sepsis is at further risk because of alterations in both systolic and diastolic function, which may be the result of inadequate fluid resuscitation and also release of a variety of inflammatory mediators. Until treatments, which are aimed at correcting the effects of these mediators, are proven to be beneficial then the septic patient will continue to be managed according to the physiological principles as outlined by Starling.

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BibTeXRIS

L Steele, N R Webster. 2001. Altered cardiac function.. https://pubmed.ncbi.nlm.nih.gov/11242740/

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We investigated whether insulin resistance in patients with chronic heart failure (CHF) is associated with impaired insulin signalling in skeletal muscle and whether exercise training would lead to an improvement in insulin signalling, concomitant with enhanced insulin action. Fourteen men with CHF due to idiopathic dilated cardiomyopathy, with mild-to-moderate limitation of physical activity and a left-ventricular ejection fraction of less than 45 %, were studied before and after either a 5 month exercise training programme (n = 7) or standard care (n = 7). Seven healthy men participated as controls. Whole-body insulin-stimulated glucose uptake was determined by the euglycaemic hyperinsulinaemic clamp technique and skeletal muscle biopsy samples were obtained before and after the insulin infusion for insulin signalling measurements. Insulin-stimulated glucose uptake was 20 % lower in CHF patients versus healthy subjects. Physiological hyperinsulinaemia increased tyrosine phosphorylation of insulin receptor substrate (IRS)-1 by approximately 2.5-fold, IRS-1-associated phosphatidylinositol 3-kinase (PI-3-kinase) activity by approximately 2-fold and Akt (protein kinase B) phosphorylation by approximately 3-fold, with similar responses between healthy subjects and CHF patients. Insulin-mediated glucose uptake was not altered in patients after standard care, whereas exercise training elicited a 25 % increase in glucose uptake. Neither standard care nor exercise training altered insulin-stimulated tyrosine phosphorylation of IRS-1, IRS-1-associated PI-3-kinase activity or Akt phosphorylation. In conclusion, the CHF patients demonstrated impaired insulin-stimulated glucose uptake, despite normal signal transduction in skeletal muscle at the level of IRS-1, PI-3-kinase and Akt. Of clinical relevance is the finding that exercise training improves glucose uptake. However, these changes in insulin action after exercise training appear to be independent of enhanced insulin signalling at the level of IRS-1, PI-3-kinase or Akt.

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