Matches in SemOpenAlex for { <https://semopenalex.org/work/W2078398891> ?p ?o ?g. }
Showing items 1 to 83 of
83
with 100 items per page.
- W2078398891 endingPage "1275" @default.
- W2078398891 startingPage "1272" @default.
- W2078398891 abstract "One of the major risks of coronary bypass surgery is the impact of transient ischemia-reperfusion of the myocardium inherent to the surgical technique, with or without the use of extracorporeal circulation. The ensuing reversible postoperative myocardial dysfunction, referred to as myocardial “stunning,” can have severe consequences because low cardiac output can evoke failure of other vital organs. Myocardial dysfunction necessitates pharmacological and/or mechanical support of the heart and prolongs the time in intensive care and the hospital. A metabolic strategy to protect the myocardium from the deleterious effects of ischemia and reperfusion that was suggested almost five decades ago by Dr. Sodi-Pallares is the infusion of glucose, insulin, and potassium (GIK) (1). The rationale behind this intervention was to provide the heart with an alternative metabolic substrate that requires less oxygen and to prevent arrhythmia in ischemic hearts. Indeed, the metabolic cocktail of GIK could fuel the heart with an energy-saving substrate while increasing myocardial oxygen efficiency. Shifting substrate utilization in the ischemic myocardium from predominantly free fatty acids to anaerobic glycolysis reduces oxygen consumption and can thereby protect the vulnerable (post)ischemic cardiomyocytes by optimizing the balance between oxygen supply and consumption. Increasing potassium flux into the cardiomyocytes could also reduce the risk of malignant arrhythmias. In addition to these metabolic effects of GIK, it was later shown that insulin is also a direct actor in the GIK cocktail. Via binding to the insulin receptor on cardiomyocytes and by triggering the insulin signaling cascade, intracellular survival pathways are activated that could mediate cardioprotection (2) and, in the ischemic myocardium, reduce the generation and accumulation of toxic free radicals. However, despite many studies in different experimental settings of myocardial ischemia and reperfusion, and despite valid insights into the underlying mechanisms, the definite role of GIK in clinical practice remains controversial even today, half a century after the introduction of the GIK concept by Sodi-Pallares (1, 3–5). Large clinical studies produced opposing outcomes, possibly due to variable study design and composition of GIK. Particularly GIK in high doses appeared to generate positive outcomes in randomized placebo-controlled studies of patients with acute myocardial infarction (4). But the more recent large trials (6, 7) did not confirm such a benefit of GIK therapy on cardiac mortality and morbidity. Since 2001, however, the focus of metabolic research in acute medicine shifted to the potential deleterious effects of hyperglycemia in stressed cells (8) and thereby reopened the field. The renewed interest was generated by our study of patients with critical illness treated in tertiary referral surgical intensive care (9). Sixty percent of these patients had been admitted to intensive care after complex or complicated cardiac surgery with high euroscores (9, 10). The study showed that titrating insulin infusion to prevent blood glucose exceeding the upper normal limit after the surgery and continuing during the entire stay in an intensive care unit substantially reduced morbidity and mortality, a benefit that was maintained at least up to 4 yr after surgery (10). A subsequent study confirmed the acute morbidity benefits in adult medical intensive care unit patients (11), and another extended the morbidity and mortality benefits to critically ill infants and children (12). Implementation studies also reported similar benefits (13, 14). In-depth analyses of the results suggested that the prevention of hyperglycemia, not the infusion of insulin per se, explained most of these benefits (15, 16). Studies in animal models of critical illness further unraveled this important" @default.
- W2078398891 created "2016-06-24" @default.
- W2078398891 creator A5042145557 @default.
- W2078398891 date "2011-05-01" @default.
- W2078398891 modified "2023-10-17" @default.
- W2078398891 title "Coronary Bypass Surgery: Protective Effects of Insulin or of Prevention of Hyperglycemia, or Both?" @default.
- W2078398891 cites W1511509126 @default.
- W2078398891 cites W1971685280 @default.
- W2078398891 cites W1974978275 @default.
- W2078398891 cites W1980717583 @default.
- W2078398891 cites W2022131685 @default.
- W2078398891 cites W2029436136 @default.
- W2078398891 cites W2039607936 @default.
- W2078398891 cites W2044940528 @default.
- W2078398891 cites W2046636808 @default.
- W2078398891 cites W2047760971 @default.
- W2078398891 cites W2053609044 @default.
- W2078398891 cites W2054519962 @default.
- W2078398891 cites W2073145941 @default.
- W2078398891 cites W2073519711 @default.
- W2078398891 cites W2091046505 @default.
- W2078398891 cites W2096414942 @default.
- W2078398891 cites W2102641536 @default.
- W2078398891 cites W2115285670 @default.
- W2078398891 cites W2118828771 @default.
- W2078398891 cites W2119929353 @default.
- W2078398891 cites W2122022892 @default.
- W2078398891 cites W2134369433 @default.
- W2078398891 cites W2134515711 @default.
- W2078398891 cites W2136445625 @default.
- W2078398891 cites W2136811318 @default.
- W2078398891 cites W2150481072 @default.
- W2078398891 cites W2153316233 @default.
- W2078398891 cites W2155668811 @default.
- W2078398891 cites W2163567504 @default.
- W2078398891 cites W2183831387 @default.
- W2078398891 cites W2396867810 @default.
- W2078398891 cites W303812557 @default.
- W2078398891 cites W75100703 @default.
- W2078398891 cites W1997635061 @default.
- W2078398891 doi "https://doi.org/10.1210/jc.2011-0683" @default.
- W2078398891 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21543435" @default.
- W2078398891 hasPublicationYear "2011" @default.
- W2078398891 type Work @default.
- W2078398891 sameAs 2078398891 @default.
- W2078398891 citedByCount "6" @default.
- W2078398891 countsByYear W20783988912012 @default.
- W2078398891 countsByYear W20783988912013 @default.
- W2078398891 countsByYear W20783988912014 @default.
- W2078398891 countsByYear W20783988912015 @default.
- W2078398891 crossrefType "journal-article" @default.
- W2078398891 hasAuthorship W2078398891A5042145557 @default.
- W2078398891 hasBestOaLocation W20783988911 @default.
- W2078398891 hasConcept C126322002 @default.
- W2078398891 hasConcept C134018914 @default.
- W2078398891 hasConcept C2779306644 @default.
- W2078398891 hasConcept C71924100 @default.
- W2078398891 hasConceptScore W2078398891C126322002 @default.
- W2078398891 hasConceptScore W2078398891C134018914 @default.
- W2078398891 hasConceptScore W2078398891C2779306644 @default.
- W2078398891 hasConceptScore W2078398891C71924100 @default.
- W2078398891 hasIssue "5" @default.
- W2078398891 hasLocation W20783988911 @default.
- W2078398891 hasLocation W20783988912 @default.
- W2078398891 hasOpenAccess W2078398891 @default.
- W2078398891 hasPrimaryLocation W20783988911 @default.
- W2078398891 hasRelatedWork W1983641721 @default.
- W2078398891 hasRelatedWork W1995945960 @default.
- W2078398891 hasRelatedWork W2026226896 @default.
- W2078398891 hasRelatedWork W2032033851 @default.
- W2078398891 hasRelatedWork W2041678535 @default.
- W2078398891 hasRelatedWork W2066345847 @default.
- W2078398891 hasRelatedWork W2089387278 @default.
- W2078398891 hasRelatedWork W2095179743 @default.
- W2078398891 hasRelatedWork W2124070488 @default.
- W2078398891 hasRelatedWork W2130904138 @default.
- W2078398891 hasVolume "96" @default.
- W2078398891 isParatext "false" @default.
- W2078398891 isRetracted "false" @default.
- W2078398891 magId "2078398891" @default.
- W2078398891 workType "article" @default.