ArticleAnesthesiology2011
Effects of glycemic regulation on chronic postischemia pain.
Article in Anesthesiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- The Relationship Between Pre-Operative Glycosylated Haemoglobin and Opioid Consumption After Caesarean Section in Women With Gestational Diabetes Mellitus.Frontiers in endocrinology · 2022Observational
- Animal Models of Complex Regional Pain Syndrome Type I.Journal of pain research · 2021Review
- Laboratory environmental factors and pain behavior: the relevance of unknown unknowns to reproducibility and translation.Lab animal · 2017Article
- Glycemia-dependent nuclear factor κB activation contributes to mechanical allodynia in rats with chronic postischemia pain.Anesthesiology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundIschemia-reperfusion (I/R) injuries consist of enhanced oxidative and inflammatory responses along with microvascular dysfunction after prolonged ischemia and reperfusion. Because I/R injuries induce chronic postischemia pain (CPIP) in laboratory animals, it is possible that surgical procedures using prolonged ischemia may result in chronic postoperative pain. Glycemic modulation during ischemia and reperfusion could affect pain after I/R injury because glucose triggers oxidative, inflammatory, and thrombotic reactions, whereas insulin has antioxidative, antiinflammatory, and vasodilatory properties.
methodsOne hundred ten rats underwent a 3-h period of ischemia followed by reperfusion to produce CPIP. Rats with CPIP had previously been divided into six groups with differing glycemic modulation paradigms: normal feeding; fasting; fasting with normal saline administration; fasting with dextrose administration; normal feeding with insulin administration; and normal feeding with insulin and dextrose administration. Blood glucose concentration was assessed during I/R in these separate groups of rats, and these rats were tested for mechanical and cold allodynia over the 21 days afterward (on days 2, 5, 7, 9, 12, and 21 after I/R injury).
resultsI/R injury in rats with normoglycemia or relative hyperglycemia (normal feeding and fasting with dextrose administration groups) led to significant mechanical and cold allodynia; conversely, relative hypoglycemia associated with insulin treatment or fasting (fasting, fasting with normal saline administration, and normal feeding with insulin administration groups) reduced allodynia induced by I/R injury. Importantly, insulin treatment did not reduce allodynia when administered to fed rats given dextrose (normal feeding with dextrose and insulin administration group).
conclusionStudy results suggest that glucose levels at the time of I/R injury significantly modulate postinjury pain thresholds in rats with CPIP. Strict glycemic control during I/R injury significantly reduces CPIP and, conversely, hyperglycemia significantly enhances it, which could have potential clinical applications especially in the surgical field.
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Registered trials
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