ArticleResuscitation plus2026
The role of insulin resistance in hyperglycemia following cardiopulmonary resuscitation in rats.
Article in Resuscitation plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: In-hospital hyperglycemia is common among patients after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). It is not clear whether insulin resistance contributes to this condition. This study investigates the changing patterns of blood glucose levels in rats after CA/CPR and the possible mechanisms of action. Methods: Twenty Sprague-Dawley (SD) rats were randomly divided into the SHAM operation group (SHAM group) and the experimental group (CA/CPR group) according to the random number table method, with 10 rats in each group. In the SHAM group, CA was not induced except for general surgeries, and intraperitoneal glucose tolerance tests (IPGTT) were conducted after the operation. CA was induced in the experimental group via asphyxiation. CPR was performed 6 min later, and intraperitoneal glucose tolerance test was conducted 10 min after the restoration of spontaneous circulation (ROSC). The blood glucose and serum insulin levels were measured at fasting, 0.5 h, 1 h, 2 h and 3 h. Area under the curve of insulin/area under the curve of glucose (AUC-insulin/AUC-glucose) was calculated for both groups to assess insulin sensitivity. Rat pancreatic tissues were taken for HE staining to observe the islet morphology and analyze the number of islet β cells. Results: Compared with the SHAM group, the fasting blood glucose in the CA/CPR group increased, and the post-glucose loading blood glucose significantly increased (all Conclusion: Rats developed hyperglycemia following CA/CPR, which was mediated by insulin resistance.
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