ArticleJournal of cardiothoracic surgery2026
Perioperative ropivacaine conditioning may attenuate myocardial ischemia-reperfusion injury via macrophage polarization.
Article in Journal of cardiothoracic surgery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLocal anesthetics exert anti-inflammatory and cytoprotective effects beyond sodium-channel blockade. Whether perioperative ropivacaine conditioning confers cardioprotection during myocardial ischemia-reperfusion (MI/R) injury remains unclear. This study investigated the cardioprotective effects of ropivacaine and its association with macrophage polarization in a rat MI/R model.
methodsMale Sprague-Dawley rats were randomly assigned to four groups (n = 8/group): Control, MI/R, MI/R + ropivacaine 1 mg/kg, and MI/R + ropivacaine 2 mg/kg. Ropivacaine or saline was administered intraperitoneally once daily for 7 days before MI/R induction. Plasma levels of myoglobin, CK-MB, and cardiac troponin I were measured to assess myocardial injury. Histopathological changes were evaluated by hematoxylin-eosin staining. Circulating M1 and M2 macrophage proportions were quantified by flow cytometry, and myocardial expression of inducible nitric oxide synthase (iNOS) and arginase-1 (Arg-1) was analyzed by Western blot.
resultsMyocardial ischemia-reperfusion markedly increased plasma myoglobin, CK-MB, and cardiac troponin I levels compared with controls (P < 0.001, 0.020, and 0.025, respectively), accompanied by severe histopathological injury characterized by disrupted myocardial fibers and inflammatory infiltration. High-dose ropivacaine (2 mg/kg), but not low-dose treatment, reduced plasma myoglobin and troponin I levels compared with untreated MI/R animals (P = 0.004 and 0.030) and improved myocardial histological appearance. MI/R also increased circulating M1 macrophage proportion and decreased M2 macrophages (P = 0.013 and 0.044), whereas high-dose ropivacaine reversed these changes (P = 0.001 and 0.040). Consistent with macrophage polarization, MI/R increased myocardial iNOS expression and reduced Arg-1 levels compared with controls (both P < 0.001), while high-dose ropivacaine decreased iNOS and increased Arg-1 expression (both P < 0.001), indicating a shift toward an anti-inflammatory phenotype.
conclusionPerioperative ropivacaine conditioning attenuates myocardial ischemia - reperfusion injury in rats, potentially through modulation of macrophage polarization toward an anti-inflammatory phenotype. These findings suggest an additional immunomodulatory mechanism of ropivacaine that may be relevant to perioperative cardio-protection.
Indexed as
Identifiers
42458522What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.