Background and Objectives: This is the first study to examine the role of monocyte distribution width (MDW) in predicting sepsis after cardiovascular surgery. Methods: This study included 43 consecutive patients who had undergone cardiovascular surgery between July 2021 and July 2022. All patients were examined at the following three time points (TPs): preoperative period (TP1), postoperative at 24 h (TP2), and discharge (TP3). SOFA score, leukocyte count, neutrophil-to-lymphocyte ratio (NLR), MDW, C-reactive protein (CRP), and procalcitonin (PCT) levels were tested at each TPs. The Sepsis-3 criteria were used to diagnose patients with sepsis. Results: The mean values of all variables (leukocyte count, NLR, MDW, CRP, and PCT levels) were significantly higher at TP2 and TP3 than at TP1 (p < 0.05). All these values were significantly higher at TP2 than at TP3 (p < 0.05). Patients with sepsis had significantly higher mean values for leukocyte count, NLR, MDW, CRP, and PCT levels than those without sepsis (p < 0.05). There was a significant correlation between MDW and inflammatory markers (CRP, PCT, and NLR) during the three time periods (p < 0.05). According to the ROC analysis, the optimal MDW cutoff value with the highest sensitivity and specificity for predicting sepsis in the postoperative period was 20.5. Conclusions: Our findings indicate that elevated MDW levels may be a valuable predictor of sepsis in patients following cardiovascular surgery.

Ischemia–reperfusion injury (IRI) is a clinically important consequence of blood-flow restoration after ischemia and contributes to tissue damage across multiple organ systems. This critical review evaluates the preclinical evidence for BPC 157 in rodent IRI and related reperfusion-associated vascular injury models, with particular attention to oxidative stress, endothelial and nitric oxide (NO)-related responses, inflammation, apoptosis, angiogenic signaling, and tissue injury. Searches were performed up to 24 June 2026 across PubMed/MEDLINE, Web of Science Core Collection, Scopus, PMC, publisher/DOI metadata, ClinicalTrials.gov, FDA materials, and WADA materials. Peer-reviewed rodent studies involving conventional organ-specific IRI or reperfusion-associated systemic injury were evaluated as the core IRI/reperfusion evidence according to the experimental model, BPC 157 dose, route and timing, measured outcomes, and methodological limitations, while selected major-vessel occlusion models were considered separately as related in vivo vascular evidence. Endothelial, vascular-ring, human ex vivo, and regulatory/clinical sources were used as contextual evidence rather than as evidence of IRI efficacy. Meta-analysis was not performed because of substantial heterogeneity in organ systems, injury paradigms, doses, routes, treatment timing, and outcome measures. Across the available rodent literature, BPC 157 administration has been associated with attenuation of oxidative injury, modulation of NO-related vascular responses, reductions in inflammatory and apoptotic markers, and changes in VEGF/VEGFR2–Akt–eNOS-related signaling. Organ-specific findings include biochemical, molecular, and histological protection in lower-extremity skeletal-muscle IRI; attenuation of distant-organ injury following limb IRI; neuronal and functional effects in hippocampal IRI; vascular and tissue-protective responses in intestinal/colonic IRI; and hemodynamic and histological effects in hepatic Pringle-maneuver IRI. However, the evidence base remains heterogeneous and frequently relies on short observation periods, single-dose paradigms, and incompletely characterized risk-of-bias domains. Reperfusion-like systemic and major-vessel occlusion models provide additional mechanistic context but should not be considered equivalent to conventional organ-specific IRI. Current evidence therefore supports BPC 157 as a hypothesis-generating investigational candidate for further preclinical IRI research rather than as an established therapy. Independent blinded replication, dose–response and therapeutic-window studies, pharmacokinetic/pharmacodynamic characterization, rigorous toxicology, and ultimately controlled human studies would be required before clinical translation could be considered.