Cancer constitutes a significant contributor to global morbidity and mortality rates. The stress triggered by surgical procedures leads to a systemic impact involving immune system suppression, inflammation, ischemia-reperfusion injury (IRI), activation of the sympathetic nervous system, and heightened cytokine release. This, in turn, substantially elevates the risk of cancer recurrence.  Surgical interventions incite inflammation through various means, such as wound formation and infection, which result in the release of numerous inflammatory agents and the recruitment of various immune cell types, particularly monocytes and neutrophils. Consequently, it becomes imperative to employ strategies during the perioperative phase to regulate surgical stress and inflammation, potentially mitigating postoperative complications and enhancing clinical outcomes. Even under the expertise of seasoned surgeons, tumor cells inevitably disseminate into the bloodstream and lymphatic circulations during surgical resection. The destiny of this minute cluster of tumor cells hinges on the equilibrium between anti-metastatic factors and the tumor’s capacity to invade, proliferate, and metastasize.

Angiogenesis, the process by which a cancerous tumor establishes its blood supply from the host, becomes crucial as the tumor surpasses a certain size threshold. Cancer responses driven by angiogenic mediators encompass vascular endothelial growth factor (VEGF), fibroblast growth factor acidic (aFGF), fibroblast growth factor basic (bFGF), placental growth factor, and transforming growth factor. VEGF typically facilitates new blood vessel formation post-injury to promote collateral circulation. Hypoxia-inducible factor (HIF) triggers VEGF production in hypoxic cells. The circulatory VEGF then binds to endothelial cell VEGF receptors, thereby inducing angiogenesis.

Numerous intravenous and inhaled anesthetics play a pivotal role in modulating immune and inflammatory functions by interacting with multiple receptors and ion channels on leukocytes. Propofol, functioning as a GABA receptor agonist, hampers several functions of innate immune system monocytes and neutrophils, including chemotaxis and phagocytosis. Additionally, Propofol exhibits anti-inflammatory and antioxidative effects, safeguarding against perioperative immune suppression. Inhalational anesthetics exert inhibitory effects on neutrophil function, reduce lymphocyte proliferation, and suppress cytokine release from peripheral blood mononuclear cells. Isoflurane exposure results in decreased leukocyte counts and systemic levels of proinflammatory cytokines (TNF-α, IL-6, and IL-1β), suggesting a systemic anti-inflammatory influence from volatile anesthetics. However, the precise role of this effect remains unclear.

Lidocaine, an amide-based local anesthetic, is employed both as a local anesthetic and intravenous infusion for its analgesic and anti-inflammatory properties. Recent studies have unveiled specific anti-cancer attributes of lidocaine, manifesting through interference with cancer cell viability, migration, and apoptosis.

This study aims to juxtapose the impact of anesthesia mode on perioperative immunosuppression and angiogenesis in ovarian cancer patients. Given the limited existing evidence concerning these perioperative phenomena and anesthesia modes, the study was conceived to address this gap in knowledge.