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The purpose of this review is to explore the parallel roles and interaction of hydrogen sulfide (H2S) and oxytocin (OT) in cardiovascular regulation and fluid homeostasis. Their interaction has been recently reported to be relevant during physical and psychological trauma. However, literature reports on H2S in physical trauma and OT in psychological trauma are abundant, whereas available information regarding H2S in psychological trauma and OT in physical trauma is much more limited. This review summarizes recent direct and indirect evidence of the interaction of the two systems and their convergence in downstream nitric oxide-dependent signaling pathways during various types of trauma, in an effort to better understand biological correlates of psychosomatic interdependencies.

Background: Sodium thiosulfate (Na 2 S 2 O 3 ) is a clinically established drug with antioxidant and sulphidereleasing properties. Na 2 S 2 O 3 mediated neuro-and cardioprotective effects in ischemia/reperfusion models and antiinflammatory effects in LPS-induced acute lung injury. Moreover, Na 2 S 2 O 3 improved lung function during resuscitation from hemorrhagic shock in swine with pre-existing atherosclerosis, characterized by decreased expression of cystathionine glyase (CSE), a major source of hydrogen sulfide (H 2 S) synthesis in the vasculature. Based on these findings, we investigated the effects of Na 2 S 2 O 3 administration during resuscitation from trauma-and-hemorrhage in mice under conditions of whole body CSE deficit. Methods: After blast wave-induced blunt chest trauma and surgical instrumentation, CSE knockout (CSE -/-) mice underwent 1 h of hemorrhagic shock (MAP 35 AE 5 mm Hg). At the beginning of resuscitation comprising retransfusion, norepinephrine support and lung-protective mechanical ventilation, animals received either i.v. Na 2 S 2 O 3 (0.45 mg g À1 , n ¼ 12) or vehicle (saline, n ¼ 13). Hemodynamics, acid-base status, metabolism using stable isotopes, and visceral organ function were assessed. Blood and organs were collected for analysis of cytokines, mitochondrial respiratory capacity, and immunoblotting. Results: Na 2 S 2 O 3 treatment improved arterial paO 2 (P ¼ 0.03) coinciding with higher lung tissue glucocorticoid receptor expression. Norepinephrine requirements were lower in the Na 2 S 2 O 3 group (P < 0.05), which was associated with lower endogenous glucose production and higher urine output. Na 2 S 2 O 3 significantly increased renal tissue IkBa and heme oxygenase-1 expression, whereas it lowered kidney IL-6 and MCP-1 levels. Conclusion: Na 2 S 2 O 3 exerted beneficial effects during resuscitation of murine trauma-and-hemorrhage in CSE -/mice, confirming and extending the previously described organ-protective and anti-inflammatory properties of Na 2 S 2 O 3 . The findings make Na 2 S 2 O 3 a potentially promising therapeutic option in the context of impaired CSE activity and/or reduced endogenous H 2 S availability.