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Purpose: The glycocalyx is a glycoprotein-polysaccaride layer covering the endothelium luminal surface, and plays a key regulatory role in several endothelial functions. Lung ischemia reperfusion (IR) is a clinical entity that occurs in everyday thoracic surgery and causes glycocalix destruction and a florid local and systemic immune response. Moreover, sevoflurane is able to modulate the inflammatory response triggered by IR lung injury. In this study, we evaluated the protective effects of sevoflurane on the pulmonary endothelial glycocalyx in an in-vivo lung autotransplant model in pigs. Methods: Sixteen Large White pigs underwent pneumonectomy plus lung autotransplant. They were divided into two groups depending on the hypnotic agent received (propofol or anesthetic preconditioning with sevoflurane). Glycocalyx components (syndecan-1 and heparan sulphate), cathepsin B, chemokines (MCP-1, MIP-1, and MIP-2) and adhesion molecules (VCAM and ICAM-1) were measured at four different timepoints using porcine-specific enzyme-linked immunosorbent assay (ELISA) kits. Results: There were no differences between groups in weight or in surgical and one-lung ventilation time. Greater glycocalyx destruction and higher chemokine and adhesion molecule expression were observed in the group that did not receive sevoflurane. Heparan sulphate and serum syndecan levels were higher in the propofol group ( P < 0.0001) after reperfusion, as was cathepsin B activity ( P < 0.015). MCP-1, MIP-1, MIP-2, VCAM, and ICAM-1 levels were also higher in the propofol group ( P < 0.006). Conclusion: Sevoflurane preconditioning protects pulmonary glycocalyx and reduces expression of leukocyte chemokines in an in-vivo model of pulmonary IR. [ABSTRACT FROM AUTHOR]

This study was designed to use real-time imaging to test the hypothesis that delayed cardiac protection induced by volatile anesthetics inhibits apoptosis. Rats were divided into two groups. One group was exposed to 120 min of 33 % O [control group (CON group)] and the other group was exposed to 2.5 % sevoflurane in 33 % O for 120 min [sevoflurane group (SEVO group)]. Both groups were allowed to return to their cages for 24 h. After 24 h recovery, all rats underwent 30 min myocardial ischemia by occluding coronary artery followed by 2 h of reperfusion. After reperfusion, technetium-99m-labeled annexin-V was administered intravenously to identify apoptosis. Left ventricular samples were obtained to measure infarct size and radionuclide imaging and caspase-3. Radionuclide imaging indicated that apoptosis was reduced in SEVO group (0.78 % ± 0.82) when compared with the CON group (1.15 % ± 0.61), and the infarct size was also decreased in the SEVO group (40 % ± 7). The transferase dUTP nick end labeling (TUNEL)-positive cardiomyocytes in the SEVO group (16 % ± 6) were significantly decreased in the peri-infarct zone when compared with the CON group (28 % ± 4). After reperfusion, caspase-3 expression was significantly blunted in the SEVO group than in CON group (50 % ± 11 vs. 68 % ± 10, p < 0.05). This study used technetium-99m-labeled annexin-V of real-time imaging to detect cardiomyocyte apoptosis and the results were confirmed by the TUNEL assay and caspase-3 expression. We concluded that delayed volatile anesthetic preconditioning (APC) protects against I/R in vivo. The method of technetium-99m-labeled annexin-V of real-time imaging can be used to detect cardiomyocyte apoptosis in delayed APC during ischemia/reperfusion. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO), when produced via inducible NO synthase (iNOS) in excess under pathological conditions (e.g., inflammation, endotoxemia, and septic shock), may lead to tissue injury and organ dysfunction. The bioavailability of NO and the activity and expression of iNOS are regulated by anesthetic agents. Volatile anesthetics mostly suppress, but in some instances may upregulate, the lipopolysaccharide-and cytokine-induced expression of iNOS in blood vessels and macrophages. Intravenous anesthetics inhibit iNOS expression in macrophages and the liver. Local anesthetics decrease the production of NO by inhibiting iNOS expression in macrophages and increase NO production in glial cells. Based on the literature reported so far, the effects of anesthetics on iNOS expression and activity under conditions of inflammation are controversial, with the observed effects depending on the experimental methods and animal species used. On the other hand, it has been shown that volatile and intravenous anesthetics consistently prevent the development of multiple organ failure elicited by endotoxemia or septic shock. Information, although still insufficient, regarding the interactions between anesthetic agents and the detrimental effects of NO formed during inflammatory processes may help us to construct advanced strategies for anesthetizing and sedating patients with inflammation and sepsis and for anesthetic preconditioning against ischemic injury. [ABSTRACT FROM AUTHOR]