Lung protection effect of EIT-based individualized protective ventilation strategy in patients with partial pulmonary resection.

OBJECTIVE: This study aimed to evaluate the lung protection effect of an individualized protective ventilation strategy based on lung impedance tomography (EIT) technology in patients with partial pulmonary resection. PATIENTS AND METHODS: Eighty patients of any gender, American Society of Anesthesiologists (ASA) classification I-II, age 30-64 years and body mass index (BMI) 18-28 kg/m2 who underwent elective thoracoscopic partial lung resection were selected and divided into 2 groups (n=40) using the random number table method: [positive end-expiratory pressure (PEEP) by electrical impedance tomography (EIT)] PEEPEIT group (experimental group) and control group. The PEEPEIT group used volume-controlled ventilation after one-lung ventilation, setting a tidal volume of 6 ml/kg and titrating the optimal PEEP value by EIT. Group C used volume-controlled ventilation after one-lung ventilation, setting a tidal volume of 6 ml/kg and a PEEP of 5 cm H2O. Clinical data were collected and recorded at 5 min after double lung ventilation (T0), single lung ventilation, 30 min after PEEP setting (T1), 60 min after PEEP setting (T2), the end of surgery, 10 min after resumption of double lung ventilation (T3) and 10 min after removal of the tracheal tube (T4), and serum surface active substance-associated protein-A (SP-A) concentrations were measured at T0, T3 and 1 d after surgery (T5). RESULTS: PEEP values were higher in the PEEPEIT group than in the control group at T1 and T2 (p-value <0.05); oxygenation index (OI) was higher in the PEEPEIT group compared to the control group at T2 and T3 (p-value <0.05); pulmonary dynamic compliance (Cdyn) was higher in the PEEPEIT group compared to the control group at T1 and T2 (p-value <0.05); intrapulmonary shunt rate (Qs/Qt) was lower in the PEEPEIT group compared to the control group at T1, T2 and at T3, the intrapulmonary shunt rate (Qs/Qt) was reduced in the PEEPEIT group compared to group C (p-value <0.05); at T5, the SP-A protein was reduced in the PEEPEIT group compared to group C. There was no statistically significant difference in the incidence of postoperative pulmonary complications between the two groups (p-value >0.05). CONCLUSIONS: The EIT-guided individualized protective ventilation strategy has a lung-protective effect in patients undergoing thoracoscopic partial lung resection.

Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-ε in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-preconditioned rats

This study aimed to determine the role of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels and protein kinase C (PKC)-ε in the delayed protective effects of sevoflurane preconditioning using Langendorff isolated heart perfusion models. Fifty-four isolated perfused rat hearts were randomly divided into 6 groups (n=9). The rats were exposed for 60 min to 2.5% sevoflurane (the second window of protection group, SWOP group) or 33% oxygen inhalation (I/R group) 24 h before coronary occlusion. The control group (CON) and the sevoflurane group (SEVO) group were exposed to 33% oxygen and 2.5% sevoflurane for 60 min, respectively, without coronary occlusion. The mitoKATP channel inhibitor 5-hydroxydecanoate (5-HD) was given 30 min before sevoflurane preconditioning (5-HD+SWOP group). Cardiac function indices, infarct sizes, serum cardiac troponin I (cTnI) concentrations, and the expression levels of phosphorylated PKC-ε (p-PKC-ε) and caspase-8 were measured. Cardiac function was unchanged, p-PKC-ε expression was upregulated, caspase-8 expression was downregulated, cTnI concentrations were decreased, and the infarcts were significantly smaller (P<0.05) in the SWOP group compared with the I/R group. Cardiac function was worse, p-PKC-ε expression was downregulated, caspase-8 expression was upregulated, cTnI concentration was increased and infarcts were larger in the 5-HD+SWOP group (P<0.05) compared with the SWOP group. The results suggest that mitoKATP channels are involved in the myocardial protective effects of sevoflurane in preconditioning against I/R injury, by regulating PKC-ε phosphorylation before ischemia, and by downregulating caspase-8 during reperfusion.

Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-ε in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-preconditioned rats.

This study aimed to determine the role of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels and protein kinase C (PKC)-ε in the delayed protective effects of sevoflurane preconditioning using Langendorff isolated heart perfusion models. Fifty-four isolated perfused rat hearts were randomly divided into 6 groups (n=9). The rats were exposed for 60 min to 2.5% sevoflurane (the second window of protection group, SWOP group) or 33% oxygen inhalation (I/R group) 24 h before coronary occlusion. The control group (CON) and the sevoflurane group (SEVO) group were exposed to 33% oxygen and 2.5% sevoflurane for 60 min, respectively, without coronary occlusion. The mitoKATP channel inhibitor 5-hydroxydecanoate (5-HD) was given 30 min before sevoflurane preconditioning (5-HD+SWOP group). Cardiac function indices, infarct sizes, serum cardiac troponin I (cTnI) concentrations, and the expression levels of phosphorylated PKC-ε (p-PKC-ε) and caspase-8 were measured. Cardiac function was unchanged, p-PKC-ε expression was upregulated, caspase-8 expression was downregulated, cTnI concentrations were decreased, and the infarcts were significantly smaller (P<0.05) in the SWOP group compared with the I/R group. Cardiac function was worse, p-PKC-ε expression was downregulated, caspase-8 expression was upregulated, cTnI concentration was increased and infarcts were larger in the 5-HD+SWOP group (P<0.05) compared with the SWOP group. The results suggest that mitoKATP channels are involved in the myocardial protective effects of sevoflurane in preconditioning against I/R injury, by regulating PKC-ε phosphorylation before ischemia, and by downregulating caspase-8 during reperfusion.