Dynamic Indices Fail to Predict Fluid Responsiveness in Patients Undergoing One-Lung Ventilation for Thoracoscopic Surgery.

Thoracic surgery using CO2 insufflation maintains closed-chest one-lung ventilation (OLV) that may provide the necessary heart-lung interaction for the dynamic indices to predict fluid responsiveness. We studied whether pulse pressure variation (PPV) and stroke volume variation (SVV) can predict fluid responsiveness during thoracoscopic surgery. Forty patients were enrolled in the study. OLV was performed with a tidal volume of 6 mL/kg at a positive end-expiratory pressure of 5 cm H2O, while CO2 was insufflated to the contralateral side at 8 mm Hg. Patients whose stroke volume index (SVI) increased ≥15% after fluid challenge (7 mL/kg) were defined as fluid responders. The predictive ability of PPV and SVV on fluid responsiveness was investigated using the area under the receiver-operator characteristic curve (AUROC), which was also assessed according to the right or left lateral decubitus position considering the intrathoracic location of the right-sided superior vena cava. AUROCs of PPV and SVV for predicting fluid responsiveness were 0.65 (95% confidence interval 0.47-0.83, p = 0.113) and 0.64 (95% confidence interval 0.45-0.82, p = 0.147), respectively. The AUROCs of indices did not exhibit any statistical significance according to position. Dynamic indices of preload cannot predict fluid responsiveness during one-lung ventilation with CO2 gas insufflation.

Overexpressed p32 localized in the endoplasmic reticulum and mitochondria negatively regulates calcium­dependent endothelial nitric oxide synthase activit.

The p32 protein plays a crucial role in the regulation of cytosolic Ca2+ concentrations ([Ca2+]c) that contributes to the Ca2+­dependent signaling cascade. Using an adenovirus and plasmid p32­overexpression system, the aim of the study was to evaluate the role of p32 in the regulation of [Ca2+] and its potential associated with Ca2+­dependent endothelial nitric oxide synthase (eNOS) activation in endothelial cells. Using electron and confocal microscopic analysis, p32 overexpression was observed to be localized to mitochondria and the endoplasmic reticulum and played an important role in Ca2+ translocation, resulting in increased [Ca2+] in these organelles and reducing cytosolic [Ca2+] ([Ca2+]c). This decreased [Ca2+]c following p32 overexpression attenuated the Ca2+­dependent signaling cascade of calcium/calmodulin dependent protein kinase II (CaMKII)/AKT/eNOS phosphorylation. Moreover, in aortic endothelia of wild­type mice intravenously administered adenovirus encoding the p32 gene, increased p32 levels reduced NO production and accelerated reactive oxygen species (ROS) generation. In a vascular tension assay, p32 overexpression decreased acetylcholine (Ach)­induced vasorelaxation and augmented phenylephrine (PE)­dependent vasoconstriction. Notably, decreased levels of arginase II (ArgII) protein using siArgII were associated with downregulation of overexpressed p32 protein, which contributed to CaMKII­dependent eNOS phosphorylation at Ser1177. These results indicated that increased protein levels of p32 caused endothelial dysfunction through attenuation of the Ca2+­dependent signaling cascade and that ArgII protein participated in the stability of p32. Therefore, p32 may be a novel target for the treatment of vascular diseases associated with endothelial disorders.

Korean red ginseng water extract restores impaired endothelial function by inhibiting arginase activity in aged mice.

Cardiovascular disease is the prime cause of morbidity and mortality and the population ages that may contribute to increase in the occurrence of cardiovascular disease. Arginase upregulation is associated with impaired endothelial function in aged vascular system and thus may contribute to cardiovascular disease. According to recent research, Korean Red Ginseng water extract (KRGE) may reduce cardiovascular disease risk by improving vascular system health. The purpose of this study was to examine mechanisms contributing to age-related vascular endothelial dysfunction and to determine whether KRGE improves these functions in aged mice. Young (10±3 weeks) and aged (55±5 weeks) male mice (C57BL/6J) were orally administered 0, 10, or 20 mg/mouse/day of KRGE for 4 weeks. Animals were sacrificed and the aortas were removed. Endothelial arginase activity, nitric oxide (NO) generation and reactive oxygen species (ROS) production, endothelial nitric oxide synthase (eNOS) coupling, vascular tension, and plasma peroxynitrite production were measured. KRGE attenuated arginase activity, restored nitric oxide (NO) generation, reduced ROS production, and enhanced eNOS coupling in aged mice. KRGE also improved vascular tension in aged vessels, as indicated by increased acetylcholine-induced vasorelaxation and improved phenylephrine-stimulated vasoconstriction. Furthermore, KRGE prevented plasma peroxynitrite formation in aged mice, indicating reduced lipid peroxidation. These results suggest KRGE exerts vasoprotective effects by inhibiting arginase activity and augmenting NO signaling and may be a useful treatment for age-dependent vascular diseases.

Stress-induced cardiomyopathy after general anesthesia for total gastrectomy -A case report-.

Stress-induced cardiomyopathy, which is also known as takotsubo cardiomyopathy, is a cardiac syndrome of a transient, reversible left ventricular dysfunction that is caused by emotional and/or physical stress and surgery. Its clinical manifestations are similar to those of myocardial ischemia without a coronary artery lesion. Stress-induced cardiomyopathy is more common in middle-aged women, and the prognosis is favorable. We report the case of a 50-year-old female patient who underwent a total gastrectomy and developed stress-induced cardiomyopathy after surgery.