[Comparison of pulse pressure variation, stroke volume variation, and plethysmographic variability index in pediatric patients undergoing craniotomy].

OBJECTIVE: To compare well-known preload dynamic parameters intraoperatively including stroke volume variation (SVV), pulse pressure variation (PPV), and plethysmographic variability index (PVI) in children who underwent craniotomy for epileptogenic lesion excision. METHODS: A total of 30 children aged 0 to 14 years undergoing craniotomy for intracranial epileptogenic lesion excision were enrolled. During surgery, we measured PPV, SVV (measured by the Flotrac/Vigileo device), and PVI (measured by the Masimo Radical-7 monitor) simultaneously and continuously. Preload dynamic parameter measurements were collected at predefined steps: after induction of anesthesia, during opening the skull, intraoperative electroencephalogram monitoring, excision of epileptogenic lesion, skull closure, at the end of the operation. After exclusion of outliers, agreement among SVV, PPV, and PVI was assessed using repeated measures of Bland-Altman approach. The 4-quadrant and polar plot techniques were used to assess the trending ability among the changes in the three parameters. RESULTS: The mean SVV, PPV, and PVI were 8%±2%, 10%±3%, and 15%±7%, respectively during surgery. We analyzed a total of 834 paired measurements (3 to 8 data sets for each phase per patient). Repeated measures Bland-Altman analysis identified a bias of -2.3 and 95% confidence intervals between -1.9 and -2.7 (95% limits of agreement between -6.0 and 1.5) between PPV and SVV, showing significant correlation at all periods. The bias between PPV and PVI was -5.0 with 95% limits of agreement between -20.5 and 10.5, and that between SVV and PVI was -7.5 with 95% limits of agreement between -22.7 and 7.8, both not showing significant correlation. Reflected by 4-quadrant plots, the con-cordance rates showing the trending ability between the changes in PPV and SVV, PPV and PVI, SVV and PVI were 88.6%, 50.4%, and 50.1%, respectively. The concordance rate between PPV and SVV was higher (92.7%) in children aged less than 3 years compared with those aged 3 and more than 3 years. The mean angular bias, radial limits of agreement, and angular concordance rate in the polar analysis were not clinically acceptable in the changes between arterial pressure waveform-based parameters and volume-based PVI (PPV vs. PVI: angular mean bias 8.4°, angular concordance rate 29.9%; SVV vs. PVI: angular mean bias 2.4°, angular concordance rate 29.1%). There was a high concordance between the two arterial pressure waveform-based parameters reflected by the polar plot (angular mean bias -0.22°, angular concordance rate 86.6%). CONCLUSION: PPV can be viewed as a surrogate for SVV, especially in children aged less than 3 years. The agreement between arterial pressure waveform-based preload parameters (PPV and SVV) and PVI is poor and these two should not be considered interchangeable. Attempt to combine PVI and PPV for improving the anesthesiologist's ability to monitor cardiac preload in major pediatric surgery is warranted.

The apoptosis in arsenic-induced oxidative stress is associated with autophagy in the testis tissues of chicken.

The aim of this study is to investigate whether arsenic (As) could induce testicular poisoning and influence the oxidative stress, apoptosis and autophagy in chickens. Seventy-two 1-day-old male Hy-line chickens were divided into 4 groups which were exposed to 0, 0.625, 1.25, and 2.5 mg/kg body weight (BW) of arsenic trioxide (As2O3) for 30, 60 and 90 days, respectively. Histological and ultrastructural changes, antioxidant enzyme activity, mRNA and protein levels of apoptosis and autophagy-related genes were detected. Oxidative stress injuries were obvious in the testes exposure to As2O3, which resulted in the decreased activities of antioxidant enzymes, such as catalase (CAT) and superoxide dismutases (SOD). Meanwhile, the changes of mRNA and protein levels of apoptosis and autophagy-related genes showed that As2O3 exposure induced enhanced testicular apoptosis and increased the levels of autophagy markers such as Microtubule associated protein light chains 3-II (LC3-II), dynein, Beclin-1, Autophagy associated gene 5 (ATG5) and ATG4B but not LC3-I and mammalian target of rapamycin (mTOR), and demonstrated the cross-talk between apoptosis and autophagy. Histological and ultrastructural abnormalities confirm the changes of the above indicators. Taken together, our findings provide deeper insights into roles of excessive apoptosis and autophagy in the aggravation of testicular damage, which could contribute to a better understanding of As2O3-induced testicular poisoning in chickens.