The Ohio State University Wexner Medical Center
ORCID: 0000-0003-0715-4347Publishes on Aortic Disease and Treatment Approaches, Aortic aneurysm repair treatments, Mechanical Circulatory Support Devices. 127 papers and 2.3k citations.
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BACKGROUND: Intraocular pressure (IOP) increases in steep Trendelenburg positioning, but the magnitude of the increase has not been quantified. In addition, the factors contributing to this increase have not been studied in robot-assisted prostatectomy cases. In this study, we sought to quantify the changes in IOP and examine perioperative factors responsible for these changes while patients are in the steep Trendelenburg position during robotic prostatectomy. METHODS: In this prospective study, we measured IOP using a Tono-pen XL in 33 patients undergoing robot-assisted prostatectomy. The IOP was measured before anesthesia while supine and awake (baseline T1), anesthetized and supine (T2), anesthetized after insufflation of the abdomen with carbon dioxide (CO(2)) (T3), anesthetized in steep Trendelenburg (T4), anesthetized in steep Trendelenburg at the end of the procedure (T5), anesthetized supine before awakening (T6), and 1 hr after awakening in the supine position (T7). RESULTS: On average, IOP was 13.3 +/- 0.58 (mean +/- SE) mm Hg higher at the end of the period of steep Trendelenburg position (T5) compared with supine position T1 (P < 0.0001). The least square estimates for each time point in mm Hg were as follows: T1 = 15.7, T2 = 10.7, T3 = 14.6, T4 = 25.2, T5 = 29.0, T6 = 22.2, T7 = 17.0. Using univariate mixed effects models for the T1-T5 time periods, peak airway pressure, mean arterial blood pressure, ETco(2), and time were significant predictors of the IOP increase, whereas age, body mass index, blood loss, volume of IV fluid administered, mean airway pressure, and desflurane concentration were not predictive. In T4-T5, which involved no significant positional or perioperative interventions, we performed a multivariate analysis to evaluate predictors of IOP increases. Surgical duration (in minutes) and ETco(2) were the only significant variables predicting changes in IOP during stable and prolonged Trendelenburg positioning. On average, IOP increased 0.21 mm Hg per mm Hg increase in ETco(2) after adjusting for time. An increase of 0.05 mm Hg in IOP per minute of surgery on average was observed during this period in the Trendelenburg position after adjusting for ETco(2). CONCLUSIONS: IOP reached peak levels at the end of steep Trendelenburg position (T5), on average 13 mm Hg higher than the preanesthesia induction (T1) value. Surgical duration and ETco(2) were the only significant predictors of IOP increase in the Trendelenburg position (T4-T5).
Brain inflammation plays a central role in multiple sclerosis (MS). Besides lymphocytes, the astroglia and microglia mainly contribute to the cellular composition of the inflammatory infiltrate in MS lesions. Several studies were able to demonstrate that cortical lesions are characterized by lower levels of inflammatory cells among activated microglia/macrophages. The underlying mechanisms for this difference, however, remain to be clarified. In the current study, we compared the kinetics and extent of microglia and astrocyte activation during early and late cuprizone-induced demyelination in the white matter tract corpus callosum and the telencephalic gray matter. Cellular parameters were related to the expression profiles of the chemokines Ccl2 and Ccl3. We are clearly able to demonstrate that both regions are characterized by early oligodendrocyte stress/apoptosis with concomitant microglia activation and delayed astrocytosis. The extent of microgliosis/astrocytosis appeared to be greater in the subcortical white matter tract corpus callosum compared to the gray matter cortex region. The same holds true for the expression of the key chemokines Ccl2 and Ccl3. The current study defines a model to study early microglia activation and to investigate differences in the neuroinflammatory response of white vs. gray matter.