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Evaluation of stroke volume variation obtained by autocalibrated arterial pulse contour analysis to predict fluid responsiveness during different intraoperative positons

ABSTRACT: Interventions: Group G:the protocol for goal direced fluid therapy;C:the protocol of fluid therapy Primary outcome(s): Length of hospital stay Study Design: Randomized parallel controlled trial

DISEASE(S): Colorectal Cancer

PROVIDER: 2675566 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Fluid Challenge and Plasma Volume, During Surgery

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A clinical study to see the effects of two different methods of fluid administration (Fluid volumeestimated by anaesthetist compared with volume estimated by a machine) during Cytoreductive Surgery with Hyperthermic Intraperitoneal Chemotherapy

Project description:Intervention1: Stroke volume variation (SVV) (using Flotrac) guided fluid therapy: The CI will be maintained at values greater than or equal to 2.5 l/min/m2 , stroke volume variation 12%, Stroke Volume Index (SVI) 35ml/m2/ beat, Systemic Vascular Resistance Index (SVRI) more than equal to 1900 dynes-sec/cm-5/m2 . Basal infusion of crystalloids will be at 4 ml/kg/h. If CI 2.5 l/min/m2, SVI 35 ml/m2 and SVV 12% crystalloid challenge and colloid bolus will be given. In the case of CI 2.5 l/min/m2 and SVI 35 ml/m2 with SVV 12% an infusion with dobutamine will be initiated alongwith colloid bolus. Control Intervention1: Fluid therapy guided by clinical parameters like mean arterial pressure (MAP), central venous pressure (CVP) and urine output: to maintain end organ perfusion, general fluid management with IV infusion of crystalloid (lactate free) will be done aiming at a Mean arterial pressure (MAP) of 65 mm Hg, urinary output of at least 0.5 (CRS phase), 2 (HIPEC phase), and 1 (post HIPEC phase) ml/ kg/ hr, respectively and CVP of 8-12 mm hg. Basal infusion of crystalloid will be at 4 ml/kg/hour, with bolus of crystalloid, colloid and use of noradrenaline depending on MAP, Urine output and CVP. Primary outcome(s): Serum Lactate levelsTimepoint: At baseline, then at one hour interval during Cytoreductive phase, half hourly interval during HIPEC phase and every 6 hourly interval post operatively for 24 hours. Study Design: Randomized, Parallel Group, Active Controlled Trial Method of generating randomization sequence:Computer generated randomization Method of allocation concealment:Sequentially numbered, sealed, opaque envelopes Blinding and masking:Participant Blinded

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Human fetal chylothorax: pleural fluid vs. ascites fluid

Project description:Transcriptional profile comparison of the pleural and ascites fluids in hydropic fetuses affected with chylothorax. Two-condition experiment, pleural fluid vs. ascites fluid. Comparison of the transcriptional profile between sample collected before and after OK-432 treatment and between fetuses with and without a G404S mutation in the ITGA9 gene

2012-12-31 | E-GEOD-33872 | biostudies-arrayexpress

SMAD4 maintains the Fluid Shear Stress set point to protect against Arterial-Venous Malformations

Project description:Vascular networks form, remodel and mature under the influence of both fluid shear stress (FSS) and soluble factors. Physiological FSS promotes and maintains vascular stability via synergy with Bone Morphogenic Protein 9 (BMP9) and BMP10. Conversely, mutation of the BMP receptors ALK1, Endoglin or the downstream effector SMAD4 leads to Hereditary Hemorrhagic Telangiectasia (HHT), characterized by fragile and leaky arterial-venous malformations (AVMs). But how endothelial cells (EC) integrate FSS and BMP signals in vascular development and homeostasis, and how mutations give rise to vascular malformations is not well understood. Here, we aimed to elucidate the mechanism of synergy between fluid shear stress and SMAD signaling in vascular stability and its failure in HHT. We have now found that loss of Smad4 increases ECs’ sensitivity to flow by lowering the FSS set point with resulting AVMs exhibiting features of excessive flow-mediated morphological responses. Mechanistically, loss of Smad4 disinhibits flow-mediated Klf4-Tie2-PI3K/Akt signaling leading to increased EC proliferation and loss of arterial identity due to Klf4-mediated repression of cyclin dependent Kinase (CDK) inhibitors, CDKN2A and CDKN2B. Thus, AVMs caused by Smad4 deletion are characterized by chronic high flow remodeling with excessive EC proliferation and loss of arterial identity as triggering events.

2023-07-03 | GSE232443 | GEO