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Angiotensin Ii in Septic Shock: Effects on Tissue Perfusion, Organ Function and Mitochondrial Respiration in a Porcine Model Of ANGIOTENSIN II IN SEPTIC SHOCK: EFFECTS ON TISSUE PERFUSION, ORGAN FUNCTION AND MITOCHONDRIAL RESPIRATION IN A PORCINE MODEL OF FECAL PERITONITIS Supplemental Digital Content Authors: Thiago D Corrêa, MD, PhD; Victor Jeger, MD; Adriano José Pereira, MD, PhD; Jukka Takala, MD, PhD; Siamak Djafarzadeh, PhD; Stephan M Jakob, MD, PhD. 1 Supplemental Digital Content Word text file containing additional information about the methods, along with related references and the Figure S1 which describes the hemodynamic protocol. The results section contains additional 6 Tables and 7 Figures. Table S1 describes hemodynamics of non-septic sham controls; Table S2 gives an overview about the effect of untreated peritonitis; Table S3 gives the acid-base-balance parameters and respiratory system variables; Table S4 describes systemic and regional hemodynamics and arterial lactate level; Table S5 summarizes electrolytes and blood glucose analysis and Table S6 describes the main results of thrombelastography. Figure S1 depicts the hemodynamic protocol; Figure S2 shows the administered infusion rate of angiotensin II to non-septic sham controls; Figure S3 shows individual mean arterial blood pressure and vasopressor infusion rates; Figure S4 describes the stability of arterial PAH concentrations; Figure S5 represents respiration rates of isolated heart mitochondria; Figure S6 shows respiration rates of isolated liver mitochondria and Figure S7 shows respiration rates of permeabilized heart fibers. METHODS SEDATION, ANALGESIA AND VENTILATION The pigs were sedated with intramuscular ketamine (20 mg/kg) and xylazine (2 mg/kg) and a catheter was inserted in an ear vein for administration of fluids and drugs. Anesthesia was induced with midazolam (0.5 mg/kg) and atropine (0.02 mg/kg). Orotracheal and gastric tubes were inserted, and anesthesia maintained with propofol (4 mg/kg/h) and fentanyl (2-10 µg/kg/h). Additional fentanyl (50 µg) or midazolam (5 mg) were administered as needed. Volume-controlled ventilation with a positive end-expiratory pressure (PEEP) of 5 cm H2O, a fractional inspiratory oxygen concentration (FiO2) of 30%, and a tidal volume of 8 ml/kg (Servo-i®; Maquet Critical Care, Solna, Sweden) was adjusted to maintain an arterial carbon dioxide partial pressure (PaCO2) between 35 and 45 mmHg. HEMODYNAMIC SUPPORT Throughout the resuscitation period, the volume status was evaluated clinically every hour. If signs of hypovolemia became evident, alternating boluses of 150 mL Ringer’s lactate (RL) and 6% hydroxyethyl starch (HES 130/0.4) were given (Figure S1). Fluid boluses were repeated as long as the stroke volume was increased by 10% or more after fluid administration. The maximum dose of HES administered was 30 ml/kg. After this maximal dose was reached, only boluses of Ringer’s lactate were given. If the mean arterial blood pressure was lower than 75 mmHg, vasopressors (norepinephrine or angiotensin II) were administrated. If the mixed venous oxygen saturation (SvO2) was less than 50%, dobutamine administration was started at a dose of 5.0 mg per hour. This dose was increased by 5.0 mg per hour every 30 minutes until the SvO2 was 50% or higher or until a maximal dose of 20 mg per hour was given (Figure S1). 2 Further treatment consisted of antibiotics (piperacillin-tazobactam (Tazobac®) 2.25 g/8h, i.v.), tight blood glucose control and deep vein thrombosis prophylaxis (continuous i.v. infusion of 10,000 IU of non-fractionated heparin/24 hours). Ringer’s lactate and Glucose 50% were infused adding up to 1.5 mL/kg/h (observation period), and to 3.0 mL/kg/h (resuscitation period), adjusted to keep blood glucose in the range of 3.5 to 5.0 mmol/L. MONITORING Hemodynamics, temperature and respiratory parameters (S/5 Critical Care Monitor®; Datex-Ohmeda, GE Healthcare, Helsinki, Finland) thermodilution cardiac output, mixed venous oxygen saturation (SvO2;Vigilance®; Edwards Lifesciences LLC, Irvine, CA, USA), and carotid and femoral artery blood flows (Transonic Systems Inc., Ithaca, NY, USA) were continuously measured and recorded (Soleasy™; National Instruments Corp., Austin, TX, USA Centricity Clinisoft®; GE Healthcare, Helsinki, Finland). Systemic VO2 was calculated based on the Fick principle (3). BLOOD SAMPLING Blood from the carotid artery was withdrawn at baseline and every six hours from the indwelling catheter and immediately analyzed in a blood gas analyzer (GEM Premier 3000 analyzer; Bedford, MA, USA) for PaO2, PaCO2 (adjusted to central body temperature), pH, lactate (mmol/L), base excess (BE), sodium, potassium and calcium. Arterial oxygen saturation and total hemoglobin concentration were measured at baseline and every six hours using a separate analyzer (OSM 3; Radiometer, Copenhagen, Denmark, porcine mode). 3 Plasma interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) were determined using a porcine immunoassay kit (R&D Systems Europe Ltd; Abingdon, Oxon, UK). Hemoglobin, platelets, white blood cell count, serum creatinine, total bilirubin, IL-6 and TNF-alpha were measured with blood samples from the carotid artery at baseline, the end of the observation period, and at the end of the study (48 hours of resuscitation or before death, for animals that died before completion of the study). Blood from the pulmonary artery was withdrawn at baseline and every 6 hours for mixed oxygen saturation measurement using a Radiometer OSM 3 blood gas analyzer (OSM 3; Radiometer, Copenhagen, Denmark, porcine mode). Blood from the kidney vein was withdrawn at baseline, end of the observation period, and at the end of the study (48 hours of resuscitation or before death, for animals that died before completion of the study) for kidney vein oxygen saturation measurement using a Radiometer OSM 3 blood gas analyzer (OSM 3; Radiometer, Copenhagen, Denmark, porcine mode). THROMBELASTOGRAPHY Thrombelastography (TEG) was performed by a TEG® thrombelastograph 5000 (Haemonetics Corporation, Braintree, MA, USA). Temperature was set to 37°C for all samples. Citrated whole blood samples (340 µl) for TEG assays were recalcified by adding 0.2M CaCl2 (20 µl) and coagulation was activated by kaolin. Heparinase coated cups were used to prevent any heparin effect. TEG instruments were tested for quality control before the measurement of baseline parameters using standardised samples provided by the manufacturer and all measured quality control parameters were always within the range. TEG samples were analysed at induction of anaesthesia, at the end of observation period and at the end of the experiment 4 (Figure 1, main manuscript). Four main TEG parameters were analyzed in this study: R (reaction time, time from start of test till begin of clot formation), K (time from activation of coagulation till 20 mm of amplitude), α-angle and maximal amplitude (MA). ESTIMATION OF RENAL BLOOD FLOW AND FUNCTION Renal blood flow was estimated using primed, continuous infusion of para- amininohippurate (PAH; Aminohippurate sodium; Merck & CO., INC, Whitehouse Station, NJ). After a priming bolus (8 mg/kg), para-amininohippurate (PAH; Aminohippurate sodium; Merck & CO., INC, Whitehouse Station, NJ) of 20% paraaminohippurate [PAH; was continuously at 8mg/min for 95 minutes. Urine samples were collected at 30, 60 and 90 minutes. Blood samples from carotid artery and kidney vein were collected at 30, 60, 85, 90 and 95 minutes. PAH concentration was measured using the colorimetric PAH assay kit from BioVision (Milpitas, CA, USA). PAH clearance was calculated as PAH infusion rate/arterial-renal vein PAH concentration difference (1, 2) at time of highest renal PAH extraction PAH extraction <0.20, was disregarded. The reproducibility of PAH measurements was assessed from 244 duplicate blood samples. Colorimetric PAH assay were performed in duplicates, and measurements were repeated if the coefficient of variation (standard deviation of measurements divided by their average) was >10%. Six hours urine samples were collected before baseline, end of observation period and end of the experiment. Creatinine, sodium and potassium concentrations were measured using standard analysis from these samples and fractional excretions of sodium and potassium were calculated following the formula: FE = (urineelectrolyte x serumcreatinine x 100) / (serumelectrolyte x urinecreatinine). Sodium results “<10 mmol/L” = 5 below detection threshold (51/120 measurements, 43%), were replaced by 10 in order to calculate FENa+ in all animals. Acute kidney injury (AKI) was defined according to the AKIN criteria as an absolute increase in serum creatinine ≥0.30 mg/dl (≥26.4 µmol/L) or a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline) (3, 4). MITOCHONDRIAL FUNCTION ANALYSIS Tissue samples were taken from the kidney, liver and heart at the end of the experiment. In animals that died earlier, the final samples were taken when the animals were still alive, receiving the maximal vasopressor dose (5000 mcg/h of norepinephrine or 1000 ng/kg/min of angiotensin II), and when mean arterial blood pressure approached 30 mmHg. Complex I-, II- and IV-dependent respiration rates were measured as described previously using high-resolution respirometry (Oxygraph-2k; Oroboros Instruments, Innsbruck, Austria) (5, 6) and is expressed as pmol/second/mg mitochondrial protein. For heart fibers, state 3 respiration was measured using glutamate/malate, succinate and ascorbate/TMPD as substrates for complex I, II and IV, respectively. Maximal electron transport system capacity
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