CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 AFRICA 71 allocated to two groups. The patients in group 1 (n = 15) were primed with a 6% HES (1 200 ml 6% HES, Voluven®; Fresenius Kabi, Germany), while the patients in group 2 were primed with a crystalloid solution (1 200 ml 0.9 % NaCl; n = 15, Polifleks®; Polifarma, Istanbul, Turkey). Exclusion criteria were assigned as the patient’s age not being between 18 and 65 years, left ventricular ejection fraction < 40%, emergent/urgent operations, additional valvular diseases, impaired renal function (estimated glomerular filtration rate > 60 ml/min) and co-morbid disease (except for hypertension). Anaesthetic and surgical management of the patients was performed by the same anaesthetist and surgical team. A standard monitoring regimen, including invasive arterial pressure, central venous pressure, peripheral oxygen saturation, five-lead electrocardiogram, regional cerebral oxygen saturation and end-tidal CO2 monitoring was performed. A 5-Fr femoral arterial thermistor-tipped catheter connected to the pulse index contour continuous cardiac output analysis monitor (PiCCO Technology, Pulsion Medical Systems, Germany) was inserted into each patient. The extravascular lung water index (ELWI), stroke volume index (SVI), systemic vascular resistance index (SVRI), cardiac index (CI) and global end-diastolic volume index (GEDI) were measured using the thermodilution and pulse contour analysis methods. The anaesthesia regimen was intravenously induced with fentanyl and propofol. Tracheal intubation was intravenously facilitated with rocuronium. Anaesthesia was maintained with sevoflurane at one minimum alveolar concentration in air/ oxygen and a maintenance dose of rocuronium and fentanyl. Ventilation of the patients was adjusted to maintain normoxia and normocapnia. Heparin (300 IU/kg) and additional heparin were given until the activated clotting time was > 400 seconds. As the CPB concluded, protamine sulphate was administered at the same dosage as the initially administered heparin dose to antagonise the heparin effect. Dopamine, dobutamine, norepinephrine, epinephrine, or combinations thereof were used as inotrope or vasopressors. The patients were transferred to the cardiac ICU after surgery. Standard CPB techniques were employed. The CPB circuit was primed according to each patient’s study group. During CPB, standard cannulation of the ascending aorta and right atrium was performed. Pump flows at 2.0–2.4 l/min/m2 of the body surface area, moderate systemic hypothermia (32°C) and intermittent anterograde blood cardioplegia was used. Homogenous cooling and rewarming were provided. Packed red blood cells were transfused to maintain haemoglobin levels between 6 and 8 g/dl during the pump period and between 8 and 10 g/dl after reperfusion. Fresh frozen plasma and platelet transfusions were used, according to the laboratory and clinical findings. Normal saline solution was administered to meet the volume loss by evaporation and through the urine. Inaddition toPiCCOandoxidative stress statusmeasurements, heart rate, mean arterial pressure, the partial pressure of carbon dioxide and oxygen (pCO2–pO2), and serum level of haematocrit, glucose and lactate were recorded. The duration of extubation and ICU/hospital stay were also determined. Haemodynamic variables [heart rate (beats/min), mean arterial pressure (mmHg)], blood gas analysis [pH, pCO2 (mmHg), pO2 (mmHg), lactate (mmol/l) and biochemical variables (glucose (mg/ dl), hematocrit (%)] were obtained at the following times: T0 (zero time point), T1 (after anaesthesia induction), T2 (five minutes after the initiation of CPB), T3 (after cross-clamping), T4 (after weaning from CPB), T5 (at admission to the ICU), T6 (third hour after ICU admission) and T7 (24th hour after ICU admission). Using the transpulmonary thermodilution and PiCCO methods, ELWI, SVI, SVRI, CI and GEDI were evaluated at the T1, T4, T5, T6 and T7 time points. In addition, blood samples were obtained to evaluate the oxidative stress status and cellular integrity. For this purpose, serum advanced oxidative protein products (AOPP), total thiol (T-SH), free haemoglobin (fHb), ischaemic modified albumin (IMA) and sialic acid (SA) levels were measured at the T0, T5 and T7 time points. The AOPP levels were measured to determine the protein oxidation using a modified method of Hanasand et al.21 The measurement of IMA levels was performed to show three-dimensional modification of plasma albumin using a modification of the Bar-Or et al. method.22 The measurement of T-SH determination was performed to thiol modification of protein, which is based on the method of Sedlak and Lindsay.23 The SA levels were determined by the method of Sydow.24 The level of fHb was determined to show the oxidant-mediated homolysis using the method by Harboe.25 Statistical analysis After the determination of distribution of data sets using the Kolmogorov–Smirnov and Shapiro–Wilk tests, all data are presented as mean ± SEM. Statistical analysis was performed using GraphPad Prism v5.0 (GraphPad Software, La Jolla, CA, USA). The sample size was estimated using G*Power software (version 3.1; Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany). To this, the study power was accepted as 80%, the type 1 alpha error was 0.05 and the effect size was accepted as 58% according to the ELWI change,26 as primary outcome. A comparative analysis of the two groups at the same time point was performed using the unpaired t-test and one-way ANOVA. The Bonferroni post hoc test was used for repeated measurements. Differences between values were considered statistically significant at p < 0.05. Results Table 1 shows haemodynamic, biochemical and arterial blood gas measurements at seven time points in the groups. There were similar results in both groups at all time points (p > 0.05). For the colloid group, the IMA levels (ABS units) were measured as 0.511 ± 0.047 at T1, 0.475 ± 0.059 at T5 and 0.457 ± 0.055 at T7. For the crystalloid group, the IMA levels (ABS units) were measured as 0.388 ± 0.074 at T1, 0.355 ± 0.063 at T5 and 0.424 ± 0.080 at T7. For the colloid group, the T-SH levels (μmol/g protein) were measured as 33.6 ± 2.1 at T1, 76.7 ± 10.4 at T5 and 77.7 ± 20.7 at T7. For the crystalloid group, the T-SH levels (μmol/g protein) were measured as 39.2 ± 4.1 at T1, 55.3 ± 5.8 at T5 and 64.1 ± 6.7 at T7. For the colloid group, the AOPP levels (mmol/g protein) were measured as 24.5 ± 2.2 at T1, 34.9 ± 3.4 at T5 and 30.6 ± 3.8 at T7. For the crystalloid group, the AOPP levels (mmol/g protein) were measured as 34.0 ± 3.8 at T1, 42.1 ± 6.0 at T5 and 37.4 ± 4.8 at T7.
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