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Background: Resuscitation is the initial step for hemorrhagic shock. However, there is still controversy as to which fluid achieves the best results clinically and experimentally. Aim: It was aimed to investigate the effects of 0.9% NaCl (sodium chloride) and 6% HES (hydroxyethyl starch) on the kidney and blood environment. Methods: Twenty-four male Wistar rats were assigned as control, shock, and resuscitated (colloid: 6% HES and crystalloid: 0.9% NaCl) groups. Besides hemodynamics (mean arterial pressure and shock index) monitoring and kidney function evaluation, hemolysis, oxidative stress, inflammation, and glycocalyx degradation were evaluated in the plasma and kidney. Results: (1) Macrohemodynamics were successfully restored by both fluids. (2) Although 3 times more crystalloid volume was applied compared to the colloid resuscitation, similar hematocrit levels were found in both resuscitation strategies (32.8 ± 2.3 vs. 33.3 ± 1.0). (3) NaCl resuscitation led to increases in the hemolytic index, catalytic iron, and sialic acid compared to control, while HES administration increased the levels of malondialdehyde, ischemia-modified albumin, and sialic acid. (4) However, both fluid resuscitation strategies could inhibit inflammation and oxidative stress in the kidney and restore kidney function parameters. Conclusion: Although both NaCl and HES resuscitation showed protection of the kidney function against oxidative stress and inflammation, these fluids initiated the injury process.

Acute kidney injury (AKI) is frequently seen in patients with hemorrhagic shock due to hypotension, tissue hypoxia, and inflammation despite adequate resuscitation. There is a lack of information concerning the alteration of renal microcirculation and perfusion during shock and resuscitation. The aim of this study was to investigate the possible role of renal microcirculatory alterations on development of renal dysfunction in a pig model of non-traumatic hemorrhagic shock (HS) induced AKI.Fully instrumented female pigs were divided into the two groups as Control (n = 6) and HS (n = 11). HS was achieved by withdrawing blood until mean arterial pressure (MAP) reached around 50 mmHg. After an hour cessation period, fluid resuscitation with balanced crystalloid was started for the duration of 1 h. The systemic and renal hemodynamics, renal microcirculatory perfusion (contrast-enhanced ultrasound (CEUS)) and the sublingual microcirculation were measured.CEUS peak enhancement was significantly increased in HS during shock, early-, and late resuscitation indicating perfusion defects in the renal cortex (p In this study, we showed that the correction of systemic hemodynamic variables may not be accompanied with the improvement of renal cortical perfusion, intra-renal blood volume and renal damage following fluid resuscitation. We suggest that the measurement of renal injury biomarkers, systemic and renal microcirculation can be used for guiding to the optimization of fluid therapies.

Background and Objectives Haemodilution leads to complications in clinical practice. It is exactly unknown whether this damage is caused by the fluid or by the stretching of the vascular bed. We aimed to compare two different haemodilution techniques at the same anaemic level. Methods Normovolemic or hypervolemic haemodilution was performed on twelve adult male Wistar rats. In the normovolemic procedure, blood was withdrawn and instantaneously administered with similar amounts of 6% hydroxyethyl starch (HES 130/0.4). Fluid was administered without withdrawing blood in the hypervolemic procedure. In both models, a 25% haematocrit level was targeted and kept at this level for 90 min to deepen the anaemia effect. Besides haemodynamics measurement, renal function (creatinine, blood urea nitrogen) and injury (tissue norepinephrine, malondialdehyde) were evaluated. Also, systemic hypoxia (lactate), oxidative stress (malondialdehyde, ischaemia-modified albumin), inflammation (tumour necrosis factor-alpha [TNF-α]), osmotic stress, adrenal stress (norepinephrine, epinephrine), and vascular stretching (atrial natriuretic peptide [ANP]) were assessed. Results Arterial pressure in the normovolemic group was lower than in the hypervolemic group. Serum creatinine, blood urea nitrogen, and lactate levels were higher in the normovolemic group. Tissue norepinephrine and malondialdehyde levels were higher in the normovolemic group. Serum ANP, malondialdehyde, ischaemia-modified albumin, free haemoglobin, syndecan-1, and TNF-α were higher in both groups compared to respective baseline. Conclusions Normovolemic haemodilution may lead to hypoxic kidney injury. The hypervolemic state may be advantageous if fluid is to be administered. Thus, the effect of the fluid itself can be relatively masked.

Little is known about the impact of COVID-19 on the outcomes of patients undergoing surgery and intervention. This study was conducted between 20 March and 20 May 2020 in six hospitals in Istanbul, and aimed to investigate the effects of surgery and intervention on COVID-19 disease progression, intensive care (ICU) need, mortality and virus transmission to patients and healthcare workers. Patients were examined in three groups: group I underwent emergency surgery, group II had an emergency non-operating room intervention, and group III received inpatient COVID-19 treatment but did not have surgery or undergo intervention. Mortality rates, mechanical ventilation needs and rates of admission to the ICU were compared between the three groups. During this period, patient and healthcare worker transmissions were recorded. In total, 1273 surgical, 476 non-operating room intervention patients and 1884 COVID-19 inpatients were examined. The rate of ICU requirement among patients who had surgery was nearly twice that for inpatients and intervention patients, but there was no difference in mortality between the groups. The overall mortality rates were 2.3% in surgical patients, 3.3% in intervention patients and 3% in inpatients. COVID-19 polymerase chain reaction positivity among hospital workers was 2.4%. Only 3.3% of infected frontline healthcare workers were anaesthesiologists. No deaths occurred among infected healthcare workers. We conclude that emergency surgery and non-operating room interventions during the pandemic period do not increase postoperative mortality and can be performed with low transmission rates.

Background It is not known whether emergency surgeries and interventions are safe during the pandemic period. We investigate the effect of surgery and intervention on COVID-19 disease progression, intensive care (ICU) need, mortality, and virus transmission to patients and healthcare workers.Methods This retrospective study was conducted between 20 March -20 May 2020 in six hospitals in Istanbul. Patients were examined in three groups. Group I patients who underwent emergency surgery, Group II patients who underwent emergency nonoperating room intervention, Group III patients who underwent inpatient COVID-19 treatment but did not have any surgery or intervention. During this period, all healthcare workers and patients diagnosed with COVID-19 with any of the symptoms, PCR positivity, or Thorax CT findings were recorded. Patient and healthcare worker transmission, unplanned intensive care need, and death due to COVID-19 were also recorded.Results 1,273 surgical, 476 nonoperating room intervention patients, and 1,884 COVID-19 inpatients were examined. ICU requirement of COVID-19 patients who had surgery was 20 times higher than COVID-19 inpatients and intervention patients but there is no difference in mortality. The total mortality rates were 2.3% in surgical patients, 3.3% in intervention patients diagnosed with COVID-19, and 3% in COVID-19 inpatients. COVID-19 PCR positivity among hospital workers was % 2.4. Only 3.3% of the infected frontline healthcare workers were anesthesiologists. No deaths occurred among infected healthcare workers.Conclusions Emergency surgeries and interventions during the pandemic period did not increase mortality and can be performed safely with very low transmission rates by complying with the effective use of personal protective equipment.

PURPOSE Although it is affected at an early stage, there is a lack of studies investigating right ventricular (RV) function in patients with mitral stenosis (MS). We aimed to investigate the correlation between conventional echocardiographic variables and tricuspid annular plane systolic excursion (TAPSE), used as an indicator of RV dysfunction. METHODS We enrolled 59 consecutive patients with MS and assigned them in group 1 if TAPSE ≤16, or group 2 if: TAPSE >16. RESULTS The mean age of the patients was 42.2 ± 8 years, and 74.6% were females. In univariate analysis, maximal mitral valve gradient, mean mitral valve gradient, systolic pulmonary arterial pressure, RV strain, and RV strain rates were associated with RV dysfunction. In multivariate analysis, both strain variables were found to be independent predictors of RV dysfunction. Kaplan Maier survival analysis showed that patients with lower RV strain had more rehospitalization rate during the one-year follow-up period. CONCLUSIONS RV dysfunction is common in patients with MS and is associated with higher rehospitalization rate and morbidity. Evaluation of RV strain and strain rate for early detection of RV dysfunction and prediction of rehospitalization may be an appropriate approach in mitral stenosis.

Aim: The incidence of cardiovascular diseases has increased in patients with metabolic syndrome(MS)and left atrial functions also begin to deteriorate from the early period. This effect could be demonstrated by both ECG and Echocardiography. In this study, we investigated the relationship between left atrium volume index (LAVi), which is a sensitive indicator of left atrial dysfunction, and p-wave dispersion (Pd) in patients with MS. Material and Methods: Patients with MS were included in the study. Baseline ECG and transthoracic echocardiography (TTE) measurements were performed and the correlation between the Pd and LAVi was investigated. Results: 180 patients were included in the study. The median age of the study population was45(36-57) and 64% was male. In correlation analysis, there was a good correlation between Pd and LAVi(r:0.73 and p

We aimed to test our hypothesis that scavenging reactive oxygen species (ROS) with tempol, a membrane permeable antioxidant, affects the type and magnitude of oxidative damage and stress tolerance through mimetic aging process in Drosophila. Drosophila colonies were randomly divided into three groups: (1) no D-galactose, no tempol; (2) D-galactose without tempol; (3) D-galactose, but with tempol. Mimetic aging was induced by d-galactose administration. The tempol-administered flies received tempol at the concentration of 0.2% in addition to d-galactose. Thiobarbituric acid reacting substance (TBARS) concentrations, advanced oxidation protein products (AOPPs), Cu,Zn-superoxide dismutase (Cu,Zn-SOD), sialic acid (SA) were determined. Additionally, stress tolerances were tested. Mimetically aged group without tempol led to a significant decrease in tolerance to heat, cold, and starvation (P0.05), but tempol was used for these parameters. The Cu,Zn-SOD activity and SA concentrations were lower in both mimetically aged and tempol-administered Drosophila groups compared to control (P0.05), whereas there were no significantly difference between mimetically aged and tempol-administered groups. Mimetically aged group without tempol led to a significant increase in tissue TBARS and AOPPs concentrations (P0.05). Coadministration of tempol could prevent these alterations. Scavenging ROS using tempol also restores redox homeostasis in mimetically aged group. Tempol partly restores age-related oxidative injury and increases stress tolerance.

Catecholamines play a regulatory role in the cardiovascular system, primarily via beta (1-2)-adrenoreceptors (AR). However, in the late 1980s, the cloning of a third beta-AR subtype (beta 3-AR) in the heart has altered the conventional view on the regulation of heart function via the betaadrenergic receptors. Additionally, in blood vessels, beta 3-AR was shown to produce relaxation. Currently, the physiological role of beta 3-AR is not clearly known. Hence, the purpose of this review is to summarize the physiological evidences supporting the functional roles of beta 3-AR in various tissues, particularly cardiac and vascular. In addition, this review discusses the potential role of beta 3-AR in obesity and insulin resistance and emphasizes their putative involvement as new therapeutic targets.

Despite the identification of several of the cellular mechanisms thought to underlie the development of acute kidney injury (AKI), the pathophysiology of AKI is still poorly understood. It is clear, however, that instead of a single mechanism being responsible for its etiology, AKI is associated with an entire orchestra of failing cellular mechanisms. Renal microcirculation is the physiological compartment where these mechanisms come together and exert their integrated deleterious action. Therefore, the study of renal microcirculation and the identification of the determinants of its function in models of AKI can be expected to provide insight into the pathogenesis and resolution of AKI. A major determinant of adequate organ function is the adequate oxygen (O(2)) supply at the microcirculatory level and utilization at mitochondrial levels for ATP production needed for performing organ function. The highly complex architecture of the renal microvasculature, the need to meet a high energy demand and the borderline hypoxemic nature of the kidney makes it an organ that is highly vulnerable to injury. Under normal, steady-state conditions, the oxygen supply to the renal tissues is well regulated and utilized not only for mitochondrial production of ATP (mainly for Na reabsorption), but also for the production of nitric oxide and the reactive oxygen species needed for physiological control of renal function. Under pathological conditions, such as inflammation, shock or sepsis, however, the renal microcirculation becomes compromised, which results in a disruption of the homeostasis of nitric oxide, reactive oxygen species, and oxygen supply and utilization. This imbalance results in these compounds exerting pathogenic effects, such as hypoxemia and oxidative stress, resulting in further deterioration of renal microcirculatory function. Our hypothesis is that this sequence of events underlies the development of AKI and that integrated therapeutic modalities targeting these pathogenic mechanisms will be effective therapeutic strategies in the clinical environment.

Hypoxia causes changes in the rate of synthesis or release of neurotransmitters in the brain. The accumulation of serotonin (5-HT) in the central nervous system might cause hypoxic respiratory depression. In the present study, we aimed to examine the role of central 5-HT on normoxic and acute hypoxic ventilatory depression (AHVD) in peripheral chemoreceptors denervated rabbits. All experiments were performed in peripherally chemodenervated rabbits anesthetized with intravenous injection of urethane (400 mg/kg) and alpha-chloralose (40 mg/kg). For intracerebroventricular (ICV) administration of 5-HT (20 microg/kg) and ketanserin (10 microg/kg), a cannula was placed in left lateral ventricle by stereotaxic method. Respiratory frequency (fR), tidal volume (VT), ventilation minute volume (VE) and systemic arterial bood pressure (BP) were recorded in each experimental phases and mean arterial pressure was calculated (MAP). Heart rate (HR) was also determined from the pulsation of BP. The effects of ICV serotonin and ICV ketanserin on the indicated parameters during air breathing (normoxia) and breathing of hypoxia (8% O2--92% N2) were investigated. During hypoxia, fR, VT, VE, MAP and HR decreased, and AHVD was thus obtained. ICV injection of 5-HT during normoxia caused significant increases in VT (P0.001) and in VE (P0.01). On the other hand, ICV 5-HT injection reduced the degree of AHVD in peripherally chemodenervated rabbits during hypoxia (fR; P0.05, VT; P0.05 and VE; P0.01). After ICV injection of ketanserin, the enhancement of 5-HT on VE was prevented during normoxia. On the breathing of hypoxic gas after ICV ketanserin, the degree of AHVD was augmented. In conclusion, our findings suggested that central 5-HT increases normoxic ventilation and reduces the degree of AHVD during hypoxia and that ICV ketanserin prevents the stimulatory effect of 5-HT on respiration and augments AHVD.

International Carnahan Conference on Security Technology(2017 : Madrid; Spain), IT system risk assessments are indispensable due to increasing cyber threats within our ever-growing IT systems. Moreover, laws and regulations urge organizations to conduct risk assessments regularly. Even though there exist several risk management frameworks and methodologies, they are in general high level, not defining the risk metrics, risk metrics values and the detailed risk assessment formulas for different risk views. To address this need, we define a novel risk assessment methodology specific to IT systems. Our model is quantitative, both asset and vulnerability centric and defines low and high level risk metrics. High level risk metrics are defined in two general categories; base and attack graph-based. In our paper, we provide a detailed explanation of formulations in each category and make our implemented software publicly available for those who are interested in applying the proposed methodology to their IT systems., This work was supported by The Scientific and Technological Research Council of Turkey (TÜBİTAK), TEYDEB 1501, Grant No: 3160047.