Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation

The neurons secreting oxytocin (OXY) and vasopressin (AVP) are located mainly in the supraoptic, paraventricular, and suprachiasmatic nucleus of the brain. Oxytocinergic and vasopressinergic projections reach several regions of the brain and the spinal cord. Both peptides are released from axons, soma, and dendrites and modulate the excitability of other neuroregulatory pathways. The synthesis and action of OXY and AVP in the peripheral organs (eye, heart, gastrointestinal system) is being investigated. The secretion of OXY and AVP is influenced by changes in body fluid osmolality, blood volume, blood pressure, hypoxia, and stress. Vasopressin interacts with three subtypes of receptors: V1aR, V1bR, and V2R whereas oxytocin activates its own OXTR and V1aR receptors. AVP and OXY receptors are present in several regions of the brain (cortex, hypothalamus, pons, medulla, and cerebellum) and in the peripheral organs (heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, ovaries, uterus, thymus). Hypertension, myocardial infarction, and coexisting factors, such as pain and stress, have a significant impact on the secretion of oxytocin and vasopressin and on the expression of their receptors. The inappropriate regulation of oxytocin and vasopressin secretion during ischemia, hypoxia/hypercapnia, inflammation, pain, and stress may play a significant role in the pathogenesis of cardiovascular diseases.

MO764AVF VOLUME BLOOD FLOW REDUCTION AS THE FIRST STAGE OF TREATMENT OF CENTRAL VEIN STENOSIS IN HD PATIENTS

Background and Aims It is well-known that central vein stenosis (CVS) significantly reduces the time of AVF functioning. At the same time, according to current guidelines (KDIGO, European Vascular Surgery Society, European Best Clinical Practice), only clinically significant CVS should be treated. Often, CVS becomes clinically manifest due to a significant increase of AVF volume blood flow (Qa) through the matured dialysis access. Aim: to assess the effect of Qa reduction on the CVS clinical course. Method We performed a retrospective study included 56 patients who underwent Qa reduction as the first step of treatment, and 62 patients who received endovascular interventions without Qa reduction (balloon angioplasty supplemented with stenting if necessary). Blood flow reduction was performed using banding under intraoperative ultrasound control. Results Surgical banding leads to a clinically obvious and statistically significant decrease in Qa in all patients – fig. 1. In contrast, after endovascular intervention most of the patients show a modest but statistically significant increase in Qa - fig. 2. All surgeries were performed to reduce the severity of clinical manifestations of CVS. AVF was better available for immediate cannulation after endovascular interventions than after banding: RR=4,537 [95%CI 1,416; 14,84], p=0,0116. However, the probability of successful cannulation at the third postoperative HD session did not differ between groups: RR=3.024 [95%CI 0.674; 13.67], p=0.2126. Taking in consideration these findings, we can conclude that the short-term results of Qa reduction are satisfactory. After Qa reduction in case of recurrence of CVS symptoms or absence of their complete resolving, we supplemented the treatment with endovascular interventions. Both primary and secondary patency were significantly better than in the case of endovascular interventions without Qa reduction – fig. 3. Moreover, in patients who underwent endovascular interventions without Qa reduction, higher Qa values were associated with decrease of the primary and secondary patency – fig. 4. So, increasing or maintaining large Qa values after endovascular intervention may be an important risk factor for CVS relapse and AVF function loss. Conclusion Qa is an important factor of CVS clinical manifestation. When determining treatment strategy, it is necessary to evaluate Qa first and reduce it, if necessary. Manage of Qa allows to transfer manifest CVS into its subclinical course, which itself leads to improved treatment results. Endovascular interventions are the preferred treatment of CVS with clinical manifestations in a case of underlying normal or suboptimal Qa.

Positive and Negative Aspects of Sodium Intake in Dialysis and Non-Dialysis CKD Patients

Sodium intake theoretically has dual effects on both non-dialysis chronic kidney disease (CKD) patients and dialysis patients. One negatively affects mortality by increasing proteinuria and blood pressure. The other positively affects mortality by ameliorating nutritional status through appetite induced by salt intake and the amount of food itself, which is proportional to the amount of salt under the same salty taste. Sodium restriction with enough water intake easily causes hyponatremia in CKD and dialysis patients. Moreover, the balance of these dual effects in dialysis patients is likely different from their balance in non-dialysis CKD patients because dialysis patients lose kidney function. Sodium intake is strongly related to water intake via the thirst center. Therefore, sodium intake is strongly related to extracellular fluid volume, blood pressure, appetite, nutritional status, and mortality. To decrease mortality in both non-dialysis and dialysis CKD patients, sodium restriction is an essential and important factor that can be changed by the patients themselves. However, under sodium restriction, it is important to maintain the balance of negative and positive effects from sodium intake not only in dialysis and non-dialysis CKD patients but also in the general population.

REGULATION OF BREATHING IN A WIDE RANGE OF PHYSICAL ACTIVITIES

In modern physiology, very simplified perceptions of such an essential system for the body as the respiratory system have taken root. The system analysis showed that at a physical load of more than 50 W, the tissue respiratory subsystem is activated, providing a volume blood flow rate adequate to the amount of oxygen consumed, and in the external respiratory subsystem the regulation on oxygen voltage in arterial blood is activated, and the regulation on carbon dioxide voltage is deactivated. The role of respiratory frequency in increasing the rate of diffusion through the alveolar capillary membrane is shown. For physiologists, medical professionals and trainers.

Abstract P732: Genetic Ablation of Endothelial C3a-Receptor Confers Cerebrovascular Protection Independent of the Dynamics of Reperfusion in Stroke

Background: Stroke enhances endothelial C3a Receptor (C3aR End ) expression and humoral levels of C3a which is further exacerbated by intravenous thrombolysis (IVT). Therefore, it is critical to investigate the role of C3aR End in post-stroke neurovascular injury. Hypothesis: Genetic depletion of C3aR is vasculoprotective in stroke. Methods: Using a loxP - Cre approach (C3aR Flox/Flox xCdh5 Cre ), we generated mice conditionally deficient or sufficient in C3aR End (C3aR End-/- or C3aR End+/+ ), and subjected males (6±0.5-mo old) to thrombotic stroke (TS). Cerebral blood flow (CBF), behavioral outcomes, infarct volume, blood brain barrier (BBB) leakage, brain hemoglobin (Hb) content, brain tissue oxygen (PbtO 2 ) , neutrophil polarization ( Proinflammatory N1: Li6G + CD206 - vs. Antiinflammatory N2: Li6G + CD206 + ) and their brain infiltration were analyzed. P<0.05 was considered statistically significant. Results: TS resulted in similar degree of cerebral ischemia in both groups (N=10/gp); however, CBF, behavior, and infarct volume were significantly improved in C3aR End-/- vs. C3aR End+/+ mice at 72h post-TS. BBB-leakage and brain-Hb at 72h were less in C3aR End-/- vs. C3aR End+/+ mice but this did not meet significance (N=5/gp). Interestingly, C3a infusion 3h post-TS significantly enhanced BBB-leakage and brain-Hb in C3aR End+/+ but not in C3aR End-/- mice at 72h (N=5/gp), demonstrating that C3a in conjunction with C3aR End exacerbates neurovascular injury in TS. Moreover, late-IVT at 4h post-TS (2 mg/kgbwt; N=8/gp) significantly enhanced PbtO 2 in C3aR End-/- vs. C3aR End+/+ mice when assessed at 6h. Finally, C3aR deficiency significantly enhanced the N2/N1 ratio relative to the C3aR sufficient group at 24h post-TS (N=3/gp); thus inducing an anti-inflammatory effect and reduced neutrophil brain infiltration. Conclusion: C3aR End plays a critical role in stroke injury. Future studies targeting brain specific C3aR End are warranted.

Cerebral Ultrasound Time-Harmonic Elastography Reveals Softening of the Human Brain Due to Dehydration

Hydration influences blood volume, blood viscosity, and water content in soft tissues – variables that determine the biophysical properties of biological tissues including their stiffness. In the brain, the relationship between hydration and stiffness is largely unknown despite the increasing importance of stiffness as a quantitative imaging marker. In this study, we investigated cerebral stiffness (CS) in 12 healthy volunteers using ultrasound time-harmonic elastography (THE) in different hydration states: (i) during normal hydration, (ii) after overnight fasting, and (iii) within 1 h of drinking 12 ml of water per kg body weight. In addition, we correlated shear wave speed (SWS) with urine osmolality and hematocrit. SWS at normal hydration was 1.64 ± 0.02 m/s and decreased to 1.57 ± 0.04 m/s (p &lt; 0.001) after overnight fasting. SWS increased again to 1.63 ± 0.01 m/s within 30 min of water drinking, returning to values measured during normal hydration (p = 0.85). Urine osmolality at normal hydration (324 ± 148 mOsm/kg) increased to 784 ± 107 mOsm/kg (p &lt; 0.001) after fasting and returned to normal (288 ± 128 mOsm/kg, p = 0.83) after water drinking. SWS and urine osmolality correlated linearly (r = −0.68, p &lt; 0.001), while SWS and hematocrit did not correlate (p = 0.31). Our results suggest that mild dehydration in the range of diurnal fluctuations is associated with significant softening of brain tissue, possibly due to reduced cerebral perfusion. To ensure consistency of results, it is important that cerebral elastography with a standardized protocol is performed during normal hydration.

Application of Grid Complexity-Based Magnetic Resonance Imaging in Monitoring Electroencephalogram Signals of Anesthetized Patients

Objective: In this paper, a lattice algorithm is used to explore the effect of MRI on anesthesia when used in neurosurgery. Methods: Sixty patients with glioma were randomly divided into two groups. Thirty patients underwent intracranial glioma resection (iMRI group) under the guidance of intraoperative magnetic resonance imaging (iMRI) and functional neuronavigational, and 30 patients underwent functional neuronavigational. Guide the traditional resection of traditional craniotomy gliomas (group N), and record the general situation, anesthesia time, operation preparation time, operation time, intraoperative blood loss, infusion volume, blood transfusion rate, preoperative and postoperative hemoglobin concentrations, Postoperative body temperature, dosage of muscle relaxant, perioperative accidents related to iMRI and anesthesia. Results: Compared with the N group, the general conditions, anesthesia time, intraoperative blood loss, infusion volume, blood transfusion rate, hemoglobin concentration, and postoperative body temperature of the patients in the iMRI group were not significantly different (P > 0.05), but the time for preparation and operation. It was significantly prolonged, and the amount of muscle relaxant was significantly increased (P < 0.05). There were no accidents related to iMRI and anesthesia in both groups. Conclusion: The use of iMRI in neurosurgical surgery improves the accuracy of surgery and makes tumor resection more complete, but the operation time is significantly longer, and other perioperative characteristics are not different from traditional neurosurgery. iMRI is used for anesthesia in neurosurgery. In addition to following the general principles of neurosurgery anesthesia, attention should also be paid to the regulation of anesthesia for long-term surgery.