The Association Between Plasma Osmolarity and In-hospital Mortality in Cardiac Intensive Care Unit Patients

Objectives: Plasma osmolarity is a common marker used for evaluating the balance of fluid and electrolyte in clinical practice, and it has been proven to be related to prognosis of many diseases. The purpose of this study was to identify the association between plasma osmolarity and in-hospital mortality in cardiac intensive care unit (CICU) patients.Method: All of the patients were divided into seven groups stratified by plasma osmolarity, and the group with 290–300 mmol/L osmolarity was used as a reference group. Primary outcome was in-hospital mortality. The local weighted regression (Lowess) smoothing curve was drawn to determine the “U”-shaped relationship between plasma osmolarity and in-hospital mortality. Binary logistic regression analysis was performed to determine the effect of plasma osmolarity on the risk of in-hospital mortality.Result: Overall, 7,060 CICU patients were enrolled. A “U”-shaped relationship between plasma osmolarity and in-hospital mortality was observed using the Lowess smoothing curve. The lowest in-hospital mortality (7.2%) was observed in the reference group. whereas hyposmolarity (<280 mmol/L vs. 290–300 mmol/L: 13.0 vs. 7.2%) and hyperosmolarity (≥330 mmol/L vs. 290–300 mmol/L: 31.6 vs. 7.2%) had higher in-hospital mortality. After adjusting for possible confounding variables with binary logistic regression analysis, both hyposmolarity (<280 mmol/L vs. 290–300 mmol/L: OR, 95% CI: 1.76, 1.08–2.85, P = 0.023) and hyperosmolarity (≥330 mmol/L vs. 290–300 mmol/L: OR, 95% CI: 1.65, 1.08–2.52, P = 0.021) were independently associated with an increased risk of in-hospital mortality. Moreover, lengths of CICU and hospital stays were prolonged in patients with hyposmolarity or hyperosmolarity.Conclusion: A “U”-shaped relationship between plasma osmolarity and in-hospital mortality was observed. Both hyposmolarity and hyperosmolarity were independently associated with the increased risk of in-hospital mortality.

Immune-Mediated Mechanisms in Cofactor-Dependent Food Allergy and Anaphylaxis: Effect of Cofactors in Basophils and Mast Cells

Cofactors may explain why in some cases food ingestion leads to anaphylaxis while in others elicits a milder reaction or tolerance. With cofactors, reactions become more severe and/or have a lower allergen threshold. Cofactors are present in up to 58% of food anaphylaxis (FAn). Exercise, NSAIDs, and alcohol are the most frequently described, although the underlying mechanisms are poorly known. Several hypotheses have suggested the influence of these cofactors on basophils and mast cells (MCs). Exercise has been suggested to enhance MC activation by increasing plasma osmolarity, redistributing blood flow, and activating adenosine and eicosanoid metabolism. NSAIDs’ cofactor effect has been related with cyclooxygenase inhibition and therefore, prostaglandin E2 (PGE2) production. Indeed, overexpression of adenosine receptor 3 (A3) gene has been described in NSAID-dependent FAn; A3 activation potentiates FcϵRI-induced MC degranulation. Finally, alcohol has been related with an increase of histamine levels by inhibition of diamino oxidase (DAO) and also with and increase of extracellular adenosine by inhibition of its uptake. However, most of these mechanisms have limited evidence, and further studies are urgently needed. In conclusion, the study of the immune-related mechanisms involved in food allergic reactions enhanced by cofactors is of the utmost interest. This knowledge will help to design both tailored treatments and prophylactic strategies that, nowadays, are non-existent.

The Role of Ambient Temperature and Plasma Osmolarity on Clinical Outcomes of Acute Myocardial Infarction Patients during Hajj

Background: Performance of Hajj is physically very demanding, especially if performed during the summer season. The aim of this study is to evaluate the importance of ambient temperature and dehydration, indicated by plasma osmolarity on the clinical outcomes of cardiac patients during Hajj season in 2017. Methods: We included all patients referred to tertiary center with acute coronary syndrome during Hajj period of 2017. Plasma osmolarity was calculated using concentrations of sodium, plasma glucose, and blood urea nitrogen at admission. Patients were stratified by groups (G) of admission osmolarity, clinical outcome was compared. The primary endpoints were in-hospital mortality, length of stay, Cardiac complications (heart failure, re-infarction, arrhythmia, shock and thrombus formation), left ventricular function and readmission rate. Result: Total of 300 patients were identified with mean age 56.2 ±12.1, 84% males and 97(32%) were pilgrims. They were exposed to average heat index 61.9 ±10.6° C. Significantly longer admissions were found in the group of higher osmolarity (G2) (≥295 mos/L) as compared to patients with normal osmolarity in G1 [6.7 ±14.9 VS 4.0 ±4.5, P=0.045]. Total in-hospital death rate was 4.3% (13). Using Binary regression analysis; osmolarity Group [p=0.009], Pilrgrim [P=0.005], Heat index [ P=0.005], were independent predictor of inhospital mortality, while Heat index is the only independent predictor for MACE [P=0.001]. Conclusion: Plasma osmolarity and heat index significantly affect cardiac patient’s outcome. These finding underscore the importance of health awareness of protection from dehydration for pilgrims during summer season.

Expression and functions of N-type Cav2.2 and T-type Cav3.1 channels in rat vasopressin neurons under normotonic conditions

Arginine vasopressin (AVP) neurons play essential roles in sensing the change in systemic osmolarity and regulating AVP release from their neuronal terminals to maintain the plasma osmolarity. AVP exocytosis depends on the Ca2+ entry via voltage-gated Ca2+ channels (VGCCs) in AVP neurons. In this study, suppression by siRNA-mediated knockdown and pharmacological sensitivity of VGCC currents evidenced molecular and functional expression of N-type Cav2.2 and T-type Cav3.1 in AVP neurons under normotonic conditions. Also, both the Cav2.2 and Cav3.1 currents were found to be sensitive to flufenamic acid (FFA). TTX-insensitive spontaneous action potentials were suppressed by FFA and T-type VGCC blocker Ni2+. However, Cav2.2-selective ω-conotoxin GVIA failed to suppress the firing activity. Taken together, it is concluded that Cav2.2 and Cav3.1 are molecularly and functionally expressed and both are sensitive to FFA in unstimulated rat AVP neurons. Also, it is suggested that Cav3.1 is primarily involved in their action potential generation.

Does Oxygen Uptake Before Physical Exercise Affect Tear Osmolarity?

Recently, it has been reported that tear osmolarity (Tosm) is correlated with plasma osmolarity and will increase during exertion. We aimed to assess whether inhaling oxygen-enriched air between exercises could significantly change the Tosm value. Thirty men aged 24.9 years were included in the study. A cycloergometer was used to perform the exercise protocol. We recorded the participants’ Tosm (mOsm/L), heart rate (HR, beats/minute), oxygen saturation, and blood pressure values. After the first exhaustive exercise (T1), participants inhaled oxygen in the experimental group and a placebo in the control group. After the second exercise (T2), another set of measurements was obtained. The Tosm value before exercise was 297.4 ± 1.21 and 296.53 ± 1.11 mOsm/L (p = 0.61718) and the HR was 72.6 ± 2.59 and 73 ± 2.59 beats/minute (p = 0.39949) in the study and the control group, respectively. At T1, Tosm was 303.67 ± 1.25 and 302.2 ± 1.25 mOsm/L (p = 0.41286) and the HR reached 178.04 ± 2.60 and 176.4 ± 2.60 beats/minute (p = 0.65832), respectively. At T2, Tosm in the study group reached 305.73 ± 0.86 mOsm/L (correlation with the use of oxygen: r = −0.3818), and in the control group, it was 308.4 ± 0.86 mOsm/L (p = 0.0373), while the HR reached 172.20 ± 2.53 beats/minute in the study group and 178.2 ± 2.53 beats/minute in the control group (p = 0.057). It was concluded that inhaling oxygen before and after exercise could increase the rate of recovery after exhaustive exercise.

Character of clinical and metabolic disorders caused by acetylsalicylic acid acute poisoning

Acute poisonings with non-opioid and analgesic antipyretics are the most frequent among other nosological groups of poisonings. The purpose. To evaluate the incidence of acute chemical trauma caused by acetylsalicylic acid poisoning in the structure of poisoning in the territory, as well as the functional systems’ disorders in the toxigenic period of poisoning and options of pathogenic therapy depending on the severity of condition and results of diagnostic methods. Materials and methods. Epidemiological analysis of poisoning in the territory was held according to the report form 64. In 2 groups (intermediate degree — n = 17; severe degree — n = 10) we assessed the functional system disorders to structure the intensive therapy options. Results. The number of poisonings caused by acetylsalicylic acid in 2008–2017 did not exceed 0,84 cases per 100 thousand population. The intermediate severity group with 32,2 (6,1) mg% toxicant volume had neurotoxic effect, metabolic acidosis — рН 7,28 (0,05), НСО3 — 19,8 (3,7) mmol/l, BE — 6,5 (3,9) mmol/l, respiratory alkalosis — раСО2 32,6 (2,6) mm Hg, plasma osmolarity — 302 (11,1) mmol/l and glucose level — 7,06 (0,53) mmol/l. In case of serious poisoning while plasma toxicant volume is higher than 41 мg%, neurotoxic disorders were more expressed, indicators of acid-alkaline condition — рН 7,2 (0,07), раСО2 — 31,8 (2,8) mm Hg, НСО3 — 18,4 (4,7) mmol/l, BE — 10,5 (3,9) mmol/l, lactate — 3,6 (0,7) mmol/l, aniongape > 18 m.e/l, hyperglycemia was observed — 8,78 (5,11) mmol/l and plasma osmolarity changed — 309 (8,0) mmol/l. In case of intermediate and severe poisoning, intensive therapy should be aimed for removing the unabsorbed poison: washing of stomach, enterosorption, intestinal lavage, toxicant and its metabolites elimination (completion of OTsK — volume of blood circulation), forced diuresis, acid-alkaline balance correction (1–2 mmol/kg while toxigenic period with maintaining 7,0–7,5 urine рН gap. When using therapy options, it is necessary to consider possible development of acute renal and liver failure, coagulopathies and change of glucose level in blood. Conclusions. Definition of acute poisoning severity on the basis of violations of functional systems is the key factor in prescribing the pathogenetic therapy.

Mathematical modeling of ischemic stroke

Objective: to determine the prognostic value of the indicators of fluid and electrolyte balance in the acutest period of severe ischemic stroke (IS). Patients and methods. A total of 150 patients with severe IS of various locations and pathogenetic subtypes were examined. The impact of plasma osmolarity or sodium levels on the course and prognosis of IS was studied on day 1 of the disease. Results and discussion. It has been established that in patients with severe IS, the most common type of fluid and electrolyte imbalance is hyperosmolar hypernatremic syndrome that develops at the onset of severe IS, serves as a factor for poor outcome, and is accompanied by high mortality. The rate of fatal outcomes in hypoosmolar syndromes is higher than that in normal plasma osmolarity, but significantly lower than that in hyperosmolar syndromes. Cerebral salt wasting (CSW) is associated with a higher mortality rate than syndrome of inappropriate antidiuretic hormone secretion (SIADH), which confirms a worse prognostic value in hypovolemia than in normo- and hypervolemia. The development of diabetes insipidus at the onset of IS reflects the degree of brainstem structural destruction and, accordingly, is associated with the highest rate of fatal outcomes. The cardioembolic pathogenetic subtype of IS is characterized by a more severe course and a higher probable mortality rate in both hypoosmolar and normosmolar conditions.Conclusion. Impaired fluid and electrolyte homeostasis is of significant prognostic value for the outcome of IS. In this case, the leading role is played by the hyperosmolar hypernatremic syndrome, in which the probability of a fatal outcome is highest and there is a need for continuous patient health monitoring and high-speed decision-making aimed to correct this condition. Therapeutic policy for diabetes insipidus depends on the duration of IS. The risk for fatal outcome in the cardioembolic pathogenetic subtype of IS is higher than that in atherothrombotic stroke, at any plasma osmolarity and sodium levels.