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Objective is to identify the pathogenic factors for progression of pancreatogenic cardiac failure in the nearest and remote periods.Materials and methods. The study was carried out on 130 male Wistar rats (292±4.0 g) divided into 4 groups. The animals were anesthetized with ethyl ether. Acute destructive pancreatitis was simulated in three experimental groups by infusion of bile (0.15 ml/kg body weight) taken from the bile duct into the pancreatic tissue. The isolated isovolumically contracting rat heart (according to E. L. Fallen et al) was simulated 24 hours, 7 days and 1 month after the bile infusion. The pressure in the left ventricle was measured by electric manometer BMT and registered along with the first derivative at the device N3384P calculating the systolic and diastolic blood pressure, and the speed of contraction and relaxation. At the same time the perfusate samples passed through the coronary arteries were har vested, and aspartate aminotransferase (AST) and glucose were determined by standard methods. To identify the cardiac depression, the high contraction rhythm and hypercalcemic and hypoxic perfusion were applied.Results. It was found that in acute destructive pancreatitis the power and speed parameters of the heart con tractile function were altered that led to lowering the systolic blood pressure and velocity of contraction and relax ation of the left ventricular myocardium and increased diastolic blood pressure as an indicator of cardyomyocyte contracture rate. These abnormalities were evidently manifested in increased heartbits, including hypercalcemic and hypoxic perfusion of the isolated hearts. Glucose consumption was raised per each mmHg generated by the ventricular pressure.Conclusion. the most significant pathogenetic factors of pancreatogenic heart failure include hypoxia, car diomyocyte membrane destruction, inhibition of sarcolemma Capump, sarcoplasmic reticulum, and mitochondrial dysfunction. The maximum depression of myocardial contractility of the left ventricle is detecting during the first day and in a month after simulated pancreatic necrosis.

Highlights: [•] LTA likely affects calcium-handling of cardiomyocytes. [•] Early stimulating effect of LTA on cardiomyocyte contractility. [•] Late depression of cardiomyocyte contractility: Single-cell sarcomere contraction analysis. [•] Findings reflect the clinical sepsis situation – effects are exacerbated by reduced extracellular calcium concentrations. [ABSTRACT FROM AUTHOR]

Thaliporphine was found to ameliorate endotoxin-induced circulatory failure and mortality in rodents. The aims of the present study were to assess whether thaliporphine could improve cardiac function in endotoxemic rats and to investigate the underlying mechanisms. Cardiac function was evaluated by pressure-volume loop analysis in pentobarbital-anesthetized rats 24 h after intravenous injection of lipopolysaccharide (LPS) (4 mg/kg) with or without thaliporphine (1 mg/kg, iv). The intracellular Ca transients, nitric oxide (NO), and reactive oxygen species (ROS) in enzymatically isolated ventricular cells were measured by fluorescent indicators. Western blotting was used to analyze the change of protein expression in response to LPS with or without thaliporphine in rat ventricle, H9C2 and Raw264.7 cells. Cardiac depression was found to coincide with the decreased intracellular Ca transients and the increased expression of nitrotyrosine on SERCA2 in rat ventricles after 24-h endotoxemia. Thaliporphine decreased intracellular NO and ROS level in ventricular cells and the nitrosylation of SERCA2, which resulted in recovering the functional properties of intracellular Ca handling and cardiac contraction. In H9C2 cells, LPS-induced nuclear translocation of nuclear factor kappa B (NF-κB) could be attenuated by thaliporphine. In Raw264.7 cells, thaliporphine attenuated LPS-induced TAK-1 phosphorylation and IκBα degradation in association with the inhibition of inducible nitric oxide synthase (iNOS) and tumor necrosis factor alpha (TNF-α) expression and the production of NO and ROS. In conclusion, thaliporphine ameliorates LPS-induced cardiac depression through attenuating TLR4 signaling in the downstream of TAK-1 phosphorylation and NF-κB signaling in both cardiomyocytes and macrophage to prevent cardiac SERCA2 from nitrosylation by peroxynitrite via decreasing iNOS and TNF-α expression. [ABSTRACT FROM AUTHOR]

The article offers information on a study which examined the potentially fatal mechanisms of the tricyclic antidepressant drug imipramine in rats. Variables measured in the study included the left ventricular developed pressure (LVDP), velocity oof the change in pressure and heart rate combined with the total magnesium efflux. It concludes that cardiac depression in rats is due to imipramine-induced increase in intracellular ionized magnesium concentrations coupled with activation of extracellular signal-regulated kinases ½.

Bee venom (BV) has been used in Oriental medicine to treat inflammatory diseases, such as tendonitis, bursitis, and rheumatoid arthritis, despite the sensitivity of the victims and toxicity of the venom. This study examined the mechanisms for the effects of BV on the cardiovascular system in rats. The arterial pressure and heart rate (HR) were measured in anesthetized rats. In addition, the left ventricular development pressure (LVDP) and total magnesium efflux ([Mg]e) in isolated perfused hearts, the vascular tonic responses in the isolated aorta, and the blood ionic and biochemical changes were determined simultaneously. In the anesthetized rats, the mean arterial pressure, systolic pressure, and pulse pressure were reduced by BV in a dose-dependent manner, even though the HR was increased. BV had no effects on the relaxation of phenylephrine- or KCl-induced contraction of the aortic rings. In the isolated hearts, BV generated a reversible decrease in the LVDP and velocity with changes in pressure, which were accompanied by increases in the HR and [Mg]e. BV increased the plasma ionized and total magnesium concentrations, and decreased the total magnesium level in the red blood cells. The ratio of ionized calcium/ionized magnesium was also decreased by the BV treatment. BV caused a detectable increase in blood creatine kinase, glutamic oxaloacetic transaminase, and lactic dehydrogenase, as well as a decrease in the blood total protein albumin and globulin levels. These results suggest that BV induces cardiovascular depression by decreasing the cardiac pressure and increasing the ionized magnesium concentration in the blood. [ABSTRACT FROM AUTHOR]

Abstract: This study investigated the signaling pathways responsible for ketamine-induced cardiac depression in guinea pigs. The left ventricular development pressure (LVDP), velocity of the change in pressure (dP/dt), and heart rate (HR) accompanied with the total magnesium efflux ([Mg]e) were measured simultaneously in perfused hearts. The level of activation of the extracellular signal-regulated kinases 1/2 (ERK 1/2) and p38 mitogen-activated protein (MAP) kinase. The intracellular ionized magnesium concentration ([Mg2+]i) was measured using Mag-fura 2 AM in a single cardiomyocyte. Ketamine produced reversible decreases in the LVDP, dP/dt, and HR accompanied by increases in the [Mg]e. Ketamine also produced significant activation of p38 MAP kinase and ERK 1/2, and produced a dose-dependent increase in the [Mg2+]i, which was inhibited SB203580 and PD98059. These results suggest that ketamine-induced cardiac depression can be partly responsible for the increase in [Mg2+]i and [Mg]e, accompanied by the activation of p38 MAP kinase and ERK 1/2 in guinea pigs. [Copyright &y& Elsevier]

The pharmacokinetic properties of the short-actingµ opioid receptor-agonist remifentanil makes it possible to give cardiac surgical patients a deep intraoperative anesthesia without experiencing postoperative respiratory depression and a prolonged stay in the intensive care unit (ICU). However, previous investigations have shown that patients who received remifentanil required additional analgesia during the early postoperative period as compared to patients who received fentanyl. The aim of the present study therefore was to investigate the effects of supplementing remifentanil to a standard fentanyl-based anesthesia in coronary artery bypass grafting (CABG).The study was prospective, randomized, double-blind, and placebo-controlled. Twenty male patients aged 55–70 years were included. All patients received a standard fentanyl and isoflurane-based anesthesia. In addition, the patients were randomized to receive either remifentanil 0.5 µg kg−1 min−1 or placebo during surgery. Hemodynamic recordings and measurements of blood glucose and plasma adrenaline and noradrenaline were performed intra- and postoperatively.Remifentanil reduced the hemodynamic and metabolic response to surgical stress compared to the standard fentanyl-based anesthetic regimen. However, the patients in the remifentanil group had a lower cardiac output (CO), left ventricular stroke work index (LVSWI), and mixed venous oxygen saturation (SvO2), and a higher central venous pressure (CVP) than the patients in the placebo group during the early postoperative phase, indicating a postoperative cardiac depression in the remifentanil group.In CABG, remifentanil reduces the hemodynamic and metabolic responses during surgery but seems to give a cardiac depression in the early postoperative phase. [ABSTRACT FROM AUTHOR]

The authors discuss a study which described the contribution of the toll-like receptor (TLR) 3 to cardiac dysfunction, by Gao and colleagues, published within the issue. They provide physiological information on TLR, including its mechanism of action and association with nuclear factor-κB and messenger RNA. They commend the study authors for demonstrating the relevance of the systemic absence of TLR 3 to mitigate sepsis-induced cardiac depression.