Cardiac arrest due to accidental overdose with norepinephrine dissolved in crystalloid.

Vasoactive agents should be administered through a controlled well-marked infusor pump, ideally via a central venous catheter if given over longer periods of time. During transfer of haemodynamically unstable patients with limited staffing and resources on site, a peripheral vasopressor infusion is sometimes resorted to as a temporary measure of optimising haemodynamic parameters. We report a case of accidental norepinephrine overdose after such practice, resulting in cardiac arrest. It illustrates the importance of careful use and labelling of vasoactive agents during the transport and handover of critically ill patients. Finally, we explore human factor issues associated with transfer from the pre-hospital to the in-hospital environment when such preparations are used.

Iatrogenic Takotsubo Cardiomyopathy Following Overdose Norepinephrine Administration During Percutaneous Coronary Intervention.

Takotsubo cardiomyopathy (TTC) is characterized by reversible ventricular dysfunction induced by endogenous and, occasionally, exogenous catecholamine. We present a report on a patient who developed TTC and cardiogenic shock during percutaneous coronary intervention (PCI) secondary to inadvertent norepinephrine administration. His hemodynamic status and cardiac function were totally restored within 1 week after hemodynamic support using intra-aortic balloon pump without sequela. Thus, TTC should be considered once a patient presents with symptoms mimicking acute coronary syndrome (ACS) after catecholamine administration.

Extracellular norepinephrine reduces neuronal uptake of norepinephrine by oxidative stress in PC12 cells.

Cardiac norepinephrine (NE) uptake activity is reduced in congestive heart failure. Our studies in intact animals suggest that this effect on the cardiac sympathetic nerve endings is caused by oxidative stress and/or NE toxic metabolites derived from NE. In this study, we investigated the direct effects of NE on neuronal NE uptake activity and NE transporter (NET), using undifferentiated PC12 cells. Cells were incubated with NE (1-500 microM) either alone or in combination of Cu(2+) sulfate (1 microM), which promotes free radical formation by Fenton reaction for 24 h. NE uptake activity was measured using [(3)H]NE. Cell viability was determined with the use of Trypan blue exclusion and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay, and cellular oxidative stress by dichlorodihydrofluorescein fluorescence and the GSH/GSSG ratio. Cell viability was reduced by NE >100 microM. At lower doses, NE produced oxidative stress and a dose-dependent reduction of NE uptake activity without affecting cell viability significantly. Cu(2+), which has no direct effect on NE uptake activity, potentiated oxidative stress and reduction of NE uptake activity produced by NE. This decrease of NE uptake activity was associated with reductions of NE uptake binding sites and NET protein expression by using the radioligand assay and Western blot analysis, but no changes in NET gene expression. In addition, the free-radical scavenger mannitol, and antioxidant enzymes superoxide dismutase and catalase, reduced oxidative stress and attenuated the reductions of NE uptake activity and NET protein produced by NE/Cu. Thus our results support a functional role of oxidative stress in mediating the neuronal NE uptake reducing effect of NE and that this effect of NE on NET is a posttranscriptional event.

Role of activation of the sympathoadrenal system in the realization of immune reactions during acute poisoning with organophosphorus compounds.

Experiments on Wistar rats showed that acute poisoning with organophosphorus compound dimethyldichlorovinylphosphate (0.2 and 0.8 LD50) was accompanied by suppression of the major immune reactions. Increasing the concentration of epinephrine and norepinephrine in the plasma produced less pronounced opposite effects, except for the influence on natural killer activity.

[Non-protein sulfhydryl groups in the blood of patients with stenocardia induced by physical stress]. / Nebilkovi sul'fhidryl'ni hrupy krovi u khvorykh na stenokardiiu napruzhennia za fizychnoho navantazhennia.

Patients suffering from stress-induced angina pectoris subjected to exertion show a decreased level of non-protein SH-groups in blood plasma and erythrocytes which depends on the level of myocardial hypoxia and may indicate metabolic exhaustion of the organism. Lowered concentrations of non-protein SH-groups are not a result of lipid peroxidation. Adrenalin is known to antagonize the depletion of non-protein SH-groups under exertion, while noradrenaline promotes the process of their oxidation. When the level of non-protein SH-groups decreases under exertion, the content of atherogenic lipids in blood does not increase, which implies that SH-groups are involved into the mechanism of appearance of atherogenic lipids in blood under exertion.

[Catecholamine concentration in blood, heart, and adrenals of rats following intraperitoneal injections of a cardiotoxic dose of adrenaline against a background of arfonad and rausedyl administration]. / Soderzhanie katekholaminov v krovi, serdtse i nadpochechnikakh krys pri vnutribriushinnoi in"ektsii kardiotoksicheskoi dozy noradrenalina na fone vvedeniia arfonada i rausedila.

A study was made of the adrenaline and noradrenaline content in the blood, myocardium and adrenals of 74 male Wistar rats. Four series of experiments were conducted with administration of noradrenaline alone and noradrenaline after premedication with arfonad (ganglion-blocking agent) or rausedil (reserpine drug). Distilled water was used in control experiments. The content of adrenaline and noradrenaline in blood and tissues was shown to change 45 seconds after noradrenaline administration and to return to normal by the 7th minute. Correlation of the catecholamine content in rat blood and tissues with morphological changes in the myocardium recorded in the analogous series of experiments has shown that the increased content of catecholamines in bloods is one of the most important factors in the pathogenesis of myocardial injury since the diminution of their content during ganglionic blockade is associated with a reduced heart injury. The noradrenaline content in the myocardium does not correlate with the severity of myocardial injury.

[Glucose-6-phosphate dehydrogenase in rat liver and myocardium following toxic doses of noradrenaline]. / Gliukozo-6-fosfatdegidrogenazy pecheni i serdechnoi myshtsy krys pri vvedenii toksicheskikh doz noradrenalina.

Administration of toxic doses of noradrenaline into rats led to exhaustion of noradrenaline reserves in liver and heart tissues with the simultaneous increase in the activity of glucose-6-phosphate dehydrogenase in the tissues. Actinomycin D, administered together with noradrenaline, completely prevented the elevation of the G6PD activity in the tissues studied. The data obtained suggest that sympathetic nervous system and its mediator are responsible for regulation of the rate of enzymatic protein synthesis in tissues.

Shock provocado por administración de Nor-Adrenalina

Se presenta un caso de shock provocado por administración intravenosa de Nor-Adrenalina. Se emplea la Dihidroergotamina droga bloqueadora de los receptores Alfa Adrenérgicos, con éxito en su tratamiento (AU)