Selective solid-phase extraction of catecholamines from plasma using nanofibers doped with crown ether and their quantitation by HPLC with electrochemical detection.

A simple and convenient preparation method has been developed for polymeric crown ethers containing the dibenzo-18-crown-6 subunit and electrospun composite nanofibers composed of polymeric crown ethers with polystyrene (PCE-PS). Furthermore, this composite nanofiber was used as a sorbent for selective extraction of plasma catecholamines, viz. dopamine (DA), norepinephrine (NE), and epinephrine (E). After the protein deposition of the plasma sample, the supernatant was adjusted to neutral pH with buffer solution. Then, the mixture was loaded and pushed through a column packed with composite nanofiber sorbent, and the analytes were eluted with 50 µL of acetic acid. The effectiveness of the plasma sample cleanup method was verified by high-performance liquid chromatography with electrochemical detection (HPLC-ECD). The PCE-PS packed column may prove clinically useful, as it provides a convenient and selective method for evaluation of human plasma catecholamines. Graphical Abstract Scheme showing the selective packed fiber SPE of catecholamines from spiked plasma using nanofibers doped with ploymeric crown ether.

Thromboxane A2 in the paraventricular hypothalamic nucleus mediates glucoprivation-induced adrenomedullary outflow.

Glucoprivation stimulates a rapid sympathetic response to release and/or secrete catecholamines into the bloodstream. However, the central regulatory mechanisms involving adrenoceptors and prostanoids production in the paraventricular hypothalamic nucleus (PVN) that are responsible for the glucoprivation-induced elevation of plasma catecholamines are still unresolved. In this study, we aimed to clarify whether glucoprivation-induced activation of noradrenergic neurons projecting to the PVN can induce α- and/or ß-adrenergic receptor activation and prostanoids production in the PVN to elevate plasma catecholamine levels. We examined the effects of α- and ß-adrenergic receptor antagonists, a cyclooxygenase inhibitor, a thromboxane A synthase inhibitor, and a PGE2 subtype EP3 receptor antagonist on intravenously administered 2-deoxy-D-glucose (2-DG)-induced elevation of noradrenaline in the PVN and plasma levels of catecholamine in freely moving rats. In addition, we examined whether intravenously administered 2-DG can increase prostanoids levels in the PVN microdialysates. Intracerebroventricular (i.c.v.) pretreatment with phentolamine (a non-selective α-adrenergic receptor antagonist) suppressed the 2-DG-induced increase in the plasma level of adrenaline, whereas i.c.v. pretreatment with propranolol (a non-selective ß-adrenergic receptor antagonist) suppressed the 2-DG-induced elevation of the plasma level of noradrenaline. I.c.v. pretreatment with indomethacin (a cyclooxygenase inhibitor) and furegrelate (a thromboxane synthase inhibitor) attenuated the 2-DG-induced elevations of both noradrenaline and adrenaline levels. Furthermore, 2-DG administration elevated the thromboxane B2 level, a metabolite of thromboxane A2 in PVN microdialysates. Our results suggest that glucoprivation-induced activation of α- and ß-adrenergic receptor in the brain including the PVN and then thromboxane A2 production in the PVN, which are essential for the 2-DG-induced elevations of both plasma adrenaline and noradrenaline levels.

Level of plasma catecholamine predicts surgical outcomes of carotid body tumors: Retrospective cohort study.

BACKGROUNDS: Carotid body tumors (CBTs) are rare neoplasms and some of them produce catecholamine. Although operations for catecholamine-producing CBTs are safe, the relationship between prognosis and endocrine function has not been analyzed before. METHODS: Patients diagnosed with CBTs in our department between 2009 and 2018 were analyzed. Plasma catecholamine was examined as a variable of surgical outcomes and prognosis by using statistical methods. RESULTS: Patients who suffered CBTs and underwent operations were divided into two groups according to their plasma catecholamine. Patients in the normal group had more or heavier surgical complications, such as neurological complications (P = .008) and blood loss (P = .03), than those in the high group. However, overall survival, local recurrence, and remote metastasis were not varied significantly in both groups. CONCLUSIONS: A high level of plasma catecholamine was a predictor for the improved operative outcomes of CBTs. Hence, nonfunctional CBTs had further short-term surgical complications.

Association between internet gaming addiction and leukocyte telomere length in Korean male adolescents.

Internet gaming addiction (IGA) has been associated with many negative health outcomes, especially for youth. In particular, the potential association between IGA and leukocyte telomere length (LTL) has yet to be examined. In this study we compared LTL in Korean male adolescents with and without IGA and examined the association between LTL and autonomic functions. Specifically, plasma catecholamine, serum cortisol, and psychological stress levels were measured as autonomic functions. Data were collected using participant blood samples analyzed for LTL, catecholamine, and cortisol levels and a set of questionnaires to assess IGA and psychological stress levels of the participants. The LTL measurements were made using a qPCR-based technique, and the relative LTL was calculated as the telomere/single copy (T/S) ratio. T/S ratio was significantly shorter in the IGA group than in the non-IGA group (150.43 ±â€¯6.20 and 187.23 ±â€¯6.42, respectively; p < .001) after adjusting for age. In a univariate regression analysis, age, daily Internet gaming time, IGA score, and catecholamine level (epinephrine and norepinephrine) were significantly associated with T/S ratio. However, duration of Internet gaming exposure, dopamine, cortisol, and psychological stress levels were not found to be associated with T/S ratio. In the final multiple linear regression model, age, daily Internet gaming time, and epinephrine level showed statistically significant relationships with T/S ratio. Our results indicate that in addition to age, involvement in excessive Internet gaming may induce LTL shortening in male adolescents, which may be partially attributable to changes in autonomic function such as catecholamine level. These findings further understanding of the health effects of IGA and highlight the need for screening and intervention strategies for male adolescents with IGA.

Influence of tumor size on anesthetic management for pheochromocytoma resection.

The relationship between tumor size and the complexity of anesthetic management was studied using several values: plasma catecholamine concentrations, requirement of vasoactive agents, surgical time, blood loss, plasma glucose concentrations, and hemodynamic variables. Ten patients with clinical and laboratory diagnosis of pheochromocytoma were prospectively studied. Each anesthesia was maintained using inhalational anesthetic agents. Control of arterial blood pressure (ABP), heart rate (HR), and pulmonary artery blood pressure (PABP) was attempted with only titrating the inhalational anesthetics and adenosine triphosphate (ATP). If the titration of both the inhalational anesthetic and ATP failed to control ABP, HR, or PABP, then phentolamine, propranolol, trinitroglycerine, or norepinephrine was additionally used. Tumor weight was significantly correlated with amount of blood loss, surgical time, duration of ATP requirement, maximal dose of ATP infusion used, maximal plasma glucose concentration, and plasma total catecholamine concentration. However, the tumor weight was not correlated with hemodynamic variables. Patients who required propranolol generally had a significantly larger tumor than those who did not. In conclusion, surgical removal of large pheochromocytoma required more complicated anesthetic management than that of small pheochromocytoma.

Plasma Norepinephrine in Hypertensive Rats Reflects α(2)-Adrenoceptor Release Control Only When Re-Uptake is Inhibited.

UNLABELLED: α(2)-adrenoceptors (AR) lower central sympathetic output and peripheral catecholamine release, thereby protecting against sympathetic hyperactivity and hypertension. Norepinephrine re-uptake-transporter effectively (NET) removes norepinephrine from the synapse. Overflow to plasma will therefore not reflect release. Here we tested if inhibition of re-uptake allowed presynaptic α(2)AR release control to be reflected as differences in norepinephrine overflow in anesthetized hypertensive spontaneously hypertensive rats (SHR) and normotensive rats (WKY). We also tested if α(2)AR modulated the experiment-induced epinephrine secretion, and a phenylephrine-induced, α(1)-adrenergic vasoconstriction. Blood pressure was recorded through a femoral artery catheter, and cardiac output by ascending aorta flow. After pre-treatment with NET inhibitor (desipramine), and/or α(2)AR antagonist (yohimbine, L-659,066) or agonist (clonidine, ST-91), we injected phenylephrine. Arterial blood was sampled 15 min later. Plasma catecholamine concentrations were not influenced by phenylephrine, and therefore reflected effects of pre-treatment. Desipramine and α(2)AR antagonist separately had little effect on norepinephrine overflow. Combined, they increased norepinephrine overflow, particularly in SHR. Clonidine, but not ST-91, reduced, and pertussis toxin increased norepinephrine overflow in SHR and epinephrine secretion in both strains. L-659,066 + clonidine (central α(2)AR-stimulation) normalized the high blood pressure, heart rate, and vascular tension in SHR. α(2)AR antagonists reduced phenylephrine-induced vasoconstriction equally in WKY and SHR. CONCLUSIONS: α(2A)AR inhibition increased norepinephrine overflow only when re-uptake was blocked, and then with particular efficacy in SHR, possibly due to their high sympathetic tone. α(2A)AR inhibited epinephrine secretion, particularly in SHR. α(2A)AR supported α(1)AR-induced vasoconstriction equally in the two strains. α(2)AR malfunctions were therefore not detected in SHR under this basal condition.

Effects of Spinal and Inhalational Anesthesia on Plasma Caticholamines / 대한마취과학회지

Surgery represents a noxious stimulus to the body, which responds to the injury in the form of an endocrine metabolic reaction. This stress responsehas usually been considered to be a homeostatic defence mechanism by which the body protects itself against injury. This study was primarily undertaken to observe the modulation of stress response to the surgical stimuli under the effects of general and spinal anesthesia by measuring endogenous catecholamines. Fifteen pateints scheuled for elective surgical procedures on the lower half of the body were divided into two group: general and spinal anesthesia groups. No premedication was given to any patient. After the patient was laid down the surgical table, intravenous line was placed and secured in an antecuhital vein for maintenance of fluid and obtaining blood samples. After the intravenous cathether was inserted and a 10-minute rest period was allowed for reassurance, the first baseline sample was obtained for measurement of catecholamines and then anesthesia was induced. .General anesthesia group: Anesthesia in five patients was induced with sodium thiopental (5 mg/ kg), succinylcholine (1 mg/kg) followed by endotracheal intubation and was maintained with halothane, N2O and muscle relaxation using pancuronium. Spinal anesthesia group: Spinal anesthesia in ten patients was performed in a sitting position at L3-L4 intervertebral space using lidocaine 50-150 mg. The anesthesia level was determined by a pinprick test. Subsequent samples were obtained at 30 minutes after the surgical incision and in the recovery room at least 60 minutes after the discontiuation of inhalational anesthesia or after recovery of senastion and motor function of the lower extremites. Mean arterial pressure was measurd by a noninvasive automatic blood pressure monitor. Plasma epinephrine and norepinephrine were measured by Peuler and Johnson radioenzymatic method. The results are summerized as follows: Inhalation anesthesia group: Plasma norepinephrine was increased during surgery and epinephrine was increased during the postoperative recovery period. Spinal anesthesia group: Plasma norepinephrine and epinephrine were not increased during the intra and postoperative periods. High spinal anesthesia resulted in a suppression of both plasma norepinephrine, epinephrine with a fall of mean arterial pressure but no changes of norepinephrine, epinephrine, or mean arterial pressure were observed in the patients receiving low spinal anesthesia. There was a relationship between the sensory dermatome anesthesia level and changes of both plasma norepinephrine (r=0.748, P<0.01)and epinephrine (r=0.667, P<0.05). There is a relationship between changes of blood pressure and plasma norepinephrine levels during spinal anesthesia and inhalational anesthesia (r=0.827, p<0.01). The effect of spinal anesthesia on adrenergic tone depends on the level of anesthesia. The catecholamine responses to surgical stress were prevented by low spinal anesthesia which had no supression of efferent adrenergic tone. Therefore, low spinal anesthesia maybe useful to prevent adrenergic responses to surgical stress in high-risk patients scheduled for surgery on the lower half of the body.

The beta-adrenergic Receptor Concentration and Plasma Catecholamine in Congestive Heart Failure

To identify the role of the myocardial beta-adrenergic pathway in congestive heart failure, we examined beta-adrenergic receptor density and C-AMP by receptor assay with mononuclrear cell and polymorphonuclear cell in 7 cases of normal control and 7 cases of congestive heart failure. The results were as follows: 1)The mean serum concerntrations of norepinephrine(566.00+/-48.12 pg/ml)and epinephrine(353.14+/-44.24 pg/ml) in congestive heart failure group were significantly higher than those(218.12+/-17.08 pg/ml, 187.23+/-24.62 pg/ml)in normal contral group(P<0.05 for each comparison). 2) In normal control group, the receptor concentration of mononuclear cell was 35.51+/-19.19 fmol/mg and that of polymorphonuclrear cell was 35.53+/-15.05 fmol/mg. The affinity constant of mononuclear cell was(2.47+/-0.42)x10(9)/m and that of polymorphonuclear cell was(2.24+/-0.58)x10(9)/m. 3) In congestive heart failure group, the receptor concentration of mononuclear cell(29.31+/-5.41 fmol/mg) was significantly lower than that in normal control group(p<0.05). And the affinity constant(3.57+/-1.02)x10(9)/m) was significantly higher than that in normal control group(p<0.05). 4) In congestive heart failue group, the receptor concentration of polymorphonuclear cell(33.15+/-10.46 fmol/mg) was not significantly different from that in normal control group. And the affinity constant(2.66+/-0.43)x109/m) was not significantly different from that in normal control group. 5) In congestive heart failure group, the C-AMP concentrations of mononuclear cell(basal 119.9+/-17.2 pmol/min/mg, isoproterenol stimulation 137.2+/-23.2 pmol/min/mg) were significantly lower than those(basal 205.2+/-21.1 pmol/min/mg, isoproterenol stimulation 267.5+/-34.3 pmol/min/mg) in normal control group(p<0.05 for each comparison). 6) In congestive heart failure group, the C-AMP concentrations of polymorphonuclear cell(basal 115.2+/-34.3 pmol/min/mg, isoproterenol stimulation 142.5+/-20.5 pmol/min/mg) were significantly lower thatn those(basal 186.3+/-24.2 pmol/min/mg, isoproterenol stimulation 233.4+/-32.2 pmol/min/mg) in normal control group(P<0.05 for each comparison). In conclusion, a decrease in beta-adrenergic density in congestive heart failure leads to subsensitivity of the beta-adrenergic pathway and decreased beta-agonist-stimulated contraction. However, other factors may be important in adenylate cyclase activation, and so further research is needed.