Plasma Catecholamine Levels Research Articles

Laparoscopic resection of pediatric interaortocaval large paraganglioma

Paragangliomas (PGL) are extremely rare tumors, especially in children. While minimally invasive surgical techniques are well established in adult patients, the evidence in children is extremely limited. PGL have a rich blood flow and are located around large vessels; thus, operative exposure and resection are often difficult due to proximity to major vascular structures including renal vessels, vena cava, and aorta. In particular, surgery for interaortocaval large PGL is extremely challenging. In this report, we presented a case of a child with hormonally active interaortocaval large PGL that was resected laparoscopically. A 14-year-old girl was transferred to the emergency room due to acute chest pain and vomiting after falling from a vaulting box. At presentation, her blood pressure was 218/137 mmHg and enhanced computed tomography of her abdomen revealed a 6.5-cm hypervascular tumor with intratumoral hemorrhage in the interaortocaval area. The patient's plasma catecholamine and 24-h urinary catecholamine level were found to be elevated. 131 I-MIBG scan showed increased uptake in the tumor. The definitive diagnosis of PGL was made and we conducted elective laparoscopic excision of the retroperitoneal tumor. Careful and meticulous dissection was needed to separate the tumor from the surrounding vessels and tissues using a sealing device. Intraoperative hypertension was controlled using phentolamine, and the surgeon closely communicated with the anesthesiologist intraoperatively. Complete resection of the tumor was achieved laparoscopically. Total blood loss was 175 mL and the operating time was 422 min. Six months later, she remained well with no evidence of recurrence. The laparoscopic approach gave excellent exposure and observation of the tumor's relationship to surrounding structures. Our findings suggest that laparoscopic tumor removal for interaortocaval large PGL is a feasible and safe procedure in children with the improvement of laparoscopic surgical skills and devices.

The peripheral dopamine 2 receptor antagonist domperidone attenuates ethanol enhancement of dopamine levels in the nucleus accumbens.

Dopamine neuron firing in the ventral tegmental area (VTA) and dopamine release in the nucleus accumbens have been implicated in reward learning. Ethanol is known to increase both dopamine neuron firing in the VTA and dopamine levels in the nucleus accumbens. Despite this, some discrepancies exist between the dose of ethanol required to enhance firing in vivo and ex vivo. In the present study we investigated the effects of peripheral dopamine 2 subtype receptor antagonism on ethanol's effects on dopamine neurotransmission. Plasma catecholamine levels were assessed following ethanol administration across four different doses of EtOH. Microdialysis and voltammetry were used to assess the effects of domperidone pretreatment on ethanol-mediated increases in dopamine release in the nucleus accumbens. A place conditioning paradigm was used to assess conditioned preference for ethanol and whether domperidone pretreatment altered this preference. Open-field and loss-of-righting reflex paradigms were used to assess the effects of domperidone on ethanol-induced sedation. A rotarod apparatus was used to assess the effects of domperidone on ethanol-induced motor impairment. Domperidone attenuated ethanol's enhancement of mesolimbic dopamine release under non-physiological conditions at intermediate (1.0 and 2.0g/kg) doses of ethanol. Domperidone also decreased EtOH-induced sedation at 2.0g/kg. Domperidone did not alter ethanol conditioned place preference nor did it affect ethanol-induced motor impairment. These results show that peripheral dopamine 2 receptors mediate some of the effects of ethanol on nonphysiological dopamine neurotransmission, although these effects are not related to the rewarding properties of ethanol.

Astrocytes in the PVN are involved in corticotropin-releasing factor-induced sympathetic activation in rats

Corticotropin-releasing factor (CRF) plays a key role in stress responses in the brain. CRF activates not only the hypothalamic-pituitary-adrenal axis but also the sympathetic nervous system. We previously reported that both central administration of CRF and exposure to acute restraint stress (RS) increase plasma catecholamine levels and activate presympathetic neurons in the paraventricular hypothalamic nucleus (PVN). However, it is unclear whether glial cells in brain regions including the PVN are involved in CRF- or stress-induced sympathetic activation. In this study, we examined roles of astrocytes in the CRF-induced elevation of plasmas catecholamine levels (noradrenaline and adrenaline) using fluorocitrate which blocks glial metabolic function. Intracerebroventricular pretreatment of fluorocitrate suppressed the CRF-induced elevation of plasma levels of noradrenaline and adrenaline. On the other hand, microinjection of fluorocitrate into the PVN suppressed the CRF-induced elevation of adrenaline, but not of noradrenaline. Furthermore, we tried to examine effects of inhibition of astrocytes on RS-induced sympathetic activation. Our results suggest that astrocytic function in the brain is important for the CRF-induced sympathetic activation and the effects might be brain region-dependent.

ATP-sensitive K<sup>+</sup> channel activation in the brain is involved in elevation of plasma levels of adrenaline

Recently, we reported that restraint stress-induced elevation of plasma levels of adrenaline, but not of noradrenaline, was suppressed by intravenous and intracerebroventricular (i.c.v.) administration of glucose via brain thromboxane A2-dependent mechanisms. (Yamaguchi et al., 2022). Since glucose can be converted to ATP in the brain cells, in the present study, we investigate whether ATP-sensitive K+ channel (KATP channel) activity in the brain is involved in changes of plasma levels of catecholamines in urethane anesthetized rats. I.c.v. administered diazoxide (20 µg/rat), a KATP channel opener, and A-769662 (25 µg/rat), an AMPK activator, elevated plasma levels of adrenaline, but not noradrenaline. In contrast, i.c.v administered glibenclamide (25 µg/rat), a KATP channel antagonist, did not alter plasma levels of adrenaline. I.c.v. pretreatment with SQ29548 (10 µg/rat), a thromboxane A2 receptor antagonist, attenuated diazoxide- and A-7969662-induced elevation of plasma levels of adrenaline. These results suggest that KATP channel activation in the brain might trigger the activation of thromboxane A2 receptor, resulting in elevation of plasma levels of adrenaline.

Yokukansan, a traditional Japanese medicine, suppresses stress-induced sympathetic activation and central responses to stress in rats

Stress exposure activates the sympathetic nervous system. We previously reported that restraint stress and stress-related neuropeptides increases plasma catecholamine levels and that brain prostanoids medicate these responses in rats. Yokukansan (YKS), a traditional Japanese medicine, has been used for neurosis, night crying and irritability. Additionally, it has been reported that YKS is also effective against the behavioral and psychological symptoms of dementia in patients with Alzheimer's disease, stress-related anxiety-like behavior and stress-induced increase in plasma corticosterone in rodents. These previous findings raise the possibility that YKS can exert its action in the brain and has suppressive effects on stress responses. In this study, we examined effects of YKS on stress-induced sympathetic activation and stress responses in the brain using rats. Repeated administration with YKS suppressed stress-induced increase in plasma adrenaline level. YKS also suppressed stress-induced elevation of prostaglandin E2 and thromboxane B2 levels in the paraventricular hypothalamic nucleus (PVN). In addition, YKS suppressed stress-induced increases of acetylcholine, GABA and serotonin in the PVN. Our results suggest that YKS can ameliorate stress-induced sympathetic activation via inhibition of stress responses in the brain.

The role of β2 adrenergic receptor on infection development after ischaemic stroke

Mechanisms underlying post-stroke immune impairments and subsequent development of fatal lung infection have been suggested to involve multiple pathways, including hyperactivation of the sympathetic nervous system (SNS), which results in the excessive release of catecholamines and activation of β-adrenergic receptors (βARs). Indeed, previous reports from experimental studies demonstrated that post-stroke infection can be inhibited with treatment of β-blockers. However, the effectiveness of β-blockers in reducing post-stroke infection has yielded mixed results in retrospective clinical trials and its use remain controversial. In this study, we performed mid-cerebral artery occlusion in mice either genetically deficient in β2-adrenergic receptor (β2AR) or treated with non-selective and selective βAR antagonists to explore the contributions of the SNS in the development of post-stroke lung infection. Stroke induced a systemic activation of the SNS as indicated by elevated levels of plasma catecholamines and UCP-1 activity. However, β2AR deficient mice showed similar degrees of post-stroke immune impairment and infection rate compared to wildtype counterparts, potentially due to compensatory mechanisms common in transgenic animals. To overcome this, we treated post-stroke wildtype mice with pharmacological inhibitors of the βARs, including the non-selective antagonist propranolol (PPL) and selective β2AR antagonist ICI-118551. Both pharmacological strategies to block the action of SNS signalling were unable to reduce infection in mice that underwent ischaemic stroke. Overall, our data suggests that other mechanisms independent or in combination with β2AR activation contribute to the development of post-stroke infection.

Comparative study of dexmedetomidine vs. midazolam on plasma catecholamine levels and hemodynamics in patients with septic shock

To compare the effects of dexmedetomidine (DEX) and midazolam on the endogenous plasma catecholamine levels and the dosage of exogenous norepinephrine (NE) to maintain blood pressure in patients with septic shock. From January 2018 to December 2019, patients admitted to the department of critical care medicine of the Affiliated Hospital of Guizhou Medical University who needed invasive mechanical ventilation and had a stay of more than 48 hours in the intensive care unit (ICU) for septic shock and received DEX or midazolam for sedation were enrolled in this study. The hemodynamic data, arterial blood lactic acid (Lac) level, arterial blood gas analysis and vasoactive drug dose at 0, 12, 24, 48, 72 hours after entering the ICU were dynamically recorded, and the plasma catecholamine levels at 0, 24, 48 hours after entering the ICU were recorded. The acute physiology and chronic health evaluation II (APACHE II) score and sequential organ failure assessment (SOFA) score on ICU-admission were calculated. The parameters of prognosis were collected. A total of 24 patients were enrolled, 12 in the DEX group and 12 in the midazolam group. There were similar dynamic trends in heart rate (HR), central venous pressure (CVP), venous-arterial carbon dioxide pressure difference (Pv-aCO2), oxygenation index (PaO2/FiO2), and Lac level of patients between the two groups. Only the 12-hour CVP and 72-hour Pv-aCO2 in the DEX group were significantly higher than those in the midazolam group [CVP (mmHg, 1 mmHg = 0.133 kPa): 13±3 vs. 10±3, Pv-aCO2 (mmHg): 9.4±5.2 vs. 4.8±2.2, both P < 0.05], and the mean arterial pressure (MAP) of patients in the DEX group at 48 hours and 72 hours was significantly higher than that in the midazolam group (mmHg: 95±10 vs. 86±10, 96±9 vs. 88±7, both P < 0.05). There was no statistically significant difference in the duration of mechanical ventilation, ICU mortality or in-hospital mortality between the DEX group and the midazolam group [duration of mechanical ventilation (days): 5.6 (3.8, 9.5) vs. 10.5 (5.9, 15.0), ICU mortality: 16.7% vs. 33.3%, in-hospital mortality: 25.0% vs. 41.7%, all P > 0.05]. There was no significant difference in the dosage of propofol or sufentanil between the DEX group and the midazolam group [propofol (mg/kg): 0 (0, 9.35) vs. 4.07 (0, 13.75), sufentanil (μg/kg): 6.26 (4.90, 9.80) vs. 8.32 (3.52, 9.34), both P > 0.05]. The levels of plasma NE, dopamine and dobutamine in the DEX group at 48 hours were significantly lower than those in the midazolam group [NE (ng/L): 1 850.12 (342.16, 2 938.05) vs. 4 596.60 (3 310.56, 5 546.84), dopamine (ng/L): 119.10 (60.47, 200.71) vs. 275.40 (214.61, 418.88), dobutamine (ng/L): 51.20 (36.85, 75.59) vs. 98.97 (85.65, 107.10), all P < 0.05], but the amount of NE required to maintain MAP between 65 mmHg and 75 mmHg in the DEX group and the midazolam group was similar [μg/kg: 1 922 (1 170, 4 887) vs. 2 466 (2 043, 3 438), P > 0.05]. DEX can reduce plasma catecholamine levels in patients with septic shock more than midazolam, and does not increase the dose of exogenous NE, and has a smaller effect on hemodynamics in patients with septic shock than midazolam.

Effect of ingesting a meal and orthostasis on the regulation of splanchnic and systemic hemodynamics and the responsiveness of cardiovascular α1-adrenoceptors.

Postprandial orthostasis activates mechanisms of cardiovascular homeostasis to maintain normal blood pressure (BP) and adequate blood flow to vital organs. The underlying mechanisms of cardiovascular homeostasis in postprandial orthostasis still require elucidation. Fourteen healthy volunteers were recruited to investigate the effect of an orthostatic challenge (60°-head-up-tilt for 20 min) on splanchnic and systemic hemodynamics before and after ingesting an 800-kcal composite meal. The splanchnic circulation was assessed by ultrasonography of the superior mesenteric and hepatic arteries and portal vein. Systemic hemodynamics were assessed noninvasively by continuous monitoring of BP, heart rate (HR), cardiac output (CO), and the pressor response to an intravenous infusion on increasing doses of phenylephrine, an α1-adrenoceptor agonist. Neurohumoral regulation was assessed by spectral analysis of HR and BP, plasma catecholamine and aldosterone levels and plasma renin activity. Postprandial mesenteric hyperemia was associated with an increase in CO, a decrease in SVR and cardiac vagal tone, and reduction in baroreflex sensitivity with no change in sympathetic tone. Arterial α1-adrenoceptor responsiveness was preserved and reduced in hepatic sinusoids. Postprandial orthostasis was associated with a shift of 500 mL of blood from mesenteric to systemic circulation with preserved sympathetic-mediated vasoconstriction. Meal ingestion provokes cardiovascular hyperdynamism, cardiac vagolysis, and resetting of the baroreflex without activation of the sympathetic nervous system. Meal ingestion also alters α1-adrenoceptor responsiveness in the hepatic sinusoids and participates in the redistribution of blood volume from the mesenteric to the systemic circulation to maintain a normal BP during orthostasis.NEW & NOTEWORTHY A unique integrated investigation on the effect of meal on neurohumoral mechanisms and blood flow redistribution of the mesenteric circulation during orthostasis was investigated. Food ingestion results in cardiovascular hyperdynamism, reduction in cardiac vagal tone, and baroreflex sensitivity and causes a decrease in α1-adrenoceptor responsiveness only in the venous intrahepatic sinusoids. About 500-mL blood shifts from the mesenteric to the systemic circulation during orthostasis. Accordingly, the orthostatic homeostatic mechanisms are better understood.

Left ventricular depression and pulmonary edema in rats after short-term normobaric hypoxia: effects of adrenergic blockade and reduced fluid load

Acute normobaric hypoxia may induce pulmonary injury with edema (PE) and inflammation. Hypoxia is accompanied by sympathetic activation. As both acute hypoxia and high plasma catecholamine levels may elicit PE, we had originally expected that adrenergic blockade may attenuate the severity of hypoxic pulmonary injury. In particular, we investigated whether administration of drugs with reduced fluid load would be beneficial with respect to both cardiocirculatory and pulmonary functions in acute hypoxia. Rats were exposed to normobaric hypoxia (10% O2) over 1.5 or 6 h and received 0.9% NaCl or adrenergic blockers either as infusion (1 ml/h, increased fluid load) or injection (0.5 ml, reduced fluid load). Control animals were kept in normoxia and received infusions or injections of 0.9% NaCl. After 6 h of hypoxia, LV inotropic function was maintained with NaCl injection but decreased significantly with NaCl infusion. Adrenergic blockade induced a similar LV depression when fluid load was low, but did not further deteriorate LV depression after 6 h of infusion. Reduced fluid load also attenuated pulmonary injury after 6 h of hypoxia. This might be due to an effective fluid drainage into the pleural space. Adrenergic blockade could not prevent PE. In general, increased fluid load and impaired LV inotropic function promote the development of PE in acute hypoxia. The main physiologic conclusion from this study is that fluid reduction under hypoxic conditions has a protective effect on cardiopulmonary function. Consequently, appropriate fluid management has particular importance to subjects in hypoxic conditions.

Plasma catecholamine levels in the acute and subacute stages of takotsubo syndrome: Results from the Stockholm myocardial infarction with normal coronaries 2 study.

AimsIt is well‐accepted that takotsubo syndrome (TS) is characterized by a massive surge of plasma catecholamines despite lack of solid evidence. The objective of this study was to examine the hypothesis of a massive catecholamine elevation in TS by studying plasma‐free catecholamine metabolites in patients participating in the Stockholm myocardial infarction (MI) with normal coronaries 2 (SMINC‐2) study where TS constituted more than one third of the patients.Methods and resultsThe patients included in the SMINC‐2 study were classified, according to cardiac magnetic resonance (CMR) imaging findings (148 patients), which was performed at a median of 3 days after hospital admission. Plasma‐free catecholamine metabolites; metanephrine, normetanephrine, and methoxy‐tyramine were measured on day 2–4 after admission. Catecholamine metabolite levels were available in 125 patients. One hundred and ten (88%) of the 125 patients included in SMINC‐2 study, and 38 (86.4%) of the 44 patients with TS had completely normal plasma metanephrine and normetanephrine levels. All patients had normal plasma methoxy‐tyramine levels. Fourteen (11.2%) of the 125 patients included in SMINC‐2 study, and 5 (11.6%) of the 43 patients with TS had mild elevations (approximately 1.2 times the upper normal limits) of either plasma metanephrine or normetanephrine. One patient with pheochromocytoma‐triggered TS had marked elevation of plasma metanephrine and mild elevation of plasma normetanephrine. There were no significant differences between the number or degree of catecholamine metabolite elevations between the different groups of patients with CMR imaging diagnosis included in SMINC‐2 study.ConclusionThere was no evidence of massive catecholamine elevations in the acute and subacute stages of TS apart from one patient with pheochromocytoma‐induced TS. Most of the TS patients had normal catecholamine metabolites indicating that blood‐borne catecholamines do not play a direct role in the pathogenesis of TS.

Influence of the prehospital administered dosage of epinephrine on the plasma levels of catecholamines in patients with out-of-hospital cardiac arrest

AimThis study evaluated whether the prehospital administered dosage of epinephrine (Ep) influences the plasma levels of catecholamines in patients with out-of-hospital cardiac arrest (OHCA). MethodsThis was a prospective, observational clinical study. Patients with OHCA transferred to our hospital between July 2014 and July 2017 were analyzed. The plasma levels of catecholamines were measured using blood samples obtained immediately upon arrival at the hospital and before the administration of Ep. Patients were divided into three groups based on the prehospital administered dosage of Ep: no prehospital administration (group Z); 1 mg of Ep (group O); and 2 mg of Ep (group T). The levels of catecholamines, as well as the conditions of resuscitation prior to and after arrival at the hospital were compared between the three groups. ResultsWe analyzed 145 patients with OHCA (96, 38, and 11 patients in groups Z, O, and T, respectively). Group T exhibited the highest plasma levels of Ep with a statistically significant difference, however, there were no significant differences in the plasma levels of norepinephrine (Nep), dopamine (DOA) and vasopressin (ADH) among the three groups. ConclusionThe prehospital administered dosage of Ep influences the plasma levels of Ep; however, it does not contribute to the plasma levels of Nep, DOA and ADH in patients with OHCA.

Relationship between the Plasma Levels of Catecholamines and Return of Spontaneous Circulation in Patients with Out-of-Hospital Cardiac Arrest.

Purpose The dynamic state of epinephrine (Ep) in the plasma of patients with out-of-hospital cardiac arrest (OHCA) remains unclear. The purpose of this study was to evaluate the relationship between the plasma levels of catecholamines (such as epinephrine (Ep), norepinephrine (Nep), and dopamine) and vasopressin (antidiuretic hormone (ADH)) and the acquisition of return of spontaneous circulation (ROSC) in OHCA patients. Methods This was a prospective, observational clinical study. Patients with OHCA transferred to our hospital between July 2014 and July 2017 were enrolled. The levels of catecholamines and ADH in the plasma were measured using blood samples immediately obtained on arrival at our hospital and before the administration of Ep. Patients in whom Ep was already administered prior to obtaining blood samples were excluded. Patients were divided into two groups: with and without ROSC, that is, ROSC (+) and ROSC (−) groups, respectively. The plasma levels of these agents and the conditions of resuscitation were compared between the two groups. Results A total of 96 patients with OHCA were analyzed. The ROSC (+) and ROSC (−) groups included 34 and 62 patients, respectively. There were no significant differences observed between the two groups in age, cause of cardiopulmonary arrest, and prehospital resuscitation time. The plasma levels of Ep and Nep were significantly lower in the ROSC (+) group than in the ROSC (−) group. However, there were no significant differences in the plasma levels of dopamine and ADH between the two groups. Conclusion Increased levels of Ep in the plasma may not be associated with the acquisition of ROSC in patients with OHCA.

Depression accelerates gastric cancer invasion and metastasis by inducing a neuroendocrine phenotype via the catecholamine/β2 -AR/MACC1 axis.

BackgroundDepression is a common, easily ignored, accompanied disease of gastric cancer (GC) patients and is often observed with elevated plasma catecholamine levels. Depression frequently promotes GC progression and leads to poor clinical outcomes; however, the molecular mechanisms underlying depression‐induced GC progression remain poorly understood. We aimed to study the effects of depression on GC progression and explore possible mechanisms mediating the action of depression‐associated catecholamines on GC.MethodsDepression states of GC patients were graded using the Patient Health Questionnaire‐9, and plasma catecholamine levels were examined by high performance liquid chromatography coupled with tandem mass spectrometry. Migrative and invasive GC cells were examined using transwell assays, and metastatic GC niches were imaged using bioluminescence technology in a depression mouse model established with chronic unpredictable mild stress. Mouse depression‐like behaviors were assessed through sucrose preference, forced swimming, and tail suspension tests. Characteristics of the neuroendocrine phenotype were observed via RT‐PCR, Western blotting, flow cytometry, and transmission electron microscopy.ResultsFifty‐one GC patients (age: 53.61 ± 1.79 years; cancer duration: 3.71 ± 0.33 months; depression duration: 2.37 ± 0.38 months; male‐to‐female ratio: 1.55:1) were enrolled in the study. Depression grade was significantly higher in GC patients showing higher plasma levels of catecholamines (epinephrine: P = 0.018; noradrenaline: P = 0.009), higher oncogene metastasis‐associated in colon cancer‐1 (MACC1) level (P = 0.018), and metastasis (P < 0.001). Further, depression‐associated catecholamine specifically bound to the beta‐2 adrenergic receptor (β2‐AR) and upregulated MACC1 expression, and thus promoting neuroendocrine phenotypic transformation through direct binding between MACC1 and synaptophysin. Eventually, the neuroendocrine phenotypic transformation accelerated GC invasion in vitro and metastasis in vivo. However, β2‐AR antagonist ICI‐118,551 or MACC1 silencing effectively blocked the catecholamine‐induced neuroendocrine phenotypic transformation and eliminated depression‐enhanced GC migration and invasion. Moreover, β2‐AR blocking or MACC1 silencing prevented GC metastasis attributed to a neuroendocrine phenotype in a depression mouse model.ConclusionsCatecholamine‐induced neuroendocrine phenotypes of GC cells led to depression‐accelerated GC invasion and metastasis via the β2‐AR/MACC1 axis, while β2‐AR antagonist or MACC1 silencing could reverse it, showing promising potential therapeutic strategies for improving the outcome of GC patients with comorbid depression.

The Effect of Noise on the Neurobehavioral Function of the Occupational Population and the Content of Catecholamines.

According to the decibel level of noise detection in the working environment, the research objects were divided into high noise group (more than 85 dB), low noise group (55 to 85 dB), and control group (less than 55 dB), the neurobehavioral core test battery (NCTB) was used to systematic tests all workers, radioimmunoassay was used to detect plasma catecholamine levels, and the relationship between noise intensities and the levels of plasma catecholamine was analyzed by canonical correlation. The result shows noise exposure will affect workers' neurological function and the influence of noise on neurobehavioral function may be related to the increase of the levels of norepinephrine and dopamine in the plasma and the inhibition of the synthesis of epinephrine of noise-exposed workers.

Sympathetic Nervous System Activity in Patients with Metabolic Syndrome, Type 2 Diabetes Mellitus and Chronic Kidney Disease. Role of Renalase and Alpha Amylase

Aim: To evaluate serum renalase and salivary alpha amylase concentrations and their relationship with plasma catecholamine levels in patients with Metabolic Syndrome (MS), Type 2 Diabetes Mellitus (T2DM), and End-Stage Renal Disease (ESRD). Method: In cross-sectional study 163 patients were enrolled; 43 patients with MS, 93 withT2DM, 13 with ESRD, and 14 healthy subjects (control group). All patients had their ascription to the UMAA/UMF No. 75, in Morelia, Michoacan, Mexico. Glucose, creatinine, cholesterol, triglycerides, HDL, and renalase were measurement in serum, and Dopamine (DA), Epinephrine (E) and Norepinephrine (NE) in plasma. An aliquot of saliva was collected for alpha amylase determination. Results: High plasma concentrations of DA, E and NE (p&lt;0.0001) was founded in T2DM and ESRD patients. Renalase was lower in ESRD compared to MS and T2DM patients (p&lt;0.0001). High concentrations of alpha amylase were found in MS, T2DM, and ESRD patients in comparison with control group (p&lt;0.0001). Catecholamines correlated positively with alpha amylase and diabetes evolution. Conclusion: Sympathetic hyperactivity in MS, T2DM and ESRD patients was founded. Renalase could be proposed as biomarker of renal function and salivary alpha amylase as sympathetic hyperactivity. Additional studies are required to evaluate the pathophysiological mechanisms involved of SNS in CKD development.

High Stocking Density and Food Deprivation Increase Brain Monoaminergic Activity in Gilthead Sea Bream (Sparus aurata).

Simple SummaryFarmed fish must cope with different stressors during aquaculture procedures, such as high densities, fasting, transport, or air exposure during handling. The severity and timing of these stressors can produce important imbalances in the overall status of the animals, triggering several endocrine and physiological players. In this study, gilthead sea bream (Sparus aurata) juveniles were assigned to four experimental conditions: (1) fed at a low stocking density (LSD-F, 4 kg·m−3); (2) fed at a high stocking density (HSD-F, 40 kg·m−3); (3) food-deprived at LSD (LSD-FD); and (4) food-deprived at HSD (HSD-FD). This served to evaluate, both at the plasma and central (brain) levels, the role of several hormonal (cortisol and catecholamines) and monoamine (dopaminergic and serotonergic neurotransmitters) functionalities. Our results evidenced chronic stress exposure (i.e., a high stocking density and food deprivation) fallouts in the enhancement of the parameters related to the stress response, where monoaminergic activities in different brain regions served to reorganize the physiological response depending on the challenge applied.In teleosts, brain monoamines (dopamine and serotonin) participate in the early response to different acute stressors. However, little is known regarding their role during chronic stress. In a 2 × 2 factorial design, the influence of a high stocking density (HSD) and/or food deprivation (FD) on the brain monoaminergic activity in gilthead sea bream (Sparus aurata) was evaluated. Following a 21-day experimental design, samples from the plasma and brain regions (telencephalon, hypothalamus, and optic tectum) were collected. The dopamine (DA), serotonin (5HT), and their main metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and 5 hydroxyindoleacetic acid (5HIAA), contents were HPLC-assessed in brain tissues, and the ratios DOPAC/DA and 5HIAA/5HT were calculated as indicators of enhanced monoaminergic activity. The plasma levels of cortisol and catecholamine were also evaluated. The cortisol levels increased in fish exposed to HSD and normally fed but, also, in all FD groups, whereas the NA levels decreased in LSD-FD animals. Within the brain, the dopaminergic and serotonergic activities in telencephalon and hypothalamus increased in fish subjected to HSD and in the telencephalon of LSD-FD fish. While DA (hypothalamus) and 5HT (telencephalon) increased in the animals submitted to a HSD, food-deprived fish did not show such an increase. Taken together, our results supported the hypothesis of brain monoaminergic activity participating in maintaining and orchestrating the endocrine response to chronic stress in fish.

Plasma dopamine and catecholamine levels in patients with central serous chorioretinopathy

To evaluate plasma dopamine and catecholamine levels in patients with central serous chorioretinopathy (CSCR). In this prospective study, 32 patients with acute CSCR were included, along with 32 age- and gender-matched healthy controls without CSCR. Complete ophthalmologic examinations were performed. Plasma dopamine, epinephrine, norepinephrine levels were measured in the morning after 8-12hours of fasting. A P-value of less than 0.05 was considered statistically significant. While the mean age of the CSCR group was 40.12±7.96 years, the mean age of the control group was 37.81±7.26 years. There was no statistically significant difference between the groups in terms of age or gender (P=0.229, P=0.740, respectively). The plasma dopamine level was 29.85±9.39pg/ml in the CSCR group and 23.93±7.33pg/ml in the control group (P=0.001). The plasma epinephrine level was 60.73±25.69pg/ml in the CSCR group and 45.77±18.55pg/ml in the control group (P=0.021). The plasma norepinephrine level was 206.68±71.51pg/ml in the CSCR group and 149.33±49.69pg/ml in the control group (P=0.001). Plasma dopamine, epinephrine, and norepinephrine levels were statistically significantly higher in the CSCR group. We concluded that dopamine may be a possible factor in the etiology of CSCR, both through its receptors and by enhancing sympathetic activity.

The Effects of Acute Glucoprivation on Adrenomedullary Function in SHR and WKY Rats

We have shown previously, acute intraperitoneal administration of 2-deoxy-d-glucose (2DG) into Sprague-Dawley rats led to activation of the adrenal medulla chromaffin cells, indicated with increased protein kinase activity and increased tyrosine hydroxylase (TH) phosphorylation, as well as increased plasma adrenaline and glucose levels. Here we have used spontaneous hypertensive (SHR) and Wistar Kyoto (WKY) rats to investigate whether hypertension alters basal adrenal chromaffin cell function, or the response of these cells to acute 2DG treatment. At basal level, we found no differences in adrenal medulla TH protein, TH phosphorylation, TH activity or catecholamine levels between SHR and WKY despite a significant difference in the level of systolic blood pressure; nor were there differences in plasma catecholamine levels or blood glucose (BG). Furthermore, the vehicle animals evoked no significant changes in any parameter measured in SHR, but evoked significant increases in pSer19TH, plasma adrenaline and BG in WKY. Single episode of glucoprivation evoked increases in PKA and CDK/MAPK, pSer40TH, pSer31TH, TH activity, and plasma adrenaline and BG in SHR, and in addition evoked increases in PKC, CAMKII, and pSer19TH in WKY. These findings are significant which indicates hypertension does not impact catecholamine function in the adrenal gland. It also appears that hypertension does not alter the adrenal response to glucoprivation. The findings are also significant as WKY showed greater adrenal activation of protein kinases and TH phosphorylation in response to saline and 2DG when compared to SHR and possible reasons for these findings are further discussed.

Neurobiological Pathways Linking Acute Mental Stress to Impairments in Executive Function in Individuals with Coronary Artery Disease.

Background:Individuals with coronary artery disease (CAD) have worse executive function compared to the general population but the mechanisms are unknown.Objective:To investigate the role of acute mental stress (MS) on the executive function of patients with CAD.Methods:Participants with stable CAD underwent acute MS testing with simultaneous peripheral vascular function measurements and brain imaging using high resolution-positron emission tomography. Digital pulse wave amplitude was continuously measured using peripheral artery tonometry (PAT, Itamar Inc). Stress/rest PAT ratio (sPAT) of pulse wave amplitude during MS/baseline was calculated as a measure of microvascular constriction during MS. Plasma levels of catecholamine and interleukin-6 were assessed at baseline and after MS. Executive function was assessed both at baseline and at 2 years follow-up using the Trail Making Test parts A and B.Results:We studied 389 individuals with brain data available for 148 participants. Of this population follow-up cognitive assessments were performed in 226 individuals (121 with brain imaging). After multivariable adjustment for baseline demographics, risk factors, and medication use, a lower sPAT, indicating greater vasoconstriction, a higher inferior frontal lobe activation with MS, and increases in norepinephrine and IL-6 levels with MS were all independently associated with greater time to complete Trail B test.-38.4ptConclusion:In response to acute MS, greater peripheral vasoconstriction, higher inferior frontal lobe brain activation, and increases in the levels of norepinephrine and IL-6 are associated with worse executive function.

Changes in electrocardiogram parameters during acute nonshivering cold exposure and associations with brown adipose tissue activity, plasma catecholamine levels, and brachial blood pressure in healthy adults.

BackgroundSympathetic activity causes changes in electrocardiogram (ECG) during cold exposure and the changes have been studied mostly during hypothermia and less during mild acute nonshivering cold exposure. Cold‐induced sympathetic activity also activates brown adipose tissue (BAT) and increases arterial blood pressure (BP) and plasma catecholamine levels. We examined changes in ECG parameters during acute nonshivering cold exposure and their associations with markers of sympathetic activity during cold exposure: brachial blood pressure (BP), plasma catecholamine levels, and BAT activity measured by positron emission tomography (PET).Methods and resultsHealthy subjects (M/F = 13/24, aged 20–55 years) were imaged with [15O]H2O (perfusion, N = 37) and [18F]FTHA to measure plasma nonesterified fatty acid uptake (NEFA uptake, N = 37) during 2‐h nonshivering cold exposure. 12‐lead ECG (N = 37), plasma catecholamine levels (N = 17), and brachial BP (N = 31) were measured at rest in room temperature (RT) and re‐measured after a 2‐h nonshivering cold exposure. There were significant differences between RT and cold exposure in P axis (35.6 ± 26.4 vs. 50.8 ± 22.7 degrees, p = 0.005), PR interval (177.7 ± 24.6 ms vs.163.0 ± 28.7 ms, p = 0.001), QRS axis (42.1 ± 31.3 vs. 56.9 ± 24.1, p = 0.003), and QT (411.7 ± 25.5 ms vs. 434.5 ± 39.3 ms, p = 0.001). There was no significant change in HR, QRS duration, QTc, JTc, and T axis during cold exposure. Systolic BP (127.2 ± 15.7 vs. 131.8 ± 17.9 mmHg, p = 0.008), diastolic BP (81.7 ± 12.0 vs. 85.4 ± 13.0 mmHg, p = 0.02), and plasma noradrenaline level increased during cold exposure (1.97 ± 0.61 vs. 5.07 ± 1.32 µmol/L, p = 0.001). Cold‐induced changes in ECG parameters did not correlate with changes in BAT activity, brachial BP, plasma catecholamines, or skin temperature.ConclusionsDuring short‐term nonshivering cold exposure, there were increases in P axis, PR interval, QRS axis, and QT compared to RT in healthy adults. Cold‐induced changes in ECG parameters did not correlate with BAT activity, brachial BP, or plasma catecholamine levels which were used as markers of cold‐induced sympathetic activity.