Changes In Plasma Catecholamines Research Articles

Impact of procedural handling on the physiological effects of alfaxalone anaesthesia in the ball python (Python regius)

To describe the cardiovascular changes following intramuscular (handled) and intravascular (undisturbed, via intraarterial catheter) alfaxalone administration, we studied 20 healthy ball pythons (Python regius) in a randomised, prospective study. The pythons were instrumented with occlusive arterial catheters to facilitate undisturbed, continuous monitoring of heart rate and blood pressure. Six pythons were administered intramuscular (IM) saline, followed by 20 mg/kg IM alfaxalone, and were manually restrained for both injections. Six pythons received intraarterial (IA) saline, followed by 10 mg/kg IA alfaxalone, and remained undisturbed for both injections. Arterial blood samples were taken at 0, 12 and 60 min post-injection, and heart rate and blood pressure were recorded for 60 min. The remaining eight snakes received 20 mg/kg IM or 10 mg/kg IA alfaxalone (n = 4 per treatment) and were not handled for intubation 10 min post-injection, to examine the effects of handling during anaesthesia. IM administration of 20 mg/kg alfaxalone or an equivalent volume of saline elicited a profound tachycardia and hypertension, which recovered to resting values after 20 min. However, when 10 mg/kg alfaxalone or saline were injected IA, mild hypotension and a lower magnitude tachycardia occurred. Arterial PCO2 and PO2, pH and lactate concentrations did not change following IA alfaxalone, but an acidosis was observed during IM alfaxalone anaesthesia. There were no significant changes in plasma catecholamines and corticosterone among treatments. Handling for injection and during anaesthesia associated with intubation significantly affects cardiovascular parameters, whereas alfaxalone per se only elicits minor changes in cardiovascular physiology.

Insulin enhances contextual fear memory independently of its effect in increasing plasma adrenaline

AimsAdrenaline enhances contextual fear memory consolidation possibly by activating liver β2-adrenoceptors causing transient hyperglycaemia. Contrastingly, insulin-induced hypoglycaemia may culminate in blood adrenaline increment, hidering the separation of each hormone's action in contextual fear memory. Therefore, an adrenaline-deficient mouse model was used aiming to investigate if contextual fear memory consolidation following insulin administration requires or not subsequent increases in plasma adrenaline, which occurs in response to insulin-induced hypoglycemia. Main methodsFear conditioning was performed in wild-type (WT) and adrenaline-deficient (Pnmt-KO) male mice (129 × 1/SvJ) treated with insulin (2 U/kg, intraperitoneal (i.p.)) or vehicle (0.9 % NaCl (i.p.)). Blood glucose was quantified. Catecholamines were quantified using HPLC with electrochemical detection. Quantitative real-time polymerase chain reaction was used to assess mRNA expression of hippocampal Nr4a1, Nr4a2, Nr4a3, and Bdnf genes. Key findingsInsulin-treated WT mice showed increased freezing behaviour when compared to vehicle-treated WT mice. Also, plasma dopamine, noradrenaline, and adrenaline increased in this group. Insulin-treated Pnmt-KO animals showed increased freezing behaviour when compared with respective vehicle. However, no changes in plasma or tissue catecholamines were identified in insulin-treated Pnmt-KO mice when compared with respective vehicle. Furthermore, insulin-treated Pnmt-KO mice presented increased Bdnf mRNA expression when compared to vehicle-treated Pnmt-KO mice. SignificanceConcluding, enhanced freezing behaviour after insulin treatment, even in adrenaline absence, may indicate a key role of insulin in contextual fear memory. Insulin may cause central molecular changes promoting contextual fear memory formation and/or retrieval. This work may indicate a further role of insulin in the process of contextual fear memory modulation.

A Preliminary Comparison of Beef Carcases Stunned using DTS: Diathermic Syncope® or Captive Bolt in Terms of Selected Meat Quality Attributes and Plasma Biomarker Concentrations

A novel technology for inducing unconsciousness prior to slaughter has been developed (DTS). For commercial reasons meat quality attributes are important, and impacts on endocrine responses provide an indication of animal welfare. We compared endocrine, ultimate pH and meat quality (after 1 and 10 weeks of storage) attributes of cattle carcases processed using DTS with those processed using penetrative captive bolt (CB). There were no significant differences between treatments in the change in plasma cortisol, adrenocorticotropic hormone, β-endorphin and catecholamines between baseline and immediately post-slaughter, and no significant differences in terms of pH at 24 h post slaughter. There were no significant differences in pH, shear force, TBARS or drip loss between DTS and CB samples of round and loin at week 1 and week 10 post slaughter; DTS meat was yellower at quartering (MINOLTA b* P < 0.05). At week 1, DTS loins were redder (MINOLTA a*, P < 0.05) and yellower (MINOLTA b*, P < 0.05), while DTS rounds were lighter (MINOLTA L*, P < 0.05), than CB. At week 10, there were no significant meat color differences between treatments. Processing cattle using DTS results in endocrine changes and meat quality attributes that are comparable to CB.

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.

Effect of Morning Exercise With or Without Breaks in Prolonged Sitting on Blood Pressure in Older Overweight/Obese Adults

Both exercise and breaks in prolonged sitting can reduce blood pressure (BP) in older overweight/obese adults. We investigated whether there is an additive hypotensive effect when exercise is combined with subsequent breaks in sitting. Sex differences and changes in plasma catecholamines as a potential candidate mechanism underlying BP responses were also examined. Sedentary older adults (n=67; 67±7 years; 31.2±4.1 kg/m2) completed 3 conditions in random order-sitting (SIT): uninterrupted sitting (8 hours, control); exercise+sitting (EX+SIT): sitting (1 hour), moderate-intensity walking (30 minutes), uninterrupted sitting (6.5 hours); exercise+breaks (EX+BR): sitting (1 hour), moderate-intensity walking (30 minutes), sitting interrupted every 30 minutes with 3 minutes of light-intensity walking (6.5 hours). Serial BP and plasma epinephrine/norepinephrine measurements occurred during 8 hours. The 8-hour average systolic and diastolic BP (mm Hg 95% CI) was lower in EX+SIT -3.4 (-4.5 to -2.3), -0.8 (-1.6 to -0.04), and EX+BR -5.1 (-6.2 to -4.0), -1.1 (-1.8 to -0.3), respectively, relative to SIT (all P <0.05). There was an additional reduction in average systolic BP of -1.7 (-2.8 to -0.6) in EX+BR relative to EX+SIT ( P=0.003). This additional reduction in systolic BP was driven by women -3.2 (-4.7 to -1.7; P<0.001 EX+BR versus EX+SIT). Average epinephrine decreased in EX+SIT and EX+BR in women (-13% to -12%) but increased in men (+12% to +23%), respectively, relative to SIT ( P<0.05). No differences in average norepinephrine were observed. Morning exercise reduces BP during a period of 8 hours in older overweight/obese adults compared with prolonged sitting. Combining exercise with regular breaks in sitting may be of more benefit for lowering BP in women than in men. Clinical Trial Registration- URL: https://www.anzctr.org.au . Unique identifier: ACTRN12614000737639.

Systemic angiotensin II does not increase cardiac sympathetic nerve activity in normal conscious sheep.

While it is well established that centrally injected angiotensin II (Ang II) has potent actions on sympathetic nervous activity (SNA), it is less clear whether peripheral Ang II can immediately stimulate SNA. In particular, the contribution of cardiac sympathetic nerve activity (CSNA) to the acute pressor response is unknown. We therefore examined the effect of incremental doses of intravenous Ang II (3, 6, 12, 24, and 48 ng/kg/min each for 30 min) on CSNA in eight conscious sheep. Ang II infusions progressively increased plasma Ang II up to 50 pmol/l above control levels in dose-dependent fashion (P<0.001). This was associated with the expected increases in mean arterial pressure (MAP) above control levels from <10 mmHg at lower doses up to 23 mmHg at the highest dose (P<0.001). Heart rate and cardiac output fell progressively with each incremental Ang II infusion achieving significance at higher doses (P<0.001). There was no significant change in plasma catecholamines. At no dose did Ang II increase any of the CSNA parameters measured. Rather, CSNA burst frequency (P<0.001), burst incidence, (P=0.002), and burst area (P=0.004) progressively decreased achieving significance during the three highest doses. In conclusion, Ang II infused at physiologically relevant doses increased MAP in association with a reciprocal decrease in CSNA presumably via baroreceptor-mediated pathways. The present study provides no evidence that even low-dose systemic Ang II stimulates sympathetic traffic directed to the heart, in normal conscious sheep.

Abstract 019: Effect of CPAP on Blood Pressure and Central Sympathetic Outflow in Diabetic Patients with OSA, Resistant HTN, and CKD

Introduction: Central sympathetic hyperactivity as assessed by muscle sympathetic nerve activity recordings is thought to play a crucial role in the development and maintenance of hypertension (HTN) in patients with obstructive sleep apnea (OSA). Decreases in daytime and nocturnal blood pressure (BP) in response to treatment with continuous positive airway pressure (CPAP) are paralleled by decreases in muscle sympathetic nerve activity (MSNA). Patients with chronic kidney disease (CKD) have high MSNA. Bilateral nephrectomy, but not renal transplantation normalizes MSNA indicating central sympathoexcitatory effects by renal afferents. The objective of this study was to assess to what extent is HTN driven by central sympathetic hyperactivity in patients with diabetic CKD, OSA, and resistant HTN. Thirteen patients (age 62.2±7.4 years) with diabetic CKD, resistant HTN defined as SBP on 24-hr ABPM above 135 mmHg while on 3 or more BP lowering drugs (including diuretic) with OSA, were randomized to therapeutic CPAP or non-therapeutic CPAP for one months. 24-hr ABPM, plasma catecholamines, aldosterone, and renin, and MSNA were assessed before and 1 months after randomization. Our results show (Table) that in contrast to sham CPAP, therapeutic CPAP decreased daytime and nighttime BP. In contrast, neither therapeutic nor sham CPAP caused any changes in MSNA and plasma catecholamines. In conclusion, decreases in BP in response to CPAP in patients with in diabetic CKD, despite maintained high MSNA, indicate other mechanism contributing to HTN in these patients as well as other central sympathoexcitatory pathways activated.

Early morphologic alterations in renal artery wall and renal nerves in response to catheter-based renal denervation procedure in sheep: difference between single-point and multiple-point ablation catheters.

Renal sympathetic hyperactivity is critically involved in hypertension pathophysiology; renal denervation (RDN) presents a novel strategy for treatment of resistant hypertension cases. This study assessed effects of two RDN systems to detect acute intravascular, vascular and peri-vascular changes in the renal artery, and renal nerve alterations, in the sheep. The procedures using a single-point or multi-point ablation catheters, Symplicity Flex(TM), Medtronic versus EnligHTN(TM), St. Jude Medical were compared; the intact contralateral kidneys served as controls. Histopathological and immunohistochemical assessments were performed 48 h after RDN procedures; the kidney and suprarenal gland morphology was also evaluated. Special staining methods were applied for histologic analysis, to adequately score the injury of renal artery and adjacent renal nerves. These were more pronounced in the animals treated with the multi-point compared with the single-point catheter. However, neither RDN procedure led to complete renal nerve ablation. Forty-eight hours after the procedure no significant changes in plasma and renal tissue catecholamines were detected. The morphologic changes elicited by application of both RDN systems appeared to be dependent on individual anatomical variability of renal nerves in the sheep. Similar variability in humans may limit the therapeutic effectiveness of RDN procedures used in patients with resistant hypertension.

Sympathetic nervous system alterations with HER2+ antagonism: an early marker of cardiac dysfunction with breast cancer treatment?

BackgroundHER2 antagonists (anti-HER2; e.g., trastuzumab and lapatinib) are effective in treating an aggressive form of breast cancer (BC), but can cause cardiotoxicity due to the disruption in neuregulin (NRG)/HER2+ ligand receptor signalling. The recent data show that NRG-HER2 receptors located in the medulla oblongata are important regulators of vasomotor tone. Disrupting the NRG-HER2 signalling in mouse medulla results in increased sympathetic nerve output and blood pressure. We hypothesized that anti-HER2 agents would cause increased sympathetic tone with changes in plasma catecholamines and NRG.MethodsIn 15 newly diagnosed HER2+ BC patients receiving anti-HER2 agents, vital signs were measured along with supine plasma epinephrine (EPI), norepinephrine (NE), and NRG at baseline and three months. Serial echocardiography was performed.ResultsWith three months of anti-HER2 treatment, NE increased (2.334 ± 1.294 nmol/L vs. 3.262 ± 2.103 nmol/L; p = 0.004) and NRG decreased (12.7±15.7 ng/ml vs. 10.9 ± 13.3 ng/ml; p = 0.036) with a corresponding increase in systolic blood pressure (110 ± 10 mmHg vs. 120 ± 16 mmHg, p = 0.049) and diastolic blood pressure (67 ± 14 vs. 77 ± 10, p = 0.009). There was no change, however, in EPI (0.183 ± 0.151 nmol/L vs. 0.159 ± 0.174 nmol/L; p = 0.519) or heart rate (73 ± 12 bpm vs. 77 ± 10 bpm, p = 0.146). Left ventricular ejection function declined over the follow-up period (baseline 63 ± 6% vs. follow-up 56 ± 5%).ConclusionsAnti-HER2 treatment results in increased NE, blood pressure, and decreased NRG; this suggests that the inhibition of NRGHER2 signalling leads to increased sympathoneural tone. Larger studies are needed to determine if these observations have prognostic value and may be offset with medical interventions, such as beta-blockers.Clinical Trial RegistrationThe study was registered with www.clinicaltrials.gov (NCT00875238).

Responses to increasing exercise upon reaching the anaerobic threshold, and their control by the central nervous system.

The anaerobic threshold (AT) has been one of the most studied of all physiological variables. Many authors have proposed the use of several markers to determine the moment at with the AT is reached. The present work discusses the physiological responses made to exercise - the measurement of which indicates the point at which the AT is reached - and how these responses might be controlled by the central nervous system. The detection of the AT having been reached is a sign for the central nervous system (CNS) to respond via an increase in efferent activity via the peripheral nervous system (PNS). An increase in CNS and PNS activities are related to changes in ventilation, cardiovascular function, and gland and muscle function. The directing action of the central command (CC) allows for the coordination of the autonomous and motor systems, suggesting that the AT can be identified in the many ways: changes in lactate, ventilation, plasma catecholamines, heart rate (HR), salivary amylase and muscular electrical activity. This change in response could be indicative that the organism would face failure if the exercise load continued to increase. To avoid this, the CC manages the efferent signals that show the organism that it is running out of homeostatic potential.

Differential effects of cathinone compounds and MDMA on body temperature in the rat, and pharmacological characterization of mephedrone‐induced hypothermia

Recreational users report that mephedrone has similar psychoactive effects to 3,4-methylenedioxymethamphetamine (MDMA). MDMA induces well-characterized changes in body temperature due to complex monoaminergic effects on central thermoregulation, peripheral blood flow and thermogenesis, but there are little preclinical data on the acute effects of mephedrone or other synthetic cathinones. The acute effects of cathinone, methcathinone and mephedrone on rectal and tail temperature were examined in individually housed rats, with MDMA included for comparison. Rats were killed 2 h post-injection and brain regions were collected for quantification of 5-HT, dopamine and major metabolites. Further studies examined the impact of selected α-adrenoceptor and dopamine receptor antagonists on mephedrone-induced changes in rectal temperature and plasma catecholamines. At normal room temperature, MDMA caused sustained decreases in rectal and tail temperature. Mephedrone caused a transient decrease in rectal temperature, which was enhanced by α(1) -adrenoceptor and dopamine D(1) receptor blockade, and a prolonged decrease in tail temperature. Cathinone and methcathinone caused sustained increases in rectal temperature. MDMA decreased 5-HT and/or 5-hydroxyindoleacetic acid (5-HIAA) content in several brain regions and reduced striatal homovanillic acid (HVA) levels, whereas cathinone and methcathinone increased striatal HVA and 5-HIAA. Cathinone elevated striatal and hypothalamic 5-HT. Mephedrone elevated plasma noradrenaline levels, an effect prevented by α-adrenoceptor and dopamine receptor antagonists. MDMA and cathinones have different effects on thermoregulation, and their acute effects on brain monoamines also differ. These findings suggest that the adverse effects of cathinones in humans cannot be extrapolated from previous observations on MDMA.

The Relationships Between Plasma Adrenomedullin and Endothelin-1 Concentrations and Doppler Echocardiographic Indices of Left Ventricular Function During Static Exercise in Healthy Men

Our previous study showed a significant relationships between static exercise-induced changes in plasma adrenomedullin (ADM) and those in endothelin-1 (ET-1), noradrenaline (NA) and pre-ejection period/left ventricular ejection time ratio (PEP/LVET) in older healthy men. It is hypothesized that ADM, ET-1, NA and adrenaline (A) may function as endogenous regulators of cardiac function by modulating myocardial contractility during static exercise. The present study was undertaken to assess the relationships between exercise-induced changes in plasma ADM, ET-1, NA, A concentrations and those in ascending aortic blood flow peak velocity (PV) and mean acceleration (MA) measured by Doppler echocardiography in 24 healthy older men during two 3-min bouts of handgrip at 30% of maximal voluntary contraction, performed alternately with each hand without any break between the bouts. Plasma ADM, ET-1, NA and A as well as heart rate (HR), blood pressure (BP), PV and MA were determined. During handgrip, plasma ADM, ET-1, NA and A as well as HR, BP increased, whereas PV and MA decreased. The increases in plasma ADM correlated positively with those in ET-1, NA and diastolic BP, and correlated negatively with changes in PV (r= −0.68) and MA (r= −0.62). The increases in plasma ET-1 correlated positively with those in NA and BPs and correlated negatively with changes in PV (r= −0.67) and MA (r= −0.60). The results of this study suggest that in healthy older men the exercise-induced changes in plasma ADM, ET 1 and catecholamines are related to alterations in left ventricular contractile state and may co-operatively counteract age-related deterioration of cardiac performance in men.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

Marked increases in plasma catecholamine concentrations precede hypotension and bradycardia caused by 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) in conscious rats

Plasma noradrenaline and adrenaline responses to 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), a selective putative 5-HT1A receptor agonist, have been studied in conscious, freely moving rats. Intravenously administered 8-OH-DPAT caused dose-related and sustained increases in plasma noradrenaline (2-fold) and adrenaline (11-fold) concentrations. Neither metergoline pretreatment (0.5 mg kg-1 i.v.) nor splanchnicectomy had any effect on the noradrenaline and adrenaline elevation caused by 8-OH-DPAT (250 micrograms kg-1 i.v.). The catecholamine responses peaked early but were still present during nadirs in blood pressure and heart rate. The discrepancy between plasma catecholamine and cardiovascular changes raises further questions about the mechanism of action of 8-OH-DPAT and supports other evidence suggesting a role for vagus stimulation in the cardiovascular effects caused by this drug.

The Effect of Exogenous Glucocorticoids on Plasma Catecholamines and Metanephrines in Patients Without Phaeochromocytomas

The aim of the study was to evaluate the effects of steroid administration under standardised conditions in a range of patients both normal and with adrenal pathologies and to review the impact on plasma catecholamines and metanephrines. Corticosteroid administration has been linked to the development of hypertensive crises in patients with phaeochromocytoma, however a mechanism for this is not fully understood. We aimed to add useful information about the effect of steroids on levels of these hormones under usual circumstances. A prospective, observational cohort study of 50 patients undergoing the low-dose dexamethasone suppression test (LDDST) was undertaken. Additional blood samples were taken at the start and end of the standard LDDST. Biochemical analysis was carried out for plasma catecholamines and plasma free metanephrines. Demographic and hormonal data were acquired from review of the notes or measured at baseline. No significant changes in plasma catecholamines or metanephrines were seen at the end of the LDDST compared to baseline. This was also true of subgroup analysis, divided by age, gender, or type of underlying pathology. Our results suggest that hypertensive reaction responses, rare as they are, are unlikely to be related to normal adrenal physiology. Thus LDDST is likely to be safe under most circumstances, however caution should be exercised in patients with adrenal masses with imaging characteristics compatible with phaeochromocytoma. It may be prudent to defer glucocorticoid administration until functioning phaeochromocytoma has been excluded biochemically.

Heart rate variability and catecholamines during hypoglycemia and orthostasis

The low frequency component of heart rate variability (HRV) is believed to be affected by sympathetic activity, but an evidence for this suggestion remains controversial. This study analyzed association between HRV and plasma catecholamines in response to two distinct conditions activating sympathetic nervous system. Changes in HRV were analysed from ECG recording and plasma norepinephrine and epinephrine levels were measured in response to head-up tilt (60°, 10 min) in 14 healthy volunteers (6 males, mean age 27.2 ± 0.8) and in response to insulin-induced hypoglycemia (0.1 IU per kg, i.v. bolus) in 11 healthy volunteers (5 males, mean age 26.6 ± 0.9 yr). Normalized low frequency power, low/high frequency ratio, plasma catecholamines increased, whereas normalized high frequency power decreased in response to head-up tilt or hypoglycemia. When analyzed individual time points of orthostatic test, plasma epinephrine correlated positively with low/high frequency ratio and negatively with normalized high frequency at the 3rd min of the head-up tilt. When all data at different time points were pooled significant correlations were found between catecholamines and normalized low frequency power and low/high frequency ratio. In insulin-induced hypoglycemia test plasma epinephrine correlated negatively with normalized high frequency power at the 30th minute. When all data measured at different time points were pooled no significant correlation was found between plasma catecholamines and HRV parameters. In conclusion, the present study shows an increase in low frequency component of HRV in response to orthostasis or hypoglycemia with significant, however inconsistent association to changes in plasma catecholamines.

β-Endorphin in pressor response to hyperventilation in elderly patients with essential and secondary hypertension

Abstract It has been observed that a distinct blood pressure (BP) response to prolonged and forced hyperventilation in adult patients with essential hypertension is associated with significant changes in plasma catecholamine and β-endorphin levels. This paper investigated whether hemodynamic and neuro-endocrine responses to hyperventilation in elderly patients with essential hypertension (n = 39, mean age 81 ± 3 years) differ from those in elderly patients with secondary hypertension (isolated systolic hypertension, bilateral chronic nephropathy, nephroangiosclerosis, diabetic nephropathy and hyperparathyroidism) (n = 39, mean age 80 ± 1 years). Plasma β-endorphin levels were normal in patients with essential hypertension and increased in patients with secondary hypertension. Plasma norepinephrine levels were normal in both populations. Hyperventilation decreased BP and norepinephrine levels and increased β-endorphin levels in essential hypertensive patients, whereas it did not significantly change BP or neuro-hormonal levels in secondary hypertensive patients. Hierarchical cluster analysis based on BP response to hyperventilation disclosed a sub-group of essential hypertensive patients with the highest basal levels of norepinephrine and the lowest β-endorphin levels, in whom the BP decrease following hyperventilation was correlated with the decrease in norepinephrine and increase in β-endorphin levels. This suggests that b-endorphin may be involved in modulating sympatho-adrenergic activity in elderly patients with essential hypertension.

Urocortin 1 exhibits potent inhibition of cardiac sympathetic nerve activity in conscious sheep

Urocortin 1 (Ucn1) and the sympathetic nervous system both participate in cardiac and circulatory regulation, but little is known about their possible interactions. We report the effects of Ucn1 on the cardiac sympathetic nerve activity (CSNA), haemodynamics and plasma catecholamines in normal sheep. Bolus intravenous administration of Ucn1 at 2.5 and 10 microg in seven sheep had no significant effect on haemodynamic parameters, including heart rate, mean arterial pressure (MAP) and cardiac output. At these doses, however, Ucn1 administration reduced CSNA, with burst frequency (P = 0.011), burst incidence (P = 0.015) and burst area (P = 0.012) all significantly reduced in a dose-related manner compared with a time-matched control. At higher doses (25 and 100 microg; n = 5 sheep), Ucn1 induced significant rises in heart rate (P < 0.001) and cardiac output (P = 0.03) and reduced peripheral resistance (P = 0.03), but had no effect on MAP. Ucn1 administration at the higher doses reduced CSNA, with burst incidence (P < 0.001), burst area/min (P = 0.001) and burst area/100 beats (P < 0.001) all significantly reduced in a dose-related manner compared with a time-matched control. There was no change in plasma catecholamines at any dose. The present study shows that Ucn1 induces potent inhibition of sympathetic traffic to the heart at doses both above and below the threshold for direct actions of Ucn1 on the myocardium. These findings suggest an important role for Ucn1 in cardiovascular homeostasis and warrant further investigation for potential therapeutic applications in acute myocardial injury and heart disease.

Hemodynamic and Catecholamine Responses to Laryngoscopy and Endotracheal Intubation in Paraplegic Patients: Time Course and Relation to the Affected Level

Background: We determined whether the cardiovascular responses to endotracheal intubation change as a function of the time elapsed after injury and the level of injury in patients with spinal cord injury. Methods: One-hundred-eighty six patients with complete cord injury were grouped into 3 according to the level of injury: high- (T1−T4, n = 34), mid- (T5− T10, n = 47) and low paraplegics (＜ T10, n = 105). They were further divided into 5 according to the time elapsed since injury: ＜ 4 wks, 4 wks−1 yr, 1−5 yrs, 5−10 yrs, and ＞ 10 yrs. Twenty-five patients with no cord injury served as controls. Systolic arterial blood pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were measured. Results: The intubation caused an increase of SAP and norepinephrine concentrations in every group. However, the magnitude of their peak increases was less in high paraplegics compared with all other groups (P ＜ 0.05). HR was similarly increased in all groups (P ＜ 0.01). Pressure but not either HR or norepinephrine response was enhanced in mid- and low-paraplegics whose injury elapsed more than 10 yrs compared with controls (P ＜ 0.05). The incidence of arrhythmias did not differ among the groups. Conclusions: The pressure and plasma catecholamine changes associated with endotracheal intubation may be attenuated in high-paraplegics, and the pressure changes may be enhanced over time in mid- and low-paraplegics. (Korean J Anesthesiol 2008; 54: 160∼6)

Changes of Hemodynamic Parameters, Plasma Catecholamines and Vasopressin Level During Laparoscopic Cholecystectomy and in Recovery Period

Changes of Hemodynamic Parameters, Plasma Catecholamines and Vasopressin Level During Laparoscopic Cholecystectomy and in Recovery Period