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PubMed1994

Positron emission tomography shows high specific uptake of racemic carbon-11 labelled norepinephrine in the primate heart.

(-)-Norepinephrine is the predominant neurotransmitter of the sympathetic innervation of the heart. Racemic norepinephrine was labelled with carbon-11 and injected i.v. into Cynomolgus monkeys. Five minutes after injection there was a more than tenfold higher radioactivity in the heart than in adjacent tissue. Pretreatment with the norepinephrine reuptake inhibitor desipramine reduced the uptake by more than 80%. The high specific uptake of racemic [11C]norepinephrine indicates that enantiomerically pure (-)-[11C]norepinephrine has promising potential for detailed mapping of the sympathetic innervation of the human myocardium.

Animals↗

PubMed1978

Regulation of (Na+, K+) adenosinetriphosphatase of nerve ending membranes: action of norepinephrine and a soluble factor.

Norepinephrine added in vitro to nerve ending membranes from rat cerebral cortex stimulates the activity of (Na+, K+) adenosinetriphosphatase (ATPase) only in the presence of the soluble brain fraction. In its absence norepinephrine inhibits the enzyme. (Mg2+)ATPase also showed stimulation by norepinephrine in the presence of the soluble fraction, but of lesser magnitude. The activation of (Na+, K+)ATPase by norepinephrine is not reproduced by cyclic AMP and is not antagonized by either alpha- or beta-adrenergic blocking agents. These results suggest that the stimulation caused by norepinephrine is a direct effect on the enzyme and is not mediated by cyclic AMP or adrenergic receptors.

Adenosine Triphosphatases↗

PubMed1989

Depletion of hypothalamic norepinephrine reduces the fever induced by polyriboinosinic acid: polyribocytidylic acid (Poly I:Poly C) in rats.

Administration of either Poly I:Poly C (0.05-0.50 micrograms) or norepinephrine (2-8 micrograms) into the anterior hypothalamic area produced a dose-related fever in rats. The fever induced by Poly I:Poly C was attenuated after selective depletion of norepinephrine in the hypothalamus. However, selective depletion of hypothalamic norepinephrine did not affect the fever induced by intrahypothalamic norepinephrine. The data indicate that Poly I:Poly C may act to induce fever through the endogenous release of norepinephrine from the rat's hypothalamus.

Animals↗

PubMed1978

The metabolic response to norepinephrine in normal versus diabetic man.

Norepinephrine was infused for 60 minutes in high physiological concentration (0.08 microgram/kg/min) into seven insulin dependent diabetic subjects with no demonstrable endogenous insulin secretion and into seven normal subjects. Insulin dependent diabetic subjects had a stable, free insulin concentration of 23 +/- 5 microunits/ml which was unaffected by norepinephrine infusion. In the normal subjects, norepinephrine induced an initial inhibition of insulin secretion which lasted for approximately 20 minutes. Norepinephrine infusion caused a rapid increase in both ketone body and glucose concentrations but this response did not differ between the two groups. In contrast, plasma nonesterified fatty acid and triglyceride concentrations were increased significantly more in the normal than in the diabetic subjects. The increase in plasma glucagon concentrations was similar in the two groups of subjects. The cause of the differential metabolic response to norepinephrine between the normal and diabetic groups was not resolved, but may be related, at least in part, to suppression of endogenous insulin secretion in the normal subjects.

Adult↗

PubMed1975

The effects of morphine and halothane anaesthesia on urine norepinephrine during and after coronary artery surgery.

Urine concentrations and excretion rates of norepinephrine were measured in 28 patients anaesthetized with halothane or morphine before, during and for two hours after aortocoronary artery grafting procedures. All patients were paralyzed with d-tubocurarine, intubated and respiration was controlled. Urine was obtained for 90 minutes before induction, during induction, before, during and after bypass and postoperatively. In patients anaesthetized with halothane, urinary norepinephrine concentrations and excretion rates were not significantly different from preoperative values until the postoperative period. Patients anaesthetized with morphine did not have urine norepinephrine concentrations different from preoperative values until bypass, when they became significantly increased. All subsequent urine norepinephrine concentrations and excretion rates were significantly elevated when compared to preoperative values. These findings do not indicate a mechanism but they do demonstrate that morphine anaesthesia is associated with increased urinary and probably also increased plasma levels of norepinephrine during and after cardiopulmonary bypass in patients undergoing coronary artery operations.

Adjuvants, Anesthesia↗

PubMed2006

Review article: organ perfusion/permeability-related effects of norepinephrine and vasopressin in sepsis.

PURPOSE: One invariable hallmark of severe sepsis is generalized tissue "malperfusion" and hyperpermeability secondary to microcirculatory/capillary leakage. This review focuses on direct and/or indirect influences of norepinephrine, as a standard of care, and vasopressin, as an alternative vasoactive drug, on organ and tissue perfusion/permeability in severe sepsis. SOURCE: English and French language articles and books published between 1966 and 2005 were identified through a computerized Medline search using the terms "sepsis, permeability, norepinephrine and vasopressin". Relevant publications were retrieved and scanned for additional sources. PRINCIPAL FINDINGS: There are few randomized clinical trials comparing different vasopressors in sepsis; most available literature consists of clinical reports, animal experiments and occasional reviews. Based on the best current evidence from these sources, we describe the status of major organ perfusion/permeability in sepsis (i.e., the lung, the kidney, the heart, the intestine/gut) in the context of sepsis-induced organ dysfunction/failure. Potential and differential therapeutic effects of the vasopressors norepinephrine and arginine-vasopressin, in the setting of sepsis, are identified. CONCLUSIONS: In the treatment of sepsis, arginine-vasopressin exhibits organ-specific heterogeneity in vascular responsiveness, compared to norepinephrine. While norepinephrine is a current standard of care in sepsis, arginine-vasopressin shows promise for the treatment of septic shock.

Animals↗

PubMed2003

Norepinephrine release is reduced in cardiac tissue of Type 2 diabetic patients.

AIMS/HYPOTHESIS: The aim of this study was to assess whether cardiac catecholamine release is affected in patients with Type 2 diabetes mellitus. METHODS: A trial tissue was obtained from 19 diabetic (Type 2) and 43 non-diabetic patients undergoing coronary surgery. Endogenous norepinephrine release was examined under baseline conditions as well as during electrical field stimulation (effective voltage 5 V, stimulation frequency 4 Hz, pulse width 2 msec) by high performance liquid chromatography and electrochemical detection. Cardiac function and arterial blood pressure was assessed from coronary angiography. RESULTS: In atrial tissue from diabetic patients, stimulation-induced norepinephrine release was reduced by 25% compared with non-diabetic patients, while baseline norepinephrine release did not differ between both groups. Preoperative plasma glucose and haemoglobin A(1C) concentrations were increased in patients with diabetes, however, no relation was found to catecholamine release. Diabetic and non-diabetic patients did not differ regarding left ventricular ejection fraction and arterial blood pressure. CONCLUSION/INTERPRETATION: Cardiac norepinephrine release is suppressed in patients with Type 2 diabetes which could contribute to sympathetic neuropathy. The difference of norepinephrine release in diabetic and non-diabetic patients was independent of cardiac function and arterial blood pressure.

Aged↗

PubMed2003

Effects of epinephrine and norepinephrine on hemodynamics, oxidative metabolism, and organ energetics in endotoxemic rats.

OBJECTIVE: To determine whether epinephrine increases lactate concentration in sepsis through hypoxia or through a particular thermogenic or metabolic pathway. DESIGN: Prospective, controlled experimental study in rats. SETTING: Experimental laboratory in a university teaching hospital. INTERVENTIONS: Three groups of anesthetized, mechanically ventilated male Wistar rats received an intravenous infusion of 15 mg/kg Escherichia coli O127:B8 endotoxin. Rats were treated after 90 min by epinephrine ( n=14), norepinephrine ( n=14), or hydroxyethyl starch ( n=14). Three groups of six rats served as time-matched control groups and received saline, epinephrine, or norepinephrine from 90 to 180 degrees min. Mean arterial pressure, aortic, renal, mesenteric and femoral blood flow, arterial blood gases, lactate, pyruvate, and nitrate were measured at baseline and 90 and 180 min after endotoxin challenge. At the end of experiments biopsy samples were taken from the liver, heart, muscle, kidney, and small intestine for tissue adenine nucleotide and lactate/pyruvate measurements. MEASUREMENTS AND RESULTS: Endotoxin induced a decrease in mean arterial pressure and in aortic, mesenteric, and renal blood flow. Plasmatic and tissue lactate increased with a high lactate/pyruvate (L/P) ratio. ATP decreased in liver, kidney, and heart. The ATP/ADP ratio did not change, and phosphocreatinine decreased in all organs. Epinephrine and norepinephrine increased mean arterial pressure to baseline values. Epinephrine increased aortic blood flow while renal blood low decreased with both drugs. Plasmatic lactate increased with a stable L/P ratio with epinephrine and did not change with norepinephrine compared to endotoxin values. Nevertheless epinephrine and norepinephrine when compared to endotoxin values did not change tissue L/P ratios or ATP concentration in muscle, heart, gut, or liver. In kidney both drugs decreased ATP concentration. CONCLUSIONS: Our data demonstrate in a rat model of endotoxemia that epinephrine-induced hyperlactatemia is not related to cellular hypoxia.

Acidosis, Lactic↗

PubMed1978

Comparative influence of ouabain, norepinephrine and heart rate on myocardial oxygen consumption and inotropic state in dogs.

The purpose of this study was to compare the myocardial oxygen cost of augmented inotropic state produced by ouabain, norepinephrine, or increased heart rate. This problem was examined in dogs using an isovolumically contracting left ventricular preparation. Inotropic state was measured as the maximum observed contractile element velocity at the lowest common level of wall stress (MAX V). Peak left ventricular wall stress was maintained constant in each dog so that it would not influence changes in myocardial oxygen consumption (MVO2). Ouabain (4 X 10(-2) mumoles/Kg.) and norepinephrine (2 X 10(-3) mumoles/Kg./minute) always augmented inotropic state (MAX V) and increased MVO2. The positive slopes of the regression of MVO2 on MAX V for ouabain (45.4 +/- 12.5 microliter/beat/100 Gm./muscle length/sec; mean +/- SEM) and norepinephrine (34.5 +/- 5.6 microliter/beat/100 Gm./muscle length/sec; mean +/- SEM) were not significantly different, indicating that for an equal augmentation of inotropic state, ouabain increases myocardial oxygen demands to the same extent as does norepinephrine. When the results with ouabain or norepinephrine were compared to results obtained by altering heart rate, it was found that increasing inotropic state by these pharmacologic agents is more costly in terms of myocardial energy demands than when inotropic state is enhanced by increasing heart rate.

Animals↗

PubMed1982

Effects of pindolol and methyldopa on blood pressure and plasma norepinephrine.

Thirty patients with essential hypertension (supine diastolic blood pressure 100 to 115 mm Hg) were treated in a randomized, double-blind study with either pindolol (mean dose 28 +/- 5 mg twice a day) or methyldopa (673 +/- 158 mg three times a day) for 12 weeks after a 3-week, single-blind placebo period. In 17 pindolol-treated patients mean supine blood pressure was 163 +/- 3/106 +/- 1 during the placebo period and 155 +/- 3/99 +/- 2 mm Hg (p less than 0.01) during the high-dose period. In 13 patients treated with methyldopa mean supine blood pressure fell from 160 +/- 4/104 +/- 1 to 156 +/- 5/97 +/- 2 mm Hg. Mean standing heart rate was reduced during pindolol therapy from 84 +/- 2 to 79 +/- 2 bpm (p less than 0.05) but was unchanged during methyldopa treatment. Mean supine pretreatment plasma norepinephrine fell from 379 +/- 40 to 337 +/- 33 pg/ml in patients on pindolol therapy and from 448 +/- 76 to 223 +/- 39 pg/ml (p less than 0.02) in the methyldopa-treated group. Although norepinephrine generally decreased in pindolol responders and not in nonresponders, changes in supine diastolic blood pressure and supine plasma norepinephrine did not correlate. In contrast, norepinephrine declined consistently in methyldopa-treated patients regardless of the blood pressure response; changes in diastolic blood pressure and norepinephrine correlated (r = 0.59; p less than 0.05). The results suggest that suppression of sympathetic nervous system activity may play a role in the hypotensive effect of both pindolol and methyldopa.

Blood Pressure↗

PubMed1989

Plasma norepinephrine in Chagas' cardioneuromyopathy: a marker of progressive dysautonomia.

Chronic Chagas' disease produces pathologic changes of the cardiovascular, digestive, and autonomic nervous systems. In an attempt to elucidate the nature of the dysautonomia in patients with Chagas' disease, we measured plasma norepinephrine levels, blood pressure, and heart rate, both supine and standing in 26 patients, and compared these values of patients classified according to three clinical subsets of cardiovascular manifestations with the values of nine normal volunteers and 16 patients with nonchagasic heart failure. Results suggested (1) progressive blockade of the alpha receptor in patients with Chagas' disease who have minimal clinical symptoms (group I) and in those who have ECG alterations without congestive symptoms (group II), as reflected by normal or raised plasma norepinephrine levels without change of diastolic blood pressure during standing, which indicates absent postural reflexes; and (2) blockade associated with partial denervation in patients with Chagas' disease who have class III or IV heart failure (group III), as suggested by a lower supine plasma norepinephrine level and a fall in diastolic blood pressure in the upright position. The findings of reduced plasma norepinephrine levels are in contrast to the elevated plasma norepinephrine levels in patients without Chagas' disease with class III and IV heart failure who have sympathetic hyperactivity.

Adult↗

PubMed1991

Impaired suppression of plasma norepinephrine during head-down tilt in patients with congestive heart failure.

Neurohumoral activation is present in congestive heart failure and may contribute to vasoconstriction in this syndrome. The mechanisms leading to and maintaining neurohumoral activation in long-standing congestive heart failure are as yet undefined. The present study addresses the possibility that baroreceptor-mediated suppression of plasma norepinephrine may be abnormal in patients with long-standing congestive heart failure. Eight normal subjects and 12 patients with long-standing congestive heart failure were studied during 15 minutes of 30 degrees head-down tilt. There were no significant changes in heart rate or arterial blood pressure in either group during these maneuvers. In normal subjects, plasma norepinephrine declined from 257 +/- 38 pg/ml at control to 208 +/- 39 pg/ml during head-down tilt (p less than 0.005). Plasma norepinephrine was elevated in the patients with congestive heart failure, 475 +/- 189 pg/ml, and did not change during head-down tilt. These observations suggest that baroreflex loading maneuvers, which in this study included increased central blood volume and hydrostatic effects on the sinoaortic baroreceptor, do not suppress increased plasma norepinephrine in patients with long-standing congestive heart failure. Impaired baroreflex responsiveness could therefore contribute to either the generation or maintenance of high plasma norepinephrine in this syndrome.

Adult↗

PubMed1975

Electrophysiologic studies in the denervated transplanted human heart. II. Response to norepinephrine, isoproterenol and propranolol.

Five patients who had received a transplanted human heart 1 to 3 years previously were studied to determine the effects of norepinephrine, isoproterenol and propranolol on the atrioventricular (A-V) conduction system. Using the His bundle technique, atrial, His bundle and ventricular electrograms were recorded, and central aortic pressure was monitored during the administration of these drugs. Norepinephrine was given by continuous infusion to four patients in doses ranging from 4 to 8 mug/min, with the systolic arterial pressure increasing by an average of 72 mm Hg. Concomitantly, there was an average increase in the rate of the donor atrium of 32 beats/min, and a reflex slowing of the recipient atrium of 23 beats/min. The A-H interval shortened by an average of 27 msec. Isoproterenol dose-response curves were performed in three patients, with the maximal dose being 5.2 mug by intravenous bolus infusion. The rate of the donor atrium increased by an average of 40 beats/min, and that of the recipient atrium by 18 beats/min. The A-H time shortened by an average of 25 msec, with a drop in systolic blood pressure averaging 23 mm Hg. Propranolol (7 mg intravenously) was given to three patients and the peak doses of norepinephrine and isoproterenol were again infused. Beta adrenergic blockade was achieved at this dose of propranolol since there was only a minimal increase in the donor atrial rate after infusion of the drug. The A-H interval was not altered by catecholamine infusion after achievement of beta blockade. However, the levels of systolic hypertension noted after infusion of norepinephrine was not altered by propranolol. The denervated transplanted human heart appears to respond normally to norepinephrine and isoproterenol, and the electrophysiologic effects of these agents are blocked by propranolol. Extensive investigative work in the denervated canine model has demonstrated the presence of the alpha and beta cardiovascular receptors. Although the automonic nervous system is important in cardiac performance, this work is the first validation in man that (1) the functional integrity of the beta receptor is maintained even when the autonomic nerves are absent, and (2) the intrinsic properties of the sinus and atrioventricular nodes are the keystone in stabilizing cardiac electrophysiology after denervation.

Atrioventricular Node↗

PubMed1993

Prognostic value of plasma atrial natriuretic factor, norepinephrine and epinephrine in acute myocardial infarction.

Neurohumoral activation in acute myocardial infarction (AMI) may reflect the degree of hemodynamic compromise, contribute to the progression of heart failure and augment to the risk of serious ventricular arrhythmias. Consequently, assessment of neurohumoral variables may provide an index of prognostic value in AMI. Plasma levels of atrial natriuretic factor (ANF), norepinephrine and epinephrine were determined in 145 patients on day 3 after AMI. During the 360-day follow-up period 17 patients died. In univariate analysis, all 3 neurohormones were significantly related to 1-year mortality rates (ANF, p < 0.001; norepinephrine, p = 0.009; epinephrine, p = 0.048). After correction for age, sex, anamnestic, biochemical and clinical variables including signs of clinical heart failure in a multivariate model, ANF remained independently related to mortality. The association between plasma norepinephrine and survival failed to reach statistical significance after introduction of clinical heart failure in the model. Comparison of patients subdivided according to median hormone levels (ANF, 30.3 pmol/liter; norepinephrine, 2.29 nmol/liter) demonstrated a significantly increased mortality rate in patients with elevated ANF (p < 0.001), but not elevated norepinephrine levels. These results suggest that early plasma ANF levels are related to survival in patients with AMI, independently of signs of clinical heart failure.

Aged↗

PubMed1981

Increase in plasma norepinephrine during prazosin therapy for chronic congestive heart failure.

To investigate the mechanism of pharmacodynamic tolerance reported to occur during prazosin therapy of chronic congestive heart failure, we measured plasma norepinephrine, plasma epinephrine, plasma renin activity (PRA) and plasma aldosterone, as well as hemodynamics in eight patients with chronic congestive heart failure, functional class III and IV (NYHA), before and during 10 weeks of prazosin therapy. Initially, prazosin therapy produced significant hemodynamic improvement, but no significant changes were noted in norepinephrine, epinephrine, plasma renin activity or aldosterone. During ambulatory therapy, fluid retention developed in four patients, and three of them had symptoms or clinical evidence of congestive heart failure for which they required an increase in diuretic or prazosin therapy. Plasma norepinephrine levels for the whole group were significantly higher after four weeks of therapy (p less than 0.01). Repeat inpatient studies after 10 weeks showed a persistent hemodynamic response to prazosin in seven patients. One patient demonstrated complete hemodynamic tolerance whereas three others showed partial tolerance. In these four patients the cardiac output increased only to 3.78 +/ 1.17 liters/min compared to 5.04 +/- 2.11 liters/min during initial prazosin therapy. Plasma norepinephrine increased further and levels were significantly higher for the whole group than before prazosin therapy (p less than 0.05). No significant changes in epinephrine, plasma renin activity or aldosterone were demonstrated. This increase in plasma norepinephrine suggests that the sympathetic nervous system could be involved in the pharmacodynamic tolerance to prazosin therapy in congestive heart failure. Further studies are necessary to extend these results.

Aged↗

PubMed1982

Sympathetic responsiveness and plasma norepinephrine during therapy of chronic congestive heart failure with captopril.

The interaction of cardiac function and sympathetic tone in severe chronic heart failure was evaluated in 24 patients by assessing the cardiac index/plasma norepinephrine relationship. Potential changes were assessed during first-dose and long-term captopril therapy including sympathetic responsiveness to the gravitational stress of head-up tilt. Because cardiac index and norepinephrine levels demonstrated a significant inverse correlation (r = -0.640, p less than 0.001). Norepinephrine decreased from 803 +/- 116 to 635 +/- 76 pg/ml following first-dose captopril therapy (p less than 0.02), with overall hemodynamic improvement. However significant first-dose correlations were not observed. During long-term therapy, norepinephrine decreased from 694 +/- 118 to 457 +/- 106 pg/ml, associated with improvement of symptoms and exercise tolerance. The extent of cardiac index increase was matched by norepinephrine reduction, so that their correlation was maintained (r = -0.540, p less than 0.02). First-dose and long-term therapy were associated with improved responsiveness of sympathetic tone to the reduction of cardiac index induced by the gravitational stress of tilt. In summary, sympathetic tone was increased in severe heart failure, correlating inversely with cardiac function. Although there was improvement of cardiac function with first-dose captopril therapy, significant correlations of supine improvement with reduction of sympathetic tone were noted primarily with long-term therapy. Responsiveness of sympathetic tone to the stress of tilt however, was evident during first-dose and long-term therapy.

Adult↗

PubMed1975

Variations in the level of uterine norepinephrine during pregnancy in the guinea pig.

The uterine smooth musculature is innervated by short adrenergic neurons which are unique in that their transmitter content varies during pregnancy and under the influence of exogenous sex hormones. Uterine norepinephrine was measured fluorometrically at 25 stages throughout pregnancy in the guinea pig, which was chosen because one of the pregnant uterine horns often is devoid of fetuses and hence not subject to mechanical tension. During the initial 10 days of pregnancy, the total organ content of norepinephrine was almost doubled whether the horn contained conceptuses or not. In the horn with conceptuses, norepinephrine was subsequently reduced in the course of the remaining gestation time to reach near-zero levels at term (about 65 days post coitus). In the empty horn, the amine level was constantly elevated until the last two weeks, during which it fell to the same low values as in the contralateral horn. Cervical norepinephrine exhibited the same variations during pregnancy as the empty horn. It is suggested that the characteristic variations in uterine norepinephrine reflect a hormonal influence on the system of short adrenergic neurons, with the addition of mechanical factors in that horn containing fetuses.

Animals↗

PubMed1984

Effects of circulating levels of vasoconstrictors on systemic pressor responsiveness to angiotensin II and norepinephrine.

Pregnancy is associated with vascular refractoriness to systemic pressor responses produced by angiotensin II. The present study was designed to determine if pregnancy-induced increases in circulating levels of angiotensin II are responsible for this refractoriness. Ten ovariectomized ewes received intravenous infusions of graded doses of angiotensin II (3, 10, 30, and 100 ng/kg/min) and norepinephrine (0.1, 0.3, 1.0, and 3.0 micrograms/kg/min) prior to (control response) and during (test response) the continuous infusion of either angiotensin II (8 ng/kg/min) or norepinephrine (0.2 microgram/kg/min). Systemic pressor responses (increases in blood pressure, millimeters of mercury) to graded doses of angiotensin II were significantly depressed during the continuous angiotensin II infusion while responses to norepinephrine were not modified. In contrast, elevation of baseline levels of a second vasoconstrictor, norepinephrine, did not alter pressor responsiveness to either angiotensin II or norepinephrine. These data suggest that vascular responses to exogenously administered angiotensin II can be selectively depressed by elevated baseline levels of angiotensin II in nonpregnant sheep.

Angiotensin II↗