Convalescent anti SARS-CoV-2 plasma/norepinephrine/tocilizumab

SummaryDesmopressin acetate administration markedly stimulates release of tissue plasminogen activator (t-PA) from vascular endothelial cells. The mechanism for this effect is unknown. Because infusion of epinephrine has been shown to increase t-PA levels, we examined the role of endogenous catecholamine mediation of t-PA release by desmopressin. Intravenous desmopressin acetate (0.3 μg/kg) was infused over 30 min in 9 controls and 11 subjects with diabetes mellitus, a condition associated with abnormalities of the fibrinolytic system. Plasma was collected in the supine, overnight fasted state at 15 min intervals (0-60 min) for measurement of t-PA activity, t-PA antigen and fractionated catecholamines. t-PA activity peaked at 30-45 min and subsequently decreased. The norepinephrine levels paralleled the t-PA activity. t-PA activity increased 10-fold from 0.14 ± .12 to 1.49 ± 0.79 IU/ml (Mean ± SD) and plasma norepinephrine increased 2- fold from 426 ± 90 to 780 ± 292 pg/ml. However, epinephrine and dopamine levels did not change significantly. The response to desmopressin of control and diabetic subjects was not shown to differ and their data were combined. We conclude that desmopressin increases plasma norepinephrine in addition to t-PA and that the parallel time course of change suggests a possible role for norepinephrine in mediating endothelial cell t-PA release.

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High plasma norepinephrine concentrations at birth in infants of diabetic mothers

Diabetes ◽

10.2337/diabetes.28.7.697 ◽

1979 ◽

Vol 28 (7) ◽

pp. 697-699 ◽

Cited By ~ 14

Author(s):

J. B. Young ◽

W. R. Cohen ◽

E. B. Rappaport ◽

L. Landsberg

Keyword(s):

High Plasma ◽

Plasma Norepinephrine ◽

Infants Of Diabetic Mothers ◽

Diabetic Mothers

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Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00783.2007 ◽

2008 ◽

Vol 295 (5) ◽

pp. R1546-R1554 ◽

Cited By ~ 8

Author(s):

Melissa Li ◽

Xiaoling Dai ◽

Stephanie Watts ◽

David Kreulen ◽

Gregory Fink

Keyword(s):

Blood Pressure ◽

Sympathetic Innervation ◽

Sympathetic Ganglia ◽

Plasma Norepinephrine ◽

Sprague Dawley ◽

Surgical Ablation ◽

Arterial Blood ◽

Sprague Dawley Rats ◽

Induced Hypertension ◽

Hypertension Development

Endothelin (ET) type B receptors (ETBR) are expressed in multiple tissues and perform different functions depending on their location. ETBR mediate endothelium-dependent vasodilation, clearance of circulating ET, and diuretic effects; all of these should produce a fall in arterial blood pressure. However, we recently showed that chronic activation of ETBR in rats with the selective agonist sarafotoxin 6c (S6c) causes sustained hypertension. We have proposed that one mechanism of this effect is constriction of capacitance vessels. The current study was performed to determine whether S6c hypertension is caused by increased generation of reactive oxygen species (ROS) and/or activation of the sympathetic nervous system. The model used was continuous 5-day infusion of S6c into male Sprague-Dawley rats. No changes in superoxide anion levels in arteries and veins were found in hypertensive S6c-treated rats. However, superoxide levels were increased in sympathetic ganglia from S6c-treated rats. In addition, superoxide levels in ganglia increased progressively the longer the animals received S6c. Treatment with the antioxidant tempol impaired S6c-induced hypertension and decreased superoxide levels in ganglia. Acute ganglion blockade lowered blood pressure more in S6c-treated rats than in vehicle-treated rats. Although plasma norepinephrine levels were not increased in S6c hypertension, surgical ablation of the celiac ganglion plexus, which provides most of the sympathetic innervation to the splanchnic organs, significantly attenuated hypertension development. The results suggest that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in prevertebral sympathetic ganglia.

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Catecholamine-fuel interrelationships during exercise in fasting men

Journal of Applied Physiology ◽

10.1152/jappl.1980.48.1.109 ◽

1980 ◽

Vol 48 (1) ◽

pp. 109-113 ◽

Cited By ~ 38

Author(s):

J. M. Pequignot ◽

L. Peyrin ◽

G. Peres

Keyword(s):

Maximal Oxygen Consumption ◽

Plasma Catecholamines ◽

Plasma Free Fatty Acid ◽

Work Load ◽

Bicycle Ergometer ◽

Plasma Norepinephrine ◽

Plasma Catecholamine ◽

Adrenergic Response ◽

Response To Exercise

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.

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Plasma norepinephrine and age as determinants of systemic hemodynamics in men with established essential hypertension.

Hypertension ◽

10.1161/01.hyp.9.4.415 ◽

1987 ◽

Vol 9 (4) ◽

pp. 415-419 ◽

Cited By ~ 20

Author(s):

J L Izzo ◽

R J Smith ◽

P S Larrabee ◽

M C Kallay

Keyword(s):

Essential Hypertension ◽

Systemic Hemodynamics ◽

Plasma Norepinephrine

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Failure of plasma norepinephrine to consistently reflect sympathetic activity in humans.

Hypertension ◽

10.1161/01.hyp.8.8.641 ◽

1986 ◽

Vol 8 (8) ◽

pp. 641-649 ◽

Cited By ~ 59

Author(s):

J Floras ◽

J Vann Jones ◽

M O Hassan ◽

B A Osikowska ◽

P S Sever ◽

...

Keyword(s):

Sympathetic Activity ◽

Plasma Norepinephrine

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Influnce of the beta-adrenergic agonist clenbuterol on plasma catecholamines and lymphocyte beta-receptors

Psychiatry and Psychobiology ◽

10.1017/s0767399x00000080 ◽

1986 ◽

Vol 1 (3) ◽

pp. 234-236

Author(s):

B. Bondy ◽

M. Ackenheil ◽

G. Laakmann ◽

H.T. Munz

Keyword(s):

Specific Binding ◽

Plasma Catecholamines ◽

Adrenergic System ◽

Plasma Norepinephrine ◽

Adrenergic Agonists ◽

Adrenergic Agonist ◽

Beta Receptors ◽

Β Receptor ◽

Beta Adrenergic Agonist ◽

The Brain

SummaryThe influence of subchronic application of the β-adrenergic agonist clenbuterol on plasma norepinephrine (NE), epinephrine (E) and β-receptors on lymphocytes was investigated in 8 male, healthy volunteers. Treatment with clenbuterol (0.04 mg/day) for 6 days induced significant reduction of β-receptor specific binding in 7 of the 8 subjects with a mean decrease of 40% (p < 0.01) with no changes in affinity. Concomitantly an increase in the plasma NE concentration was observed (mean 50%, p < 0.01), but no significant overall alteration of E concentration. Our results suggest that β-adrenergic agonists exercise a similar effect on the peripheral adrenergic system and on the adrenergic system in the brain.

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Effect of chronic left ventricular failure on beta-endorphin

Journal of Applied Physiology ◽

10.1152/jappl.1992.73.6.2675 ◽

1992 ◽

Vol 73 (6) ◽

pp. 2675-2680 ◽

Cited By ~ 1

Author(s):

E. Mellow ◽

E. Redei ◽

K. Marzo ◽

J. R. Wilson

Keyword(s):

Heart Failure ◽

Blood Pressure ◽

Chronic Heart Failure ◽

Left Ventricular ◽

Plasma Norepinephrine ◽

Endogenous Opiates ◽

Beta Endorphin ◽

Arterial Blood ◽

Norepinephrine Concentration ◽

C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

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Effect of changes in myocardial epinephrine stores on plasma norepinephrine gradient across the dog heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.6.h2404 ◽

1994 ◽

Vol 266 (6) ◽

pp. H2404-H2409 ◽

Cited By ~ 2

Author(s):

F. Peronnet ◽

G. Boudreau ◽

J. de Champlain ◽

R. Nadeau

Keyword(s):

Electrical Stimulation ◽

Adrenal Medulla ◽

Pulse Width ◽

Stellate Ganglion ◽

Plasma Norepinephrine ◽

Direct Support ◽

Left Stellate Ganglion ◽

Ici 118,551 ◽

Beta 2 ◽

Stimulation Of

Plasma norepinephrine (NE) concentration ([NE]) gradient across the heart was measured under electrical stimulation of the left stellate ganglion (LSG; 4 Hz, 4 V, 2 ms pulse width, 1 min) in control (Ctrl) and in adrenalectomized (Adrx) dogs, without and with a 10-min epinephrine (Epi) infusion (92 ng.kg-1.min-1), which partly restored myocardial Epi stores in Adrx dogs (2.9 +/- 0.7 ng/g vs. 6.4 +/- 0.7 ng/g in Ctrl dogs) and slightly increased tissue Epi stores in Ctrl dogs (10.5 +/- 1.3 pg/g). Compared with Ctrl dogs (1,069 +/- 172 pg/ml), the [NE] gradient across the heart under stimulation of the LSG was not modified 1 wk after bilateral adrenalectomy (1,190 +/- 122 pg/ml) or after Epi infusion in Ctrl (1,134 +/- 276 pg/ml) and Adrx (1,259 +/- 279 pg/ml) dogs. The beta 2-antagonist ICI-118,551 significantly reduced the stimulation-induced [NE] gradient across the heart in Ctrl dogs (621 +/- 190 and 603 +/- 86 pg/ml without and with a 10-min Epi infusion, respectively) but not in Adrx dogs deprived of tissue Epi (1,345 +/- 345 pg/ml). Partial repletion of myocardial Epi stores in Adrx dogs restored the effect of ICI-118,551 on the stimulation-induced [NE] gradient (776 +/- 121 pg/ml). These results provide direct support of the hypothesis that tissue Epi, which originates from the adrenal medulla and which is released locally along with NE, is the endogenous agonist for presynaptic beta 2-receptors and potentiates NE release.

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