IMMUNOLOGICAL RELEASE OF HISTAMINE AND SLOW-REACTING SUBSTANCE OF ANAPHYLAXIS FROM HUMAN LUNG

1971 ◽  
Vol 134 (3) ◽  
pp. 136-148 ◽  
Author(s):  
Robert P. Orange ◽  
W. Gerald Austen ◽  
K. Frank Austen
Keyword(s):  
Inhibitory Activity ◽  
Human Lung ◽  
Blocking Agent ◽  
Adrenergic Stimulation ◽  
Temperature Dependent ◽  
Myeloma Protein ◽  
Adrenergic Agents ◽  
Myeloma Proteins ◽  
Ige Myeloma ◽  
Adrenergic Blocking

The sensitization of human lung with atopic serum is both time and temperature dependent. Highly purified IgE myeloma protein is capable of blocking sensitization of human lung with atopic serum whereas myeloma proteins of the IgG subgroups are inactive. Drugs capable of increasing cellular levels of CAMP such as ß-adrenergic agents and methylxanthines inhibit the antigen-induced release of both histamine and SRS-A from human lung and these agents demonstrate synergism when used together. The ß-adrenergic blocking agent, propranolol, prevents epinephrine-induced inhibition of the immunologic release of the mediators. Diethylcarbamazine also inhibits the antigen-induced release of histamine and SRS-A from human lung and a synergism between this drug and epinephrine is observed. Predominantly α-adrenergic stimulation achieved by combining propranolol with epinephrine or norepinephrine not only prevented the inhibitory activity of the sympathomimetic amines but also resulted in an enhanced release of histamine and SRS-A. These observations suggest that whereas increases in cellular levels of CAMP are inhibitory, decreases in cellular levels of CAMP enhance the antigen-induced release of the mediators.

Alpha 1-adrenergic stimulation of hamster brown adipocyte respiration

1983 ◽  
Vol 244 (5) ◽  
pp. C362-C368 ◽  
Author(s):  
R. J. Schimmel ◽  
L. McCarthy ◽  
K. K. McMahon
Keyword(s):  
Oxygen Uptake ◽  
Adrenergic Receptors ◽  
Blocking Agent ◽  
Brown Adipocyte ◽  
Control Of Respiration ◽  
Blocking Drug ◽  
Tetraacetic Acid ◽  
Adrenergic Stimulation ◽  
Adrenergic Blocking ◽  
Stimulation Of

Respiration was increased approximately 5-fold with 0.05 microM norepinephrine and to a maximum of 10-fold by 0.30 microM norepinephrine. Prazosin, an alpha-adrenergic blocking agent highly selective for alpha 1-type receptors, partially inhibited the response to norepinephrine (0.05 microM) by 20-25% at a concentration of 0.10-1 microM. In contrast, when the stimulus for respiration was provided by isoproterenol or 3-isobutyl-1-methylxanthine, prazosin was without effect up to a concentration of 10 microM. Yohimbine, an alpha-adrenergic blocking drug preferential for alpha 2-receptors, did not influence norepinephrine-stimulated oxygen uptake. Respiration was increased two- to fourfold by phenylephrine or methoxamine, agents preferential for alpha 1-adrenergic receptors but not at all by clonidine, an agent preferential for alpha 2-adrenergic receptors. The stimulatory effect of phenylephrine on oxygen uptake was fully blocked by prazosin but not propranolol. Removal of extracellular calcium with ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid prevented phenylephrine stimulation of respiration but was without effect when isoproterenol was the stimulus. These results support the participation of alpha 1-adrenergic receptors in control of respiration and are consistent with the possibility that changes in cell calcium are intimately involved in this response.

Contribution of Adrenaline to the Fibrinolytic Activity Evoked by E. Coli Endotoxin in the Rat

1983 ◽  
Vol 50 (02) ◽  
pp. 557-559 ◽  
Author(s):  
J F Fracasso ◽  
A M Rothschild
Keyword(s):  
Fatty Acid ◽  
Adrenal Gland ◽  
Intravenous Injection ◽  
Fibrinolytic Activity ◽  
Blocking Agent ◽  
E Coli ◽  
Adrenergic Blocking

SummaryIntravenous injection of E. coli endotoxin (ETX), of adrenaline (AD) or of carbamylcholine (CBCH), caused fibrinolytic activity (FA), directly detectable on plasminogen-rich fibrin plates, to appear in the plasma of the rat. Adrenodemedul- lation abolished responses to ETX or CBCH, but enhanced those to AD. Rats given ETX exhibited marked hypotension, followed by a compensatory phase of normotension abolished by adrenodemedullation and significantly attenuated by phenoxy- benzamine, an a-adrenergic blocking agent which however failed to block FA caused by either ETX or AD. Aspirin, but not indomethacin, inhibited FA evoked by ETX, AD or CBCH. These results suggest that FA evoked by ETX in the rat is caused by AD released from the adrenal gland and does involve the fatty acid cyclooxygenase system.

ADRENERGIC CONTROL MECHANISM FOR ACTH SECRETION IN MAN

1973 ◽  
Vol 74 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Yoshikatsu Nakai ◽  
Hiroo Imura ◽  
Teruya Yoshimi ◽  
Shigeru Matsukura
Keyword(s):  
Intravenous Infusion ◽  
Human Subjects ◽  
Blocking Agent ◽  
Inhibitory Effect ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Glucose Levels ◽  
Alpha Receptors ◽  
Normal Human ◽  
Adrenergic Blocking

ABSTRACT In order to determine if an adrenergic mechanism is involved in the secretion of corticotrophin (ACTH), the effect of adrenergic-blocking or -stimulating agent on plasma ACTH, cortisol and glucose levels was studied in normal human subjects. The intravenous infusion of methoxamine, an alpha adrenergic-stimulating agent, caused a rise in plasma ACTH and cortisol. This increase in plasma ACTH and cortisol was significantly inhibited by the simultaneous administration of phentolamine, an alpha adrenergic-blocking agent, in combination with methoxamine. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused no significant change in plasma ACTH and cortisol, although it enhanced the plasma ACTH response to insulin-induced hypoglycaemia. On the other hand, alpha adrenergicblockade by intravenous infusion of phentolamine significantly suppressed the plasma ACTH response to insulin-induced hypoglycaemia. These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man.

Effects of endogenous and exogenous catecholamines on LPS-induced neutrophil trafficking and activation

1999 ◽  
Vol 276 (1) ◽  
pp. L1-L8 ◽  
Author(s):  
Edward Abraham ◽  
Debra J. Kaneko ◽  
Robert Shenkar
Keyword(s):  
Systemic Circulation ◽  
Mrna Levels ◽  
Adrenergic Stimulation ◽  
Neutrophil Accumulation ◽  
Adrenergic Agonist ◽  
Nitric Oxide Synthase Inhibitor ◽  
Adrenergic Agents ◽  
Adrenergic Antagonist ◽  
Tnf Α ◽  
Synthase Inhibitor

Endotoxemia produces elevations in catecholamine levels in the pulmonary and systemic circulation as well as rapid increases in neutrophil number and proinflammatory cytokine expression in the lungs. In the present experiments, we examined the effects of endogenous and exogenous adrenergic stimulation on endotoxin-induced lung neutrophil accumulation and activation. Levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and macrophage inflammatory protein (MIP)-2 mRNAs were increased in lung neutrophils from endotoxemic mice compared with those present in lung neutrophils from control mice or in peripheral blood neutrophils from endotoxemic or control mice. Treatment with the β-adrenergic antagonist propranolol before endotoxin administration did not affect trafficking of neutrophils to the lungs or the expression of IL-1β, TNF-α, or MIP-2 by lung neutrophils. Administration of the α-adrenergic antagonist phentolamine before endotoxemia did not alter lung neutrophil accumulation as measured by myeloperoxidase (MPO) levels but did result in significant increases in IL-1β, TNF-α, and MIP-2 mRNA expression by lung neutrophils compared with endotoxemia alone. Administration of the α1-adrenergic agonist phenylephrine before endotoxin did not affect trafficking of neutrophils to the lungs but was associated with significantly increased expression of TNF-α and MIP-2 mRNAs by lung neutrophils compared with that found after endotoxin alone. In contrast, treatment with the α2-adrenergic agonist UK-14304 prevented endotoxin-induced increases in lung MPO and lung neutrophil cytokine mRNA levels. The suppressive effects of UK-14304 on endotoxin-induced increases in lung MPO were not affected by administration of the nitric oxide synthase inhibitor N-nitro-l-arginine methyl ester. These data demonstrate that the initial accumulation and activation of neutrophils in the lungs after endotoxemia can be significantly diminished by α2-adrenergic stimulation. Therapy with α2-adrenergic agents may have a role in modulating inflammatory pulmonary processes associated with sepsis-induced acute lung injury.

Massive Clonidine Ingestion with Hypertension in a 9-Month-Old Infant

PEDIATRICS ◽  
1983 ◽  
Vol 72 (4) ◽  
pp. 500-502
Author(s):  
Pablo Yagupsky ◽  
Rafael Gorodischer
Keyword(s):  
Blood Pressure ◽  
Antihypertensive Drugs ◽  
Complete Recovery ◽  
Blocking Agent ◽  
Assisted Ventilation ◽  
Antagonistic Effect ◽  
Arterial Blood ◽  
Clonidine Poisoning ◽  
Adrenergic Blockers ◽  
Adrenergic Blocking

The antihypertensive drug clonidine has a double and antagonistic effect on arterial blood pressure. As a result of activation of peripheral α-adrenergic receptors, it causes a transient increase in blood pressure; by a central action it decreases sympathetic tone which results in sustained bradycardia and hypotension. Both central and peripheral effects are experimentally blocked by tolazoline, an α-adrenergic blocking agent. The toxic symptoms seen in clonidine poisoning are usually produced by the central effect. A case of severe clonidine poisoning in a 9-month-old infant is reported. The clinical picture included coma, miosis, apneic spells, bradycardia, and hypertension. Rapid and complete recovery was obtained with supportive treatment that included assisted ventilation. No adrenergic blockers or antihypertensive drugs were given. Use of tolazoline in cases of clonidine overdose in children remains controversial. Supportive measures alone may be adequate for even the most severe cases.

Occurrence of Myeloma-Like γ-Globulin in C.S.F of A Four-Month Old Infant with Hydrocephalus

PEDIATRICS ◽  
1964 ◽  
Vol 33 (3) ◽  
pp. 435-440
Author(s):  
G. M. HOCHWALD ◽  
G. J. THORBECKE
Keyword(s):  
Paper Electrophoresis ◽  
Reticulum Cell ◽  
Reticulum Cell Sarcoma ◽  
Myeloma Protein ◽  
Characteristic Appearance ◽  
Myeloma Proteins ◽  
Group I ◽  
Immune Globulins ◽  
Γ Globulins ◽  
Narrow Bands

Myeloma-like immune globulins present themselves as narrow bands upon paper electrophoresis, and usually show a characteristic appearance in immunoelectrophoresis. Two antigenically different groups of myeloma proteins have been described: groups I and II. Recently, 60% of normal γ-globulin, throughout the mobility range of γ-globulin, has been shown to possess the antigen characteristic for group I, and 30% that for group II myeloma. Occurrence of myeloma-like proteins in the serum is not restricted to multiple myeloma. They may also be seen with other tumors, such as reticulum cell sarcoma, and various carcinomas. In addition, Sonnet and Milhaux have reported on the frequent occurrence of myeloma-like ("monoclonal") γ-globulins in the serum of adult Bantus with different diseases. When large amounts of a myeloma protein are present in the serum, it may be found in a much lower concentration in the spinal fluid.

The Usefulness of Dapiprazole, an Alpha-Adrenergic Blocking Agent, in Pigmentary Glaucoma

1996 ◽  
Vol 27 (9) ◽  
pp. 806-809
Author(s):  
Leonardo Mastropasqua ◽  
Paolo Carpineto ◽  
Marco Ciancaglini ◽  
Pier Enrico Gallenga
Keyword(s):  
Blocking Agent ◽  
Pigmentary Glaucoma ◽  
Adrenergic Blocking

Cardiovascular responses to insulin in the absence of hypoglycemia

1962 ◽  
Vol 202 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Santiago A. Pereda ◽  
John W. Eckstein ◽  
François M. Abboud
Keyword(s):  
Pressor Response ◽  
Direct Action ◽  
Cardiovascular Responses ◽  
Blocking Agent ◽  
Neuromuscular Blocking ◽  
Right Atrial ◽  
Systemic Vein ◽  
Anesthetized Dogs ◽  
Adrenergic Blocking ◽  
The Brain

Cardiovascular responses to intravenous administration of insulin were studied in lightly anesthetized dogs treated with a neuromuscular blocking agent. An early transient pressor response was observed. This abrupt increase in arterial pressure appeared 2–9 min after insulin was given. It was accompanied by increases in cardiac output and right atrial pressure. It occurred in the presence of hyperglycemia and in the absence of hypoglycemia. It was not altered by glucagon but it could be antagonized by ganglionic and adrenergic blocking drugs and by pentobarbital. The response could be produced when insulin was given in the carotid artery in doses that caused no effect when injected in a systemic vein. The experiments suggest that insulin may have a direct action on the brain.

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