Significance of Catecholamine-Induced Ganglionic Blockade and of Reflex Inhibition of Adrenergic Discharge at a Peripheral Locus as Mechanisms Producing Reflex Vasodilatation

1971 ◽  
Vol 49 (7) ◽  
pp. 688-698
Author(s):  
A. A. Pollard ◽  
L. Beck
Keyword(s):  
Spinal Anesthesia ◽  
Intravenous Injection ◽  
De Novo ◽  
Sympathetic Chain ◽  
Reflex Inhibition ◽  
Beta Receptors ◽  
Preganglionic Stimulation ◽  
Peripheral Locus ◽  
Ganglionic Transmission ◽  
Stimulation Of

An analysis has been made of the various factors which contribute to the vasodilatation observed in the innervated perfused hindlimb when catecholamines are injected intravenously. Bilateral transection of the lumbar sympathetic chains abolishes all dilatation in some animals and greatly reduces dilatations in all animals. When the sympathetic tone lost by chain transection is restored by preganglionic stimulation, the residual hindlimb dilatation still present after chain section is often increased, and a component of dilatation appears de novo in the hindlimb of many animals. This dilatation was blocked by spinal anesthesia. It is concluded that: (1) the peripheral dilatation produced in the hindlimb of the dog by intravenously administered catecholamines is almost entirely reflex in origin; (2) blockade of ganglionic transmission by intravenously injected adrenergic amines does not contribute significantly to the production of reflex dilatation; (3) the residual dilatation remaining after transection of the sympathetic chains is also reflex in origin because it is blocked by spinal anesthesia; (4) the hindlimb vasodilatation which appears de novo during stimulation of the sympathetic chain is also abolished by spinal anesthesia and is apparently due to inhibition of adrenergic discharge at a peripheral locus; (5) in the pentobarbital anesthetized dog, little, if any, of the hindlimb dilatation resulting from the intravenous injection of epinephrine is due to predominant activation of beta receptors.

Antiparasitic Treatment of Patients with P. falciparum Malaria Reduces the Ability of Patient Serum to Induce Tissue Factor by Decreasing NF-κB Activation

1995 ◽  
Vol 73 (01) ◽  
pp. 039-048 ◽  
Author(s):  
A Bierhaus ◽  
Ch J Hemmer ◽  
N Mackman ◽  
R Kutob ◽  
R Ziegler ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Falciparum Malaria ◽  
De Novo ◽  
Neutralizing Antibody ◽  
Mobility Shift ◽  
Before And After ◽  
Tf Gene ◽  
Electrophoretic Mobility Shift Assays ◽  
Antiparasitic Treatment ◽  
Stimulation Of

SummarySerum from patients with P. falciparum malaria at day 1 (pretherapy) induces tissue factor (TF) in cultured endothelial cells. TF induction depends on de novo transcription as shown in Nuclear Run On assays. Electrophoretic mobility shift assays demonstrated binding of AP-1 and NF- κB/Rel proteins to their recognition sites in the TF promotor. After therapy (day 28), stimulation of TF antigen by patient serum is reduced by 70%. When serum obtained before and after therapy was compared, a decrease of NF-κB activation was evident. Activation of NF-κB-like proteins was in part dependent on TNFα in patient serum, since a TNFα neutralizing antibody reduced induction of TF transcription and translation and induction of NF-κB-like proteins. Induction of TF activity was suppressed by pDTC, an inhibitor of NF-κB activation. When different promotor constructs of the TF gene were tested, induction was dependent upon the presence of the intact NF-κB-like binding site in the TF promotor. A mutant with deleted NF-κB, but intact AP-1 sites was not inducible. Mutation of the AP-1 sites did not prevent induction, but reduced inducibility by pretherapy serum. Therefore, NF-κB/Rel proteins are responsible for induction of TF transcription by pretherapy serum, but AP-1 is needed for highest inducibility. The effect of antiparasitic therapy on the induction of TF by serum from patients with complicated P. falciparum malaria is dependent on a therapy-mediated loss of activation of NF-κB-like proteins in post-treatment patient serum.

CATECHOLAMINE ANTAGONISM TO OXYTOCIN-INDUCED MILK-EJECTION

1971 ◽  
Vol 68 (1_Suppla) ◽  
pp. S5-S38 ◽  
Author(s):  
Helmuth Vorherr
Keyword(s):  
Receptor Blockade ◽  
Milk Ejection ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Beta Receptors ◽  
Alpha Receptors ◽  
Adrenergic Blockers ◽  
Beta Receptor Blockade ◽  
Second Pain ◽  
Stimulation Of

ABSTRACT In lactating rats and rabbits the mode of antagonism of sympathomimetics, angiotensin or pain toward oxytocin-induced milk-ejection was investigated. In rats intra-arterial (intrafemoral) doses of 0.01–0.02 μg or intravenous (iv) doses of 0.1–0.5 μg of either epinephrine, isoproterenol, norepinephrine, angiotensin or 10 μg of phenylephrine injected simultaneously with, or 30 seconds before an oxytocin dose (10 μU intrafemoral, 300 μU iv) greatly inhibited or suppressed the oxytocin response. A 15 second pain stimulus caused moderate inhibition. With alpha-receptor blockade pain, epinephrine, isoproterenol, norepinephrine, phenylephrine and angiotensin inhibition were, respectively, 70%, 75%, 100%, 40%, 0% and 100%. Under beta-receptor blockade the corresponding values were 14%, 40%, 0%, 70%, 100% and 100%; with simultaneous intrafemoral injections neither catecholamine was inhibitory toward oxytocin. In corresponding rabbit experiments approximately 10-fold higher iv drug dosages were applied and similar results were observed. In both species, combined alpha and beta-receptor blockade nearly eliminated the antagonistic actions of sympathomimetics toward oxytocin, whereas angiotensin inhibition persisted unchanged. The results indicate: 1) Mammary myoepithelial cells contain beta-adrenergic receptors but no alpha-receptors; 2) Inhibition of oxytocin-induced milk-ejection by isoproterenol and phenylephrine is meditated through stimulation of myoepithelial beta-receptors (myoepithelial relaxation) and vascular alpha-receptors (vasoconstriction), respectively; 3) Epinephrine and norepinephrine inhibition of milk-ejection is due to stimulation of vascular alpha-receptors and myoepithelial beta-receptors; 4) Angiotensin effects are unrelated to adrenergic receptor mechanisms; 5) Administration of both alpha and beta-adrenergic blockers is desirable for stabilizing the sensitivity of the oxytocin milk-ejection assay preparation against interference from endogenous or exogenous catecholamines; 6) Other than using adrenergic blockers, pharmacologic doses of oxytocin can correct nursing difficulties in animals and man with hyperfunction of the adrenal-sympathetic system.

Stimulation of Adrenergic Beta Receptors by Halothane and its Antagonism by Two New Drugs

1969 ◽  
Vol 48 (1) ◽  
pp. 58-65 ◽  
Author(s):  
ALAN M. KLIDE ◽  
MARIO PENNA ◽  
DOMINGO M. AVIADO
Keyword(s):  
New Drugs ◽  
Beta Receptors ◽  
Stimulation Of

scholarly journals STUDIES ON THE EFFECT OF CERTAIN TOXIC SUBSTANCES IN BACTERIAL CULTURES ON THE MOVEMENT OF THE INTESTINES

1926 ◽  
Vol 43 (6) ◽  
pp. 785-795 ◽  
Author(s):  
E. E. Ecker ◽  
A. Rademaekers
Keyword(s):  
Intravenous Injection ◽  
Toxic Substances ◽  
Propulsive Efficiency ◽  
Spasmodic Contraction ◽  
Strong Stimulation ◽  
Small Intestines ◽  
Slight Rise ◽  
Longitudinal Muscles ◽  
Stimulation Of

Following intravenous injection, filtrates of young cultures of B. paratyphosus B often produce marked diarrhea in rabbits. A study was made of the effect of these toxic filtrates on the motility of the small intestines of the rabbit. The observations were made on a segment of the small intestines in situ, and in the living animal. It was found that an immediate slight rise of tone of the longitudinal muscles occurred following intravenous injection of sterile broth. The same rise was noted after the injection of the toxic filtrate; but with these it was followed later (10 minutes elapsing at least) by a very strong but gradual rise of the diastolic and systolic tone, i.e., by spasmodic contraction of the intestinal muscle, which persisted at times for as long as 2 hours. In order to record simultaneously the effect on the longitudinal and circular muscles, and the propulsive efficiency of the segment the Sollmann and Rademaekers modification of Baur's technique was employed. This arrangement showed that the stimulation of the longitudinal muscles is accompanied by a similarly strong stimulation of the circular muscles, by peristalsis, and therefore by a greatly increased propulsion of intestinal contents which was sufficient to overcome the inhibition that usually occurs after preparation of the animal. With this arrangement an instance of peristaltic spasm was also noted. Broth alone failed to produce the phenomenon. Isotonic magnesium chloride or sulfate added to the bath relaxed the muscles again. Animals under deep urethane anesthesia did not show the diarrhea occurring in the intact controls, but sometimes exhibited it after the effect of the anesthetic had disappeared. So far no effects have been observed on the isolated strip (Magnus method), and further studies are being made to localize the effect, to neutralize it with a specific antiserum, and to observe the effect of filtrates of other members of the bacterial group including the dysentery bacilli.

Intravenous injection of hypertonic NaCl solution stimulates pulmonary C-fibers in dogs

1991 ◽  
Vol 260 (5) ◽  
pp. H1522-H1530 ◽  
Author(s):  
T. E. Pisarri ◽  
A. Jonzon ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Intravenous Injection ◽  
Pulmonary Circulation ◽  
Bronchial Artery ◽  
Dependent Manner ◽  
Nacl Solution ◽  
Impulse Frequency ◽  
Minimum Effective Concentration ◽  
C Fibers ◽  
Hypertonic Solutions ◽  
Stimulation Of

Intravenous injection of hypertonic NaCl solution evokes reflex bradycardia and hypotension, effects thought to result from stimulation of afferent vagal endings in the lungs. To identify the afferents responsible for these effects, we recorded vagal impulses arising from endings in the lungs and lower airways of anesthetized dogs and examined the response to injection of hypertonic solutions into the pulmonary circulation. Injection of 4,800 mmol/l NaCl solution (1 ml/kg) stimulated 39 of 49 pulmonary C-fibers, their impulse frequency increasing 35-fold. Stimulation was concentration dependent, the minimum effective concentration being between 1,200 and 4,800 mmol/l. Rapidly adapting receptors were also stimulated in a concentration-dependent manner, 35 of 41 receptors being stimulated by 4,800 mmol/l NaCl solution, firing increasing fivefold. Bronchial C-fibers were not stimulated by injection into the pulmonary circulation but were by injection into the bronchial artery. Hypertonic urea solutions had qualitatively similar but smaller effects on pulmonary C-fibers and rapidly adapting receptors. The results suggest that the reflex effects of intravenous injection of hypertonic solutions result principally from stimulation of pulmonary C-fibers.

Cardiac arrhythmias of sympathetic origin in the dog

1977 ◽  
Vol 233 (5) ◽  
pp. H535-H540
Author(s):  
L. S. D'Agrosa
Keyword(s):  
Cardiac Arrhythmias ◽  
Sympathetic Nerves ◽  
Nerve Fibers ◽  
Cardiac Contraction ◽  
Cardiac Rate ◽  
Atrioventricular Junction ◽  
Cardiac Nerve ◽  
Sympathetic Nerve Fibers ◽  
Beta Receptors ◽  
Stimulation Of

The effects of ventrolateral and ventromedial cardiac nerve (left sympathetics) stimulation on cardiac force, on rate, and on arrhythmogenic responses were characterized and quantitated. The stimulation of left sympathetic nerves produced augmentation in cardiac contraction in 45% of the experiments, an augmentation of both a cardiac rate and force in 47%, and in cardioacceleration alone in 8%. Two characteristic patterns of arrhythmogenic responses were elicited from stimulations of 100 sympathetic nerves. The two types of neurally induced arrhythmias were atrioventricular junctional or ventricular in origin. The onset and duration of the arrhythmias were quantitated. Both types of neurally induced arrhythmias were prevented either by blocking the beta receptors with propranolol or by preventing the neural release of norepinephrine with bretylium tosylate. The neurally induced arrhythmias were probably the result of enhanced automaticity in the atrioventricular junction area and in the ventricles produced by stimulating the sympathetic nerve fibers. This report thus implicates the ventromedial cardiac nerve in the genesis of cardiac arrhythmias.

Reflex Inhibition of Normal Cramp Following Electrical Stimulation of the Muscle Tendon

2007 ◽  
Vol 98 (3) ◽  
pp. 1102-1107 ◽  
Author(s):  
Serajul I. Khan ◽  
John A. Burne
Keyword(s):  
Electrical Stimulation ◽  
Maximum Voluntary Contraction ◽  
Voluntary Contraction ◽  
Muscle Cramp ◽  
Emg Activity ◽  
Reflex Inhibition ◽  
Experimental Conditions ◽  
Inhibitory Feedback ◽  
Two Phases ◽  
Stimulation Of

Muscle cramp was induced in one head of the gastrocnemius muscle (GA) in eight of thirteen subjects using maximum voluntary contraction when the muscle was in the shortened position. Cramp in GA was painful, involuntary, and localized. Induction of cramp was indicated by the presence of electromyographic (EMG) activity in one head of GA while the other head remained silent. In all cramping subjects, reflex inhibition of cramp electrical activity was observed following Achilles tendon electrical stimulation and they all reported subjective relief of cramp. Thus muscle cramp can be inhibited by stimulation of tendon afferents in the cramped muscle. When the inhibition of cramp-generated EMG and voluntary EMG was compared at similar mean EMG levels, the area and timing of the two phases of inhibition (I1, I2) did not differ significantly. This strongly suggests that the same reflex pathway was the source of the inhibition in both cases. Thus the cramp-generated EMG is also likely to be driven by spinal synaptic input to the motorneurons. We have found that the muscle conditions that appear necessary to facilitate cramp, a near to maximal contraction of the shortened muscle, are also the conditions that render the inhibition generated by tendon afferents ineffective. When the strength of tendon inhibition in cramping subjects was compared with that in subjects that failed to cramp, it was found to be significantly weaker under the same experimental conditions. It is likely that reduced inhibitory feedback from tendon afferents has an important role in generating cramp.

scholarly journals Induction of dopa (3,4-dihydroxyphenylalanine) decarboxylase in blowfly integument by ecdysone. A demonstration of synthesis of the enzyme de novo

1975 ◽  
Vol 146 (1) ◽  
pp. 121-126 ◽  
Author(s):  
E G Fragoulis ◽  
C E Sekeris
Keyword(s):  
Enzyme Activity ◽  
Steroid Hormones ◽  
De Novo ◽  
Steroid Hormone ◽  
Dopa Decarboxylase ◽  
Double Labelling ◽  
Labelling Technique ◽  
Immune Precipitation ◽  
Enzyme Molecules ◽  
Stimulation Of

The activity of the enzyme dopa (3,4-dihydroxyphenylalanine) decarboxylase, present in the epidermis cells of blowfly larvae, increases during the late third instar under the influence of the steroid hormone, ecdysone. By using the double-labelling technique and immune precipitation with univalent antibody to dopa decarboxylase, we demonstrated that the increase in enzyme activity was due to a stimulation of synthesis of enzyme molecules de novo. In this respect, the action of ecdysone is similar to the action of other steroid hormones.

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