Cerebral venous outflow in the dog; influence of adrenergic and cholinergic substances

1959 ◽  
Vol 197 (6) ◽  
pp. 1183-1190 ◽  
Author(s):  
Claude McClure ◽  
Harold D. Green
Keyword(s):  
Jugular Vein ◽  
Venous Blood ◽  
Jugular Bulb ◽  
Metabolic Effects ◽  
Lateral Sinus ◽  
Adrenergic Stimulation ◽  
Venous Outflow ◽  
Jugular Veins ◽  
Vascular Beds ◽  
Stimulation Of

In the intact dog, jugular vein outflow markedly decreased during adrenergic stimulation. After occlusion of both jugular bulbs and both vertebral venous sinuses with celloidin and ligation of all collateral communications along the jugular veins, in the orbit and underlying masseter muscle, lateral sinus outflow was not appreciably influenced by intra-arterial injections of 50 µg of epinephrine or arterenol, or by stimulation of the headward end of the severed vasosympathetic trunk, but intra-arterial injections of methacholine caused a weak vasodilator response. It was concluded that, in the dog, prominent communications exist between intra- and extracranial venous structures. Apparent vasoconstrictor responses are due to a reduced contribution to the jugular bulb from extracranial structures and/or to a deflection of some of the cerebral venous blood into channels other than the jugular bulb, as a result of vasoconstriction in the extracranial beds. Vasoconstrictor and cerebral metabolic effects reported in man, using the nitrous oxide technique, might be due similarly to varying contamination of the internal jugular vein blood by blood draining from adrenergically reactive facial vascular beds.

Adrenergic Stimulation of Regional Plasminogen Activator Release in Rabbits

1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin
Keyword(s):  
Lower Extremity ◽  
Plasminogen Activator ◽  
Beta Blocker ◽  
Time Course ◽  
Vascular System ◽  
Adrenergic Stimulation ◽  
Epinephrine Administration ◽  
Adrenergic Antagonist ◽  
Vascular Beds ◽  
Stimulation Of

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.

Simple Method for Entering Scalp Veins for Venous Blood Samples or Venoclysis

PEDIATRICS ◽  
1965 ◽  
Vol 36 (5) ◽  
pp. 790-791
Author(s):  
HERBERT S. KAUFMAN
Keyword(s):  
Healthy Child ◽  
Jugular Vein ◽  
Venous Blood ◽  
Jugular Veins ◽  
Simple Method ◽  
Blood Samples ◽  
Femoral Blood

The dangers of venipuncture by an experienced pediatrician are minimal. Nevertheless, some slight risk does attend femoral or jugular vein puncture; moreover, many parents recoil from witnessing femoral blood samples being taken from their healthy child. Many techniques have been described and although laboratory microprocedures may be performed by the "heel-stick" method, many tests require more blood. Anke has modified the technique of Manús and has noted a preference for the scalp veins over other peripheral vessels.Our method for obtaining blood samples requires even less material and does not involve the somewhat hazardous pressure on both jugular veins. PROCEDURE

scholarly journals The omohyoid and sternocleidomastoid muscles entrapment of the internal jugular vein: Which role in Mèniére disease patients? Treatment perspective description

2018 ◽  
Vol 7 (3) ◽  
Author(s):  
Davide Piraino ◽  
Girolamo Garofalo ◽  
Antonella Faletra ◽  
Aldo Messina
Keyword(s):  
Inner Ear ◽  
Internal Jugular Vein ◽  
Jugular Vein ◽  
Color Doppler ◽  
Venous Outflow ◽  
Meniere Disease ◽  
Jugular Veins ◽  
Physiotherapy Program ◽  
Doppler Evaluation ◽  
Menière Disease

The objectives were to analyze the Internal Jugular vein entrapment caused by muscles compression and the possible role and correlation in Mèniére disease. We describe the eco-color Doppler evaluation of a sternocleidomastoid and omohyoid muscles compression of internal jugular vein in a Mèniére patient, responsible of an anomalous venous cerebral and ear outflow. The proposed treatment was a three months muscolar decontractration physiotherapy program. The physiotherapy session allowed a complete muscles relaxation with an improvement of Internal Jugular vein caliber associated to a normalized cerebral and inner ear venous outflow and a progressive attenuation of Mèniére symptoms during the treatment and its disappearance at the end of the physiotherapy program. The comfort of the patient was confirmed during one-year follow-up. Muscles entrapment of Internal Jugular veins may be correlated with an anomalous cerebral and inner ear venous outflow, promoting the Mèniére disease symptoms. Physiotherapy treatment may represent an intriguing option alternatively of muscle surgical. The present case seems to indicate a possible first line treatment by physiotherapy, reserving surgical resection to not responders. Further studies with a wider sample of patients are warranted.

Reduction of cerebrovascular reactivity during hypercapnia

1982 ◽  
Vol 242 (5) ◽  
pp. R441-R446 ◽  
Author(s):  
A. L. Lopez de Pablo ◽  
M. C. Gonzalez ◽  
G. Dieguez ◽  
B. Gomez ◽  
S. Lluch
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Reactivity ◽  
Cerebral Vessels ◽  
Maxillary Artery ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Cervical Sympathetic ◽  
Vascular Beds ◽  
Stimulation Of

The effects on cerebral blood flow of alpha- or beta-adrenergic receptor stimulation of cerebral vessels were examined in 13 unanesthetized goats before and during hypercapnia produced by inhalation of 10% CO2 in air. This procedure increased the PCO2 from 34 to 52 and was accompanied by a fall in pH from 7.39 to 7.26. Electrical stimulation of the cervical sympathetic nerve and injections of norepinephrine and tyramine into the internal maxillary artery produced reductions in cerebral blood flow that were abolished or reduced in hypercapnia. The increase in cerebral blood flow in response to beta-adrenergic stimulation with isoproterenol was also reduced. Hypercapnia caused a similar depression of the constrictor and dilatory effects of the nonadrenergic drugs vasopressin and diazoxide. The results show a decreased response of cerebral vessels to adrenergic and nonadrenergic stimuli in hypercapnia. The findings do not suggest any difference between the refractoriness of cerebral vessels in hypercapnia and that described in other vascular beds.

Styloidogenic Jugular Venous Compression Syndrome: Diagnosis and Treatment: Case Report

Neurosurgery ◽  
2011 ◽  
Vol 70 (3) ◽  
pp. 783-783 ◽  
Author(s):  
Shervin R. Dashti ◽  
Peter Nakaji ◽  
Yin C. Hu ◽  
Don F. Frei ◽  
Adib A. Abla ◽  
...  
Keyword(s):  
Jugular Vein ◽  
Pseudotumor Cerebri ◽  
Styloid Process ◽  
Clinical Results ◽  
Venous Hypertension ◽  
Diagnosis And Treatment ◽  
Outflow Obstruction ◽  
Venous Outflow ◽  
Jugular Veins ◽  
Venous Outflow Obstruction

Abstract Background and Importance: Intracranial venous hypertension is known to be associated with venous outflow obstruction. We discuss the diagnosis and treatment of mechanical venous outflow obstruction causing pseudotumor cerebri. Clinical Presentation: We report 2 patients presenting with central venous outflow obstruction secondary to osseous compression of the internal jugular veins at the craniocervical junction. The point of jugular compression was between the lateral tubercle of C1 and a prominent, posteriorly located styloid process. In both cases, catheter venography showed high-grade jugular stenosis at the level of C1 with an associated pressure gradient. The dominant jugular vein was decompressed after the styloid process was resected. Postoperative imaging confirmed resolution of the jugular stenosis and normalization of preoperative pressure gradients. In both cases, the symptoms of intracranial hypertension resolved. Conclusion: Intracranial venous hypertension may result from extrinsic osseous compression of the jugular veins at the skull base. Although rare, this phenomenon is important to recognize because primary stenting not only is ineffective but also may actually exacerbate the outflow obstruction. The osseous impingement of the dominant jugular vein can be relieved via a decompressive styloidectomy, and the clinical results can be excellent.

Aspiration of blood from the jugular vein during intracarotid drug infusion in monkeys

1985 ◽  
Vol 62 (4) ◽  
pp. 576-579
Author(s):  
W. Craig Clark ◽  
Cheryl E. Daniels ◽  
Robert L. Dedrick ◽  
Mary E. Girton ◽  
John L. Doppman ◽  
...  
Keyword(s):  
Drug Exposure ◽  
Jugular Vein ◽  
Venous Blood ◽  
Systemic Exposure ◽  
Jugular Bulb ◽  
Constant Infusion ◽  
High Dose ◽  
Extracorporeal Circuit ◽  
Drug Infusion ◽  
Drug Removal

✓ Circulation of blood in the ipsilateral jugular vein through an extracorporeal circuit for drug removal during intracarotid chemotherapy has recently been reported to decrease the systemic drug exposure. The reduced systemic exposure achieved by the use of this technique should permit a several-fold increase of the intracarotid dose of chemotherapy without increasing systemic toxicity. To determine the influence of the rate of blood removal from the jugular vein on the fraction of the blood flowing through the ipsilateral internal carotid artery (ICA) collected for extracorporeal drug removal, the authors aspirated blood from the jugular bulb into an extracorporeal circuit at varying rates during a constant infusion of the indicator dye, indocyanine green (ICG), into the ICA of rhesus monkeys. The fraction of the ipsilateral carotid blood channeled into the extracorporeal circuit increased linearly with the rate of aspiration of jugular blood. This suggests that the absence of valves in the intracranial venous system should permit increasing fractions of drug removal during intracarotid infusion by increasing the rate of collection of venous blood from the ipsilateral jugular bulb. The measurement of ICG concentrations in a similar manner in patients undergoing isolated perfusion may prove to be a clinically useful method for estimating the maximum safe dose in high-dose intra-arterial chemotherapy.

Activation of Hageman Factor by α-Adrenergic Stimulation

1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Adrenergic Receptor ◽  
Adrenergic Stimulation ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Receptor Sites ◽  
High Doses ◽  
Stimulation Of

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.

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