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At least 919 records · Page 51Linked to original sources
PubMed1976

Coronary vascular sympathetic beta-receptor innervation.

Recent studies indicate that coronary vessels have alpha- and beta-2-adrenergic receptors and that the alpha receptors are functionally innervated. We studied whether the beta-2-vasodilator receptors are functionally innervated, using a dog in situ modified Langendorff preparation with constant coronary perfusion pressure. The beating, nonworking heart and systemic circulation were supported with a pump oxygenator. Stimulation of the left stellate ganglion increased coronary blood flow and decreased coronary sinus oxygen tension from prestimulation control values. After beta-1-receptor blockade (practolol, 10 mg/kg), stellate stimulation decreased coronary blood flow and decreased coronary sinus oxygen tension from prestimulation control values, revealing alpha-receptor vasoconstriction. After the addition of alpha-receptor blockade (Dibozane, 5 mg/kg), stellate stimulation increased coronary blood flow and coronary sinus oxygen tension a small amount from prestimulation values. Finally, after the addition of beta-2-receptor blockade (propranolol, 2 mg/kg), stellate stimulation increased flow and coronary sinus oxygen tension slightly from prestimulation control values. Direct intracoronary injections of isoproterenol, norepinephrine, and epinephrine gave results consistent with the presence of beta-1 myocardial receptors and alpha and beta-2 coronary receptors. We conclude that there is little functional innervation of coronary vascular beta-2 receptors. Intracoronary injections of isoproterenol and epinephrine activated beta-2-receptor coronary vasodilation after beta-1-receptor blockade, but norepinephrine did not.

Adrenergic alpha-Antagonists↗
PubMed1978

Studies on the mechanism of the vasodilator effects of prazosin in dogs and rabbits.

In pentobarbital (35.0 mg/kg) anaesthetised dogs, bolus injections of prazosin into the femoral artery (3.0--300.0 microgram) provoked a dose-related fall in the vascular resistance of the innervated hind limb. In contrast to papaverine, prazosin failed to produce the same effect in dogs under spinal anaesthesia even when the intrinsic femoral vascular tone was increased with vasopressin. However, vasodilator effects of prazosin were again observed when the tone of the limb was elevated by either stimulating the sympathetic lumbar chain or by infusing alpha-adrenoceptor agonists. A significant reduction of both aortic blood pressure and pressor response to bilateral carotid artery occlusion was noted in a group of normotensive dogs anaesthetised 12 h after the last dose of prazosin given twice daily at 0.5 mg/kg, p.o., for 3 day period. This short-term treatment modified neither the resting heart rate nor the positive chronotropic effect induced by either intravenous noradrenaline or electrical stimulation of pre- and post-ganglionic nerve fibres of the right stellate ganglion. However, it prevented the larger increase in heart rate in response to bilateral carotid occlusion in placebo-treated dogs after section of the vagi. A decrease in baseline sympathetic tone of the perfused hind limb as well as vasoconstrictor effects produced by i.a. injections of several alpha-adrenoceptor agonists and electrical stimulation of the lumbar sympathetic chain was observed in prazosin-treated animals. The dose--pressor response profiles to these alpha-adrenoceptor stimulants after prazosin were not parallel to those obtained in the control group. The vasoconstrictor response to angiotensin II was not changed by prazosin. In rabbit aortic strips, prazosin (0.1--3.0 micrometer) produced competitive antagonism of the contractile responses induced by cirazoline, noradrenaline and phenylephrine. In contrast to papaverine, prazosin in concentrations up to 100.0 micrometer neither relaxed the aortic strips contracted by potassium ions nor modified the concentration-response curve to calcium ions. These studies indicate that blood pressure lowering effects of prazosin given acutely or for three days can be accounted for by a clear-cut functional impairment of vascular postsynaptic alpha-adrenoceptors. No evidence for a direct myorelaxant property of prazosin could be obtained in these studies.

Adrenergic alpha-Agonists↗
PubMed1999

Effects of sympathetic nerve blockades on low-frequency oscillations of human earlobe skin blood flow.

Earlobe skin blood flow measured by laser Doppler flowmetry often shows low-frequency oscillations with a frequency around 0.1 Hz. We evaluated the effects of different sympathetic blocking techniques on the oscillations. Power spectrum of 5-min time series of beat-to-beat peak earlobe skin blood flow showed a distinct spectral peak at a frequency around 0.1 Hz (mean +/- SD, 0.107+/-0.016 Hz). The power of the spectral peak measured as coefficient of component variance (CCV) was diminished with total spinal anesthesia (TSA, n = 4) and cervicothoracic epidural anesthesia (CTEA, n = 4; P<0.05 for both). The CCV was unchanged significantly with bilateral thoracic sympathetic ganglionic excision (TSGE, n = 5). Right stellate ganglion block (RSGB, n = 6) caused a trend towards an increase in the CCV on the right (blocked)-side (P = 0.072) but no change on the left (intact)-side. Cross-spectrum analysis revealed that the low-frequency oscillations were not coherent between the right- and left-side earlobes or with low-frequency oscillations in systolic blood pressure either before or after RSGB. TSA and CTEA are known to cause extensive sympathetic nerve blockade in a broad area, while TSGE and RSGB are known to cause local and partial sympathetic blockade. Our results suggest that although the low-frequency oscillations in earlobe skin blood flow may be mediated non-neurally, magnitude of the oscillations may be modified by sympathetic vasomotor tone.

Adult↗
PubMed1978

Unilateral stellate block in the treatment of hypertension after coronary bypass surgery. Implications of a new therapeutic approach.

Unilateral stellate ganglion block (right or left) was achieved by local injection of 15 ml of lidocaine in 27 patients with hypertension after coronary bypass surgery. The stellate block led to rapid and sustained control of blood pressure in 18 patients (9 of 15 with right stellate block and 9 of 12 with left stellate block). The reduction in arterial pressure was associated with significant (P less than 0.01) reductions in total peripheral resistance and heart rate but no significant changes in cardiac output or central venous or left atrial pressures. This hemodynamic pattern as well as effectiveness of a unilateral approach suggests that the stellate block reduced arterial pressure by interrupting the afferent limb of a pressor reflex from the heart or great vessels, or both. The procedure was free from side effects and helped avoid prolonged parenteral administration of potent antihypertensive drugs.

Adult↗
PubMed2004

Age-related differences in the response of blood stroke volume to stimulation of the sympathetic ganglion in rats with beta-adrenoceptor blockade.

Blood stroke volume in rats aging 21 and 56 days decreased during beta-adrenoceptor blockade with propranolol, but increased again by the 15th minute after treatment. Suprathreshold stimulation of the stellate ganglion decreased the stroke volume and increased the heart rate in control animals. Electrical stimulation after beta-adrenoceptor blockade was followed by a further decrease in stroke volume in young rats. In 100-day-old animals this parameter remained unchanged, while the cardiac output improved.

Adrenergic beta-Antagonists↗
PubMed1995

Mechanisms of physiological gustatory sweating and flushing in the face.

Mechanisms of physiological gustatory sweating and flushing were investigated in 21 patients with a facial nerve lesion compromising parasympathetic outflow to the lacrimal gland, and in 13 patients undergoing diagnostic blockade of the stellate ganglion. Vascular responses and electrodermal activity (which reflects sweating) were monitored on each side of the forehead before and during gustatory stimulation with chillies or Tabasco sauce (derived from chillies). Vascular responses in the cheeks were also monitored in 14 patients with a facial nerve lesion. Sympathetic blockade increased gustatory vasodilatation but prevented gustatory sweating on the blocked side of the forehead. A facial nerve lesion did not affect gustatory sweating in the forehead or vasodilatation in the cheeks. However, a facial nerve lesion impaired vasodilatation in the forehead in all six patients who ate chillies, and also in four of five patients whose blood vessels dilated extensively on the normally-innervated side of the forehead when the patients tasted Tabasco sauce. These findings suggest that sympathetic sudomotor activity mediates physiological gustatory sweating in the forehead, whereas sympathetic vasoconstrictor tone inhibits gustatory vasodilatation in the forehead. A parasympathetic vasodilator reflex in the facial nerve contributes actively to gustatory flushing in the forehead, but some other unidentified mechanism influences vascular responses in the cheeks.

Adrenergic Fibers↗
PubMed1987

Coronary artery vasodilation in the canine: physiological and pharmacological roles of beta-adrenergic receptors.

The role of beta 1- and beta 2-receptors as modulators of coronary artery vasodilation was studied in the anesthetized dog. The left circumflex coronary artery was cannulated and perfused under constant pressure with blood drawn from the right femoral artery. Coronary blood flow myocardial contractile force were measured with a cannulating electromagnetic flow probe and Walton-Brodie strain gauges, respectively. The left stellate ganglion was isolated distally, and the postganglionic nerves were stimulated with a bipolar electrode. Coronary artery blood flow and regional myocardial contractile force increased in response to stellate nerve stimulation and to the intracoronary administration of norepinephrine (NE), isoproterenol (ISO), and zinterol (ZIN) before selective beta 1-adrenergic receptor blockade with celiprolol (0.3 mg/kg intravenously, i.v.). The administration of celiprolol inhibited the positive inotropic response to both stellate stimulation and to the intracoronary administration of the selected beta-adrenergic receptor agonists. The increase in coronary artery blood flow observed in response to stellate stimulation or to the intracoronary administration of NE was converted to a decrease in flow in the presence of celiprolol. In contrast, however, the intracoronary administration of ISO or ZIN continued to cause coronary vasodilation despite the presence of beta 1-selective adrenergic receptor blockade with celiprolol. Addition of propranolol (1.0 mg/kg i.v.) in the presence of celiprolol completely inhibited the increase in coronary blood flow in response to ISO and ZIN.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1992

[A study of cerebral circulation following cervical sympathetic ganglion block].

Cerebral circulation following cervical epidural block or stellate ganglion block at the transverse process of the 6th cervical vertebra (C6-SGB) was evaluated by single photon emission computed tomography of inhaled Xenon-133. Cerebral blood flow before and 15 min after both blocks was measured in eight patients after cervical epidural block and ten patients after C6-SGB. Cerebral blood flow decreased slightly following cervical epidural block, but it was not a statistically significant difference. Cerebral blood flow following C6-SGB could be separated into two groups; in one it increased and in the other it decreased slightly. In conclusion, cerebral circulation is not influenced by cervical epidural block, but it is probably affected by C6-SGB. The manner in which C6-SGB increases cerebral blood flow seems that local anesthetics reached the superior cervical ganglion and block it. C6-SGB without superior cervical ganglion block does not influence cerebral circulation, and it only dilates extracranial vessels.

Adult↗
PubMed1994

Autologous transplantation of the cervical sympathetic ganglion into the parkinsonian brain: case report.

The authors have reported a clinical trial of an autologous cervical sympathetic ganglion transplanted into the brain of a parkinsonian patient. A 45-year-old woman presented with bradykinesia and a gait disturbance for 8 years under L-dopa treatment. The patient underwent stereotactic transplantation of the right stellate ganglion into the right putamen. She showed marked amelioration of bradykinesia and gait disturbance 1 month after the operation, and she was able to conduct her activities of daily living without requiring L-dopa administration. The patient continued to improve gradually until 3 months after the operation. Two years after surgery, the patient functions independently as a housewife. The right hand tremor, however, became slightly worse after the operation, but it was transient. The patient developed a permanent right-sided Horner's syndrome after resection of the cervical sympathetic ganglion. Taken together with our previous data obtained from animal experiments, this case suggests that the autologous cervical sympathetic ganglion can be donor tissue for neural transplantation in Parkinson's disease.

Activities of Daily Living↗
PubMed1994

The cervical sympathetic trunk--a new hypothesis.

There is a sympathetic ganglion, in relation to most if not all thoracic and lumbar segments whereas there are only 3 or 4 sympathetic ganglia in the cervical region. Thus it may be inferred that sympathetic ganglia are not directly related to spinal nerves. Therefore, the hypothesis is put forward that sympathetic ganglia are associated chiefly with intersegmental vessels such as the intercostal and lumbar arteries and that the differences seen in the neck region are due to the disappearance of most of the cervical intersegmental arteries and the subsequent modifications that follow during development. This results in the fusion of the upper 4 cervical ganglia to form the superior cervical sympathetic ganglion in relation to the developing external carotid artery which seems to provide the necessary inductive stimulus. Furthermore, the antero-inferior migration of the heart, its corresponding arch arteries and the dorsal aorta bring about the formation of the ansa subclavia around the subclavian artery and the positioning of the stellate ganglion behind the vertebral artery.

Aorta↗
PubMed2000

Skeletal muscle vasodilatation during sympathoexcitation is not neurally mediated in humans.

Evidence for the existence of sympathetic vasodilator nerves in human skeletal muscle is controversial. Manoeuvres such as contralateral ischaemic handgripping to fatigue that cause vasoconstriction in the resting forearm evoke vasodilatation after local alpha-adrenergic receptor blockade, raising the possibility that both constrictor and dilator fibres are present. The purpose of this study was to determine whether this dilatation is neurally mediated. Ten subjects (3 women, 7 men) performed ischaemic handgripping to fatigue before and after acute local anaesthetic block of the sympathetic nerves (stellate ganglion) innervating the contralateral (resting) upper extremity. Forearm blood flow was measured with venous occlusion plethysmography in the resting forearm. In control studies there was forearm vasoconstriction during contralateral handgripping to fatigue. During contralateral handgripping after stellate block, blood flow in the resting forearm increased from 6.1 +/- 0.7 to 18.7 +/- 2.2 ml dl-1 min-1 (P < 0.05). Mean arterial pressure measured concurrently increased from approximately 90 to 130 mmHg and estimated vascular conductance rose from 6.5 +/- 0.7 to 14.0 +/- 1.5 units, indicating that most of the rise in forearm blood flow was due to vasodilatation. Brachial artery administration of beta-blockers (propranolol) and the nitric oxide (NO) synthase inhibitor N G-monomethyl-L-arginine (L-NMMA) after stellate block virtually eliminated all of the vasodilatation to contralateral handgrip. Since vasodilatation was seen after stellate block, our data suggest that sympathetic dilator nerves are not responsible for limb vasodilatation seen during sympathoexcitation evoked by contralateral ischaemic handgripping to fatigue. The results obtained with propranolol and L-NMMA suggest that beta-adrenergic mechanisms and local NO release contribute to the dilatation.

Adolescent↗
PubMed1991

Prolonged stellate block in treatment of reflex sympathetic dystrophy.

Prolonged continuous stellate ganglion blockade has been found useful in treatment of post-traumatic reflex sympathetic dystrophy under the following circumstances: 1) When conservative treatment with outpatient physical therapy, tranquilizers and mild analgesics has failed. 2) When conservative therapy plus intermittent stellate blocks (q.l to 4 weeks) has failed. A three-year average follow-up of a group of 26 unselected patients has shown 25% relapse rate and 75% marked to complete improvement.

Autonomic Nerve Block↗
PubMed1988

Differential response to right and left ansae subclaviae stimulation of early afterdepolarizations and ventricular tachycardia induced by cesium in dogs.

Early afterdepolarizations (EADs) are depolarizing potentials that occur before complete repolarization. They may be important in the acquired and possibly the idiopathic long QT syndrome and associated ventricular tachycardia (VT). The purpose of these experiments was to study in 20 open-chest dogs the effects of sympathetic stimulation on EADs and VT produced with cesium chloride (84 mg/kg i.v.) alone or combined with left (LAS), right (RAS), or bilateral (BAS) ansae subclaviae stimulation (2 Hz, 4 msec, 2 mA). We compared the EAD amplitude and area as a percentage of monophasic action potential amplitude and area, respectively, recorded simultaneously with contact electrodes from right (RV) and left ventricular (LV) endocardium and recorded the prevalence of VT induction during each intervention. Both LAS and BAS produced left ventricular EADs with larger amplitudes and areas than did RAS or cesium alone. BAS and LAS produced larger EADs recorded from the LV than from the RV. Cesium produced VT in six of 20 dogs, RAS in three of 20, BAS in 12 of 20, and LAS in 16 of 20. Norepinephrine (0.1-1.5 micrograms/kg/min) caused VT in all dogs by producing a dose-related increase in EAD amplitude that was similar in RV and LV, suggesting that the response of RV and LV EADs to catecholamine stimulation was not intrinsically different. During stimulation of left ansae subclaviae at increasing frequencies (1, 2, 4, and 6 Hz), EADs were significantly larger in LV than in RV at all stimulus frequencies, and the amplitude of EADs in both ventricles increased with increasing stimulus frequencies. Based on the increased LV amplitude and area of cesium chloride-induced EADs during LAS and BAS, with EAD amplitude dependent on the frequency of LAS but with an equal RV and LV EAD amplitude during norepinephrine infusion, it is possible that more norepinephrine released into the LV during LAS and BAS compared with RAS causes larger amplitude LV EADs that reach threshold to cause VT more often. Thus, quantitative differences between the effects of left and right stellate ganglia stimulation rather than qualitative differences or imbalance may account for the arrhythmogenic potential of the left stellate ganglion.

Action Potentials↗
PubMed1977

[Study of the destruction of the sympathetic ganglia by the administration of guanethidine to newborn rats and mice].

Following the injection of guanethidine (25 mg/kg) to rats from the first day of life during 2 weeks, over 70% of sympathic neurons in the stellate ganglion die. If the injections are carried out during 4 weeks, over 99% of neurons die. The injection of guanethidine to mice during 5 weeks did not result in the destruction of nerve elements in the ganglion, as compared with the control.

Animals↗
PubMed1992

[Gustatory sweating demonstrated by infrared thermography].

A 35-year-old man, previously healthy except for a grade 1 goitre, sustained a spontaneous left pneumothorax treated with a Bülau drain. When the left pneumothorax recurred 2 months later a left thoracotomy was performed. Two bullae at the lung apex were resected and a pleurodesis performed. After the operation the patient noted hypaesthesia of the dorsum of the left upper arm, mild ptosis of the left eyelid as well as reduced sweat secretion over the left half of the face and the left rib cage. The hypaesthesia improved, but the sympathetic nerve deficits remained. There were no other neurological signs. 9 months later, within one minute of eating a sour apple, the patient developed severe sweating over the left half of the face and the left chest. The reaction was confirmed by infra-red thermography which proved that the skin temperature in the sweating region had fallen to 3 degrees C. The likely cause of localized gustatory sweating is intra-operative damage of the stellate ganglion or its preganglionic nerve connections. Treatment is limited to avoidance of the precipitating gustatory stimulus.

Adult↗
PubMedDate not supplied

The effect of unilateral stellectomy on the regulation of heart rate during behavioral stress.

Changes in heart rate were examined during classical aversive conditioning before and after either left (n = 10) or right stellectomy (n = 8). Heart rate (HR) significantly (p less than 0.01) increased in response to the conditional stimulus with a further increase noted during the unconditional stimulus. After right stellectomy (RSGx) the aversive stress elicited a significantly (p less than 0.01) smaller increase in heart rate (peak HR change: control 66.8 +/- 6.0; RSGx 36.1 +/- 6.8 beats/min). In contrast left stellectomy did not significantly alter the heart rate conditional response. Cardioselective beta-adrenergic receptor blockade, metoprolol HC1 (BB, 1.0 mg/kg, n = 8), significantly (p less than 0.01) reduced the heart-rate conditional response (peak HR change: control 66.8 +/- 6; BB 25.1 +/- 3.8 beats/min) to the same extent as noted during RSGx. These data suggest that the heart-rate increases elicited by aversive stress are mediated in part by sympathetic nerves that originate or pass through the right stellate ganglion. The residual HR increase noted after RSGx or BB probably results from the withdrawal of cardiac parasympathetic activity.

Animals↗
PubMed1993

Reflex sympathetic dystrophy syndrome: two case studies.

Reflex sympathetic dystrophy syndrome (RSDS) is a multisymptom, disabling disease that can involve peripheral nerve, muscle, bone, blood vessel and skin changes. Pain is the only common denominator among all patients. Two cases presented in this article describe patients with RSDS and demonstrate differences in symptoms and patient response. One treatment modality for RSDS is the stellate ganglion block, performed in the PACU by the anesthesiologist. Important postanesthesia nursing assessment parameters after this procedure are discussed.

Adult↗