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PubMedDate not supplied

Contralateral spread of local anesthetic with stellate ganglion block.

BACKGROUND AND OBJECTIVES. Stellate ganglion block is a technically simple procedure but is liable to many complications because of the adjacent structures. We report a contralateral and bilateral Horner's syndrome with stellate ganglion block in the same patient on different occasions. We also report a bilateral recurrent laryngeal nerve block with this procedure.

Adult↗
PubMed1995

Computerized axial tomography to define the distribution of solution after stellate ganglion nerve block.

STUDY OBJECTIVE: To define the spread of local anesthetic after C6 stellate ganglion nerve block using computerized axial tomography (CAT). DESIGN: Prospective, open descriptive study. SETTING: Outpatient pain consult center. PATIENTS: 10 ASA status I patients undergoing stellate ganglion nerve blocks for sympathetically maintained pain. INTERVENTIONS: Radiocontrast and local anesthetic was given in 5 ml increments to 20 ml total volume for C6 stellate ganglion nerve blocks in eight patients and C7 in two patients. MEASUREMENTS AND MAIN RESULTS: CAT scanning was performed at baseline and after 5, 10, 15, and 20 ml of injectate was administered. Cervical level and pattern of injectate spread was recorded after each increment. Neck pressure above C6 did not promote caudal spread. One half of the injections were beneath prevertebral fascia. Injections on top of the fascia spread more diffusely around C6. All injections in high volume reached the medial aspect of T1 around the head, not neck, of the first rib. CONCLUSIONS: Solutions injected for C6 stellate ganglion nerve block concentrate medial to the stellate ganglion at T1. Thus, they must produce upper extremity sympathectomy by a mechanism other than contact with the ganglion.

Adult↗
PubMed2002

Novel mechanism of action hypothesized for stellate ganglion block related to melatonin.

The mechanism of action of stellate ganglion block has generally been explained by vasodilation within its sphere of innervation. However, the success of treatment cannot always be explained by just one mechanism of action, because its clinical indications in Japan extend to many diseases, including systemic diseases. We propose a new mechanism of action for stellate ganglion block that is based on correction of melatonin rhythm disorder resulting from increased sympathetic nerve tone and does not involve vasodilation.

Animals↗
PubMed1995

Muscarinic and ganglionic blocking properties of atropine compounds in vivo and in vitro: time dependence and heart rate effects.

High doses (3 mg/kg) of methylatropine nitrate have been used in vivo to produce long-lasting muscarinic blockade during physiologic experiments. At these levels, the possibility exists that ganglionic blockade may also be responsible for some heart rate effects. Therefore, the effects of methylatropine nitrate (0.0012-2.4 mg.kg(-1)) and atropine sulfate (0.0036 - 0.060 mg.kg(1)) were evaluated in vivo using conscious dogs and in vitro using canine right atria and isolated stellate ganglia. The lowest doses of either agent given in vivo caused bradycardia, while intermediate doses induced excess tachycardia. High doses of methylatropine nitrate transiently decreased the heart rate, followed by slow recovery. In vitro using the canine right atria, neither drug caused pacemaker shifts nor directly altered the atrial rate, but postvagal tachycardia occurred with acetylcholine challenge and was prevented by metoprolol or 6-hydroxydopamine. In vitro studies using the canine stellate ganglia indicate that both agents depressed postganglionic compound action potentials at high doses. In conclusion, with high-dose methylatropine nitrate, ganglionic blockade yields the mechanism for a reduction of excess tachycardia as well as a likely explanation for opposing chronotropic effects in conscious and anesthetized dogs. In experimental studies where high doses of atropine compounds are used for long-term muscarinic blockade, it is possible that ganglionic blocking effects may also be produced.

Action Potentials↗
PubMed2004

Pathophysiological plasma ET-1 levels antagonize beta-adrenergic dilation of coronary resistance vessels in conscious dogs.

On the basis of in vitro experiments showing that endothelin (ET)-1 interferes with smooth muscle ATP-sensitive K(+) (K(ATP)) channel opening, which is pivotal in beta-adrenergic coronary dilation, we hypothesized that pathophysiological plasma ET-1 levels impair beta-adrenergic dilation of resistance coronary vessels. In conscious instrumented dogs, graded intravenous doses of dobutamine caused the expected inotropic responses. As myocardial O(2) consumption (MVo(2)) increased, the disproportionate rise in coronary sinus (CS) Po(2) indicates that increases in coronary blood flow (CBF) exceeded metabolic requirements, consistent with beta-adrenergic dilation. ET-1 intravenous infusions, to reach pathophysiological plasma levels, reduced slopes of the Po(2)-MVo(2) and CBF-MVo(2) relations. In contrast, the first derivative of left ventricular pressure over time responses to dobutamine were not impaired during ET-1 delivery. Clazosentan, an ET(A) receptor blocker, prevented reduction of the slope of Po(2)-MVo(2) and CBF-MVo(2) relations. After ganglionic blockade to exclude reflex influences, ET-1 still reduced slopes of Po(2)-MVo(2) and CBF-MVo(2) relations. To assess effects of ET-1 on endothelium-dependent and -independent coronary vascular responses, intracoronary ACh and nitroglycerin were given to directly target coronary vessels. CBF responses to ACh and nitroglycerin were maintained during ET-1 delivery. In contrast, responses to intracoronary K(ATP) channel-dependent dilators adenosine and lemakalim were impaired by ET-1. In conclusion, pathophysiological levels of ET-1 impaired beta-adrenergic dilation of resistance coronary vessels through an ET(A) receptor-dependent process. In contrast, left ventricular inotropic responses to dobutamine were not impaired during ET-1 delivery. Our data suggest that ET-1 may interfere with smooth muscle K(ATP) channels to impair beta-adrenergic coronary dilation.

Adenosine↗