[Effects of the stellate ganglion block on systolic time intervals (author's transl)].
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Effects of fenoldopam, a selective DA1 dopamine receptor agonist, and dipropyl dopamine and propylphenethyl dopamine, preferential DA2 dopamine receptor agonists, on ganglion transmission were studied in pentobarbital-anesthetized, open-chest dogs. Tachycardia induced by electrical stimulation (supramaximal voltage, 0.5 ms duration, 1-2 Hz) of the preganglionic cardio-accelerator nerves was monitored as a measure of ganglionic transmission. Drugs were injected into the costocervical artery (i.a.) close to the arterial supply of the ganglion. Doses required to produce 30-40% inhibition of ganglionic transmission by the i.a. route were 2-8 micrograms for dipropyl dopamine, 4-16 micrograms for propylphenethyl dopamine, and 100 micrograms for fenoldopam. At these doses none of the agonists affected tachycardia induced by electrical stimulation of the postganglionic nerve. Domperidone (5 micrograms/kg i.v.), a selective DA2 dopamine receptor antagonist, markedly antagonized the effects of dipropyl dopamine and propylphenethyl dopamine, but had only minor (and statistically insignificant) effects on the inhibitory effect of fenoldopam. SCH 23390 (5 micrograms/kg i.v.), a selective and potent DA1 antagonist, failed to modify the effects of any of the agonists. In a separate series, infusion of fenoldopam, 20 micrograms/kg per min i.v. for 5-7 min, facilitated postganglionic nerve stimulation and blocked the inhibitory effect of UK 14,304, an alpha 2-adrenoceptor agonist, on the postganglionic nerve. These results confirm and support the presence of DA2 but do not support the presence of the prototypal DA1 dopamine receptor in the mammalian ganglia. Furthermore, the alpha 2-adrenoceptor blocking property of fenoldopam points to the complication of using i.v. administration for studying its ganglionic actions while monitoring the target tissue effects in response to preganglionic nerve stimulation.
It has been considered why it is possible to inject the local anaesthetic into a vessel even though the previous aspiration-test for blood had a negative result. To avoid an intravasal injection it is to be recommended to interrupt the injection with 15-20 further aspiration tests.
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Using a technique of retrograde axonal transport of horseradish peroxidase, labeled neurons were detected in the intermedialateral nucleus (pars principalis and pars funicularis), intercalatous spinal nucleus, and in the ventral horns of the spinal cord in cats. Afferent spinal transit pathways pass in all the above branches as well as the vertebral nerve. Bodies of the labeled neurons with branches passing in the vertebral nerve are located in the T2-T7 spinal ganglia, whereas those with branches passing in other nerves--are located in the C8-T8.
By means of injection into the microcirculatory network, section staining with hallocyanine chromic alumen, hematoxylin--eosin, silver impregnation after Bielschowsky--Gross, Baginsky, unequal intensity of microvascularization in cervical and thoracic portions have been stated, as well as different forms of interrelations between capillaries, neurocytes and gliocytes (capillaries are predominantly situated in parallel fashion to the surface of neurocytes, or else surround them). The distance between the capillary and neurocyte does not usually exceed 5--10 mkm. The contact area between neurocytes and capillaries increases with enlargement of neurocyte area. Glial and connective tissue elements are clearly differentiated after staining with acridine orange.
Effects of endothelin-3 on ganglionic transmission were investigated in dog cardiac sympathetic ganglia. Positive chronotropic responses to preganglionic stellate stimulation were inhibited by endothelin-3 (0.5-2 micrograms) given directly to the ganglia through the artery. To find possible inhibitory effects of the peptide at presynaptic sites, acetylcholine released from the isolated stellate ganglia was determined. The amount of acetylcholine released during preganglionic stimulation was reduced by exposure to endothelin-3 (10(-9) to 10(-6) M). A similar reduction of acetylcholine release was observed after application of a stable thromboxane A2, a thromboxane A2/prostaglandin H2 receptor agonist, U-46619, and prostaglandin E2 at concentrations from 10(-8) to 10(-4) M, but not by the same concentrations of prostaglandins F2 alpha and I2. The reduction elicited by endothelin-3 was unaffected by a phospholipase C inhibitor, neomycin, or a protein kinase C inhibitor, H-7, but was antagonized by pretreatment with phospholipase A2 inhibitors, dexamethasone or methylprednisolone, and by cyclooxygenase inhibitors, aspirin and indomethacin. In addition, the reduction also was antagonized by pretreatment with a thromboxane A2 synthetase inhibitor, OKY-046, and a specific thromboxane A2 receptor antagonist, S-145, but not by a specific prostaglandin E2 receptor antagonist, SC-19220. Furthermore, endothelin-3 (10(-7) M) stimulated the OKY-046- and indomethacin-sensitive formation of thromboxane A2 in the ganglia. These results indicate that endothelin-3 inhibits the sympathetic ganglionic transmission by reducing acetylcholine release at preganglionic terminals and that this inhibition seems to involve activation of endogenous thromboxane A2 production.
1. Depolarization of the giant axon terminal of the squid causes local calcium influx which gives rise to transmitter release and post-synaptic response, and which under certain experimental conditions leads to a regenerative action potential in the presynaptic terminal itself.2. There has been conflicting evidence in the literature on the question whether the calcium permeability change in the terminal is rapidly inactivated, or whether it can persist with little diminution for hundreds of milliseconds during a depolarizing voltage step.3. Results are presented which show that there is little ;calcium inactivation', even when very large depolarizing steps are imposed on the terminal and maintained for periods of 1-2 sec.4. Contrary indications are examined and found to be attributable to an increase of potassium conductance, rather than direct inactivation of calcium conductance.
Sympathetic cholinergic postganglionic neurons are present in many sympathetic ganglia. Three classes of sympathetic cholinergic neuron have been reported in mammals; sudomotor neurons, vasodilator neurons and neurons innervating the periosteum. We have examined thoracic sympathetic ganglia in rats to determine if any other classes of cholinergic neurons exist. We could identify cholinergic sudomotor neurons and neurons innervating the rib periosteum, but confirmed that cholinergic sympathetic vasodilator neurons are absent in this species. Sudomotor neurons contained vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) and always lacked calbindin. Cholinergic neurons innervating the periosteum contained VIP and sometimes calbindin, but always lacked CGRP. Cholinergic neurons innervating the periosteum were usually surrounded by terminals immunoreactive for CGRP. We conclude that if any undiscovered populations of cholinergic neurons exist in the rat thoracic sympathetic chain, then they are indistinguishable in size, neurochemistry and inputs from sudomotor or cholinergic neurons innervating the periosteum. It may be that the latter two populations account for all cholinergic neurons in the rat thoracic sympathetic chain ganglia.
PURPOSE: To assess the hemodynamic changes in the upper extremity arteries after sympathetic ganglion blockade (SGB) by using spectral Doppler parameters and to determine the applicability of these parameters for the evaluation of SGB efficacy. MATERIAL AND METHODS: Spectral Doppler parameters (peak systolic velocity (PSV), end diastolic velocity (EDV), mean velocity (mean V), flow volume, resistive and pulsatility indices (RI, PI), inner arterial diameters (intima to intima) (D) with simultaneous recordings of heart rate (HR), systolic and diastolic blood pressures and upper extremity surface temperature changes) were recorded before and 5 min after during the first, fifth and tenth SGB procedures. RESULTS: SGB induced an increase in skin temperature in the ipsilateral hand and persistent dilatation of the radial diameter accompanied by reduction of RI and PI in the radial and third digital arteries in all patients. CONCLUSION: Hemodynamic changes assessed by spectral Doppler parameters could be used as sensitive and objective measurements of peripheral sympathetic nervous activity and vascular tonus, and may confirm a successfully performed SGB.
Arterial and/or central venous plasma concentrations of lidocaine were determined in 12 nonmedicated adult horses (422 +/- 59 kg of body weight, mean +/- SD) after injecting a 1% lidocaine HCl solution into the cervicothoracic ganglion (CTG). A mean dosage of 2.9 +/- 0.5 mg of lidocaine/kg of body weight was used to induce unilateral CTG blockade in 8 horses and 4.8 +/- 0.8 mg was used to induce bilateral CTG blockade in 4 horses. Blood samples were collected before and at 5, 15, 30, 45, 60, 75, 90, 105, and 120 minutes after injection. The plasma lidocaine concentrations were determined by use of gas chromatography (sensitivity less than 0.01 microgram/ml). Cervicothoracic sympathetic blockade was characterized by Horner's syndrome and by profuse sweating over the face, neck, and thoracic limbs. Mean maximal venous concentrations of lidocaine were 0.86 +/- 0.33 microgram/ml at 26.3 +/- 6.9 minutes after unilateral CTG blockade, and 1.14 +/- 0.25 micrograms/ml at 31.2 +/- 18.9 minutes after bilateral CTG blockade. The mean venous and arterial concentrations of lidocaine were not significantly different at 45 and 120 minutes after injection. Venous concentrations of lidocaine were consistently higher than were concentrations in simultaneously collected arterial blood samples in 2 horses in which the right CTG and brachial plexus were temporarily anesthetized after repeated administration of 100 ml of lidocaine into the right CTG.(ABSTRACT TRUNCATED AT 250 WORDS)