Chemical Sympathectomy with 6-Hydroxydopamine

1970 ◽  
pp. 130-143 ◽  
Author(s):  
H. Thoenen ◽  
J. P. Tranzer ◽  
G. Häusler
Keyword(s):  
Chemical Sympathectomy ◽  
6 Hydroxydopamine

Differential impairment of thermogenesis in the pigeon after chemical sympathectomy

1978 ◽  
Vol 56 (4) ◽  
pp. 578-584 ◽  
Author(s):  
E. Hohtola ◽  
H. Rintamäki ◽  
R. Hissa
Keyword(s):  
Oxygen Consumption ◽  
Electrical Activity ◽  
Plasma Free Fatty Acid ◽  
Lower Body ◽  
Plasma Lactate ◽  
Chemical Sympathectomy ◽  
Ffa Metabolism ◽  
Lactate Levels ◽  
The Stability ◽  
6 Hydroxydopamine

A dose-controlled chemical sympathectomy with 6-hydroxydopamine (6-OHDA) did not disrupt thermostasis in the pigeon at +38 °C. At +6 °C, thermogenesis was impaired, but the lower body temperature and oxygen consumption were stable and vasoconstriction was normal. The stability may partly be explained by a massive release of adrenaline from the adrenals (50% in 20 min). Despite a deficit in heat production both after sympathectomy and after acute 6-OHDA, no change in muscle electrical activity was observed. Plasma free fatty acid (FFA) concentration was significantly elevated after sympathectomy, but no changes occurred in blood glucose or plasma lactate levels. The results indicate a major compensatory role for the adrenals in avian thermogenesis. They also suggest a sympathetically mediated auxiliary thermogenic mechanism independent of muscle electrical activity and coupled to FFA metabolism.

Pulmonary hypoxic vasoconstriction: not affected by chemical sympathectomy

1979 ◽  
Vol 46 (3) ◽  
pp. 529-533 ◽  
Author(s):  
C. A. Hales ◽  
D. M. Westphal
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Systemic Blood Pressure ◽  
Lung Perfusion ◽  
Chemical Sympathectomy ◽  
Test Lung ◽  
Systemic Blood ◽  
Pulmonary Vasoconstriction ◽  
Hypoxic Vasoconstriction ◽  
Alveolar Hypoxia ◽  
6 Hydroxydopamine

The influence of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) on regional alveolar hypoxic vasconstriction and on global hypoxic pulmonary vasoconstriction was investigated. In eight dogs a double-lumened endotracheal tube allowed ventilation of one lung with nitrogen as an alveolar hypoxic challenge while ventilation of the other lung with 100% O2 maintained adequate systemic oxygenation. Distribution of perfusion to the two lungs was determined with 133Xe and external counters. Mean perfusion to the test lung was 50.9 +/- 4.9% of total lung perfusion on room air and decreased by 32.4% (P smaller than 0.01) during alveolar hypoxia. Following 6-OHDA the test lung continued to reduce perfusion during alveolar hypoxia by 27.3%. In five dogs global hypoxia induced a 106% increase in pulmonary vascular resistance (PVR) prior to 6-OHDA and a 90% increase in PVR after 6-OHDA. After 6-OHDA no rise in PRV or systemic blood pressure occurred in response to tyramine, confirming effective sympathectomy by the 6-OHDA. Thus, sympathectomy with 6-OHDA failed to substantially block regional alveolar hypoxic vasoconstriction or global hypoxic pulmonary vasconstriction.

Cardiovascular responses during feeding in newborn lambs

1989 ◽  
Vol 257 (3) ◽  
pp. R568-R573
Author(s):  
B. L. Langille ◽  
S. L. Adamson ◽  
S. A. Jones
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Gastrointestinal Tract ◽  
Pressor Response ◽  
Sympathetic Innervation ◽  
Cardiovascular Responses ◽  
Bottle Feeding ◽  
Chemical Sympathectomy ◽  
Thyroid Glands ◽  
6 Hydroxydopamine

We examined the cardiovascular responses to bottle feeding in newborn lambs. Feeding induced a persistent rise in blood pressure, from 76.3 +/- 1.9 mmHg to 114 +/- 3.8 mmHg, that lasted for the duration of the feeding episode. This was accompanied by a transient tachycardia that lasted for approximately 10 s at the beginning of each feeding episode. Vasoconstriction of the hindlimb circulation, the gastrointestinal tract, kidneys, and adrenal and thyroid glands contributed to the pressor response, whereas changes in skeletal muscle resistance were not statistically significant. Of tissues assessed, only those actively involved in feeding (tongue and esophagus) vasodilated. Feeding tachycardia was greatly inhibited or abolished by the beta-blocker propranolol but the alpha-blocker phentolamine caused only moderate inhibition of the pressor response. Furthermore, chemical sympathectomy with 6-hydroxydopamine delayed the onset of the pressor response but did not abolish the ultimate rise in pressure. These findings indicate that feeding causes a significant pressor response in newborn lambs that is only partially mediated by sympathetic innervation.

EFFECT OF CHEMICAL SYMPATHECTOMY AND GANGLION BLOCKADE ON ANGIOTENSIN-STIMULATED FLUID ABSORPTION IN THE RAT JEJUNUM

1981 ◽  
Vol 91 (2) ◽  
pp. 205-211 ◽  
Author(s):  
P. G. DOREY ◽  
K. A. MUNDAY ◽  
B. J. PARSONS ◽  
JUDITH A. POAT ◽  
MARY E. UPSHER
Keyword(s):  
Fluid Transport ◽  
Extracellular Fluid ◽  
Dopamine Antagonist ◽  
Rat Jejunum ◽  
Chemical Sympathectomy ◽  
Fluid Absorption ◽  
Dopamine Infusion ◽  
6 Hydroxydopamine ◽  
Very High

A study has been made of the effects of chemical sympathectomy and ganglion blockade on the responses of rat jejunum in vivo to intravenous doses of angiotensin and noradrenaline capable of stimulating fluid transport. Pretreatment with 6-hydroxydopamine (chemical sympathectomy) or pentolinium tartrate (ganglion blockade) abolished the stimulatory actions of angiotensin II but left the responses to noradrenaline unimpaired. Dopamine, like noradrenaline, stimulated fluid transport but this response required very high dopamine infusion rates, was refractory to the dopamine antagonist sulpiride and was inhibited by the α-blocker phentolamine. The possible interaction between angiotensin and the intestinal sympathetics is discussed with reference to control of extracellular fluid volume.

Ontogeny of positive inotropic responses to sympathomimetic agents and of myocardial adrenoceptors in rats

1994 ◽  
Vol 72 (4) ◽  
pp. 361-367 ◽  
Author(s):  
Arjumand Inayatulla ◽  
Ding-You Li ◽  
Sylvain Chemtob ◽  
Daya R. Varma
Keyword(s):  
Contractile Force ◽  
Inotropic Response ◽  
Chemical Sympathectomy ◽  
Adult Rats ◽  
Maximal Increase ◽  
Inotropic Effects ◽  
Mediated Effects ◽  
Adrenoceptor Agonist ◽  
6 Hydroxydopamine ◽  
Inotropic Responses

Positive inotropic efficacies (maximal increase in contractile force) and potencies of the α-adrenoceptor agonist methoxamine and β-adrenoceptor agonist isoprenaline were determined on electrically driven (1 Hz) ventricular strips from rats aged 0.5, 1, 2, 3, 6, and 10 (adult) weeks. The inotropic response to methoxamine significantly decreased after 2 weeks of age. The inotropic potency of isoprenaline was slightly but significantly lower at all ages than at 0.5 weeks of age. Up to 2 weeks of age, the maximal inotropic effect of methoxamine was comparable with that of isoprenaline, thereafter it was but markedly less. Phenylephrine behaved like methoxamine, and noradrenaline like isoprenaline. The effect of methoxamine was antagonized by prazosin but not by propranolol; the reverse was true for isoprenaline. Injections at birth of triiodothyronine and dexamethasone exerted minimal effects on the inotropic responses to methoxamine and isoprenaline. Chemical sympathectomy with 6-hydroxydopamine caused supersensitivity to the inotropic effects of isoprenaline but produced subsensitivity to responses to methoxamine at 1 week; effects of methoxamine at 3 and 6 weeks of age were not altered by sympathectomy. No significant differences in α1 or β1-adrenoceptor densities or affinities in ventricular membranes from 7-day-old and adult rats were found. It is concluded that the positive inotropic responses to sympathomimetic amines decline with age, the decline is most marked in the case of α1-adrenoreceptor-mediated effects, and these changes do not appear to be due to a decrease in the number or affinity of α1- and β1-adrenoceptors.Key words: myocardial adrenocepters, methoxamine, isoprenaline, phenylephrine, noradrenaline, ontogeny, inotropic responses.

Plasma extravasation induced in rat trachea by 6-OHDA is mediated by sensory nerves, not by sympathetic nerves

1994 ◽  
Vol 76 (2) ◽  
pp. 701-707 ◽  
Author(s):  
I. Sulakvelidze ◽  
P. Baluk ◽  
D. M. McDonald
Keyword(s):  
Tyrosine Hydroxylase ◽  
Substance P ◽  
Knee Joint ◽  
Vascular Permeability ◽  
Sympathetic Nerves ◽  
Sensory Nerves ◽  
Plasma Extravasation ◽  
Chemical Sympathectomy ◽  
6 Hydroxydopamine ◽  
Rat Trachea

6-Hydroxydopamine (6-OHDA) stimulates the release of catecholamines from sympathetic nerves. This stimulation has been proposed as the basis of the 6-OHDA-induced increase in vascular permeability in the rat knee joint. We sought to determine whether 6-OHDA increases vascular permeability in the rat trachea through a similar mechanism. We also sought to determine whether sympathetic nerves contribute to the plasma extravasation caused by stimulating sensory nerves with capsaicin. In anesthetized rats, an intratracheal infusion of 6-OHDA caused more Monastral blue extravasation than did an infusion of vehicle (area density, 23 +/- 3% vs. 9 +/- 1%). Chemical sympathectomy, which reduced the number of tyrosine hydroxylase-immunoreactive nerves by 98%, did not reduce the amount of extravasation induced by 6-OHDA. However, pretreatment with capsaicin, which reduced the number of substance P-immunoreactive nerves by 95%, reduced the Monastral blue extravasation induced by 6-OHDA by 98%. Extravasation induced by stimulating sensory nerves with capsaicin was not significantly different in tracheae with or without sympathetic nerves. We conclude that in the rat trachea infusion of 6-OHDA causes plasma extravasation by stimulating sensory nerves, not by stimulating sympathetic nerves. Furthermore, sympathetic nerves are not essential for the plasma extravasation induced by capsaicin.

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