Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The roles played by the cerebral monoamines (dopamine, noradrenaline and serotonin) in stimulation-produced analgesia (SPA) have been investigated in the rat employing the tail flick test. SPA was elicited through bipolar electrodes chronically implanted in the mesencephalic periaqeductal gray matter, an area previously shown to yield potent and reliable analgesic effects. Four approaches were used to alter transmission in monoamine pathways. (1) Depletion of monoamines by administration of tetrabenazine (TBZ), p-chlorophenylalanine (PCPA), alpha-methyl-para-tyrosine (AMPT), or disulfiram. (2) Replacement of depleted monoamine stores by appropiate precursors (5-HTP or L-DOPA) in combination with a peripheral decarboxylase inhibitor. (3) Potentiation of monoamine systems by administration of precursors to previously untreated animals or by administration of a dopamine receptor stimulator, apomorphine. (4) Blockade of catecholamine receptors by haloperidol or of dopamine receptors by pimozide. These four approaches yielded internally consistent results. Depletion of all 3 monoamines (TBZ) led to a powerful inhibition of SPA. Original levels of SPA were restored by injection of either 5-HTP or L-DOPA. Specific depletion of serotonin (PCPA) caused a reduction in SPA, whereas elevation of serotonin levels (5-HTP) caused an increase in SPA. Dopamine receptor blockade (pimozide) decreased SPA, whereas the precursor (L-DOPA) and a dopamine receptor stimulator (apomorphine) increased SPA. On the other hand, selective depletion of noradrenaline (disulfiram) caused an increase in SPA; and at a time when noradrenaline levels are depressed and dopamine levels are elevated (AMPT + L-DOPA), SPA was seen to be particularly enhanced. thus, dopamine and serotonin appear to facilitate SPA, whereas noradrenaline appears to inhibit it. When a general catecholamine receptor blocker (haloperidol) was employed, SPA was diminished, suggesting that the influence of dopamine in SPA is greater than that of noradrenaline. Most of the drugs used in this study significantly altered SPA at doses which left baseline tail flick latency unaffected. It would appear, therefore, that SPA has a neural substrate at least partly independent of that underlying baseline pain responsiveness. Consideration is given to various ascending and descending monoamine system as possible component paths in this neural substrate of SPA. Finally, the present results are discussed in relation to studies by others on the site and mechanism of morphine's analgesic action. Some striking parallels between SPA and morphine analgesia are noted. These suggest the existence of a common pain-inhibitory system in the brain activated by morphine and by focal electrical stimulation.
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PMID:Monoaminergic mechanisms of stimulation-produced analgesia. 12 41

The haemodynamic effects of dobutamine (2 microgram/kg . min and 4 microgram/kg . min) and dopamine (4 microgram/kg . min and 8 microgram/kg . min) were studied in 17 patients with coronary artery disease prior to coronary bypass surgery. The study was performed under general anaesthesia (modified neurolept analgesia) and controlled ventilation. Dopamine improved cardiac index significantly, increased mean aortic pressure slightly while heart rate and total peripheral resistance remained unchanged. Dobutamine failed to increase cardiac and stroke index significantly, but increased mean aortic pressure distinctly due to an elevated total peripheral resistance. Both catecholamines increased left ventricular filling and mean pulmonary artery pressure. The HR x ASP-product which is closely related to left ventricular oxygen consumption was found to be augmented to a greater extent during dobutamine. For the above reasons dopamine should be favoured for increasing cardiac output in patients undergoing aortocoronary bypass surgery. Our study does not confirm earlier results which have shown dobutamine to be the preferable catecholamine. The possible reasons for this discrepancy are discussed.
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PMID:[The haemodynamic effects of dobutamine and dopamine in patients with coronary artery disease. A study performed under general anaesthesia (author's transl)]. 31 60

This review summarized some articles on the effect of the septal area in acupuncture analgesia. The data showed that the pain threshold of animal was increased when septal area was stimulated by electro-acupuncture, and that electrical stimulation of septal area had a marked inhibitory effect on the pain discharges of cells in parafascicular nucleus of thalamus, lateral habenular nucleus, periaqueductal gray and dorsal raphe nucleus. The septal area play an important role in acupuncture analgesia. The majority of the cholinergic neurons in septal area are located in nucleus of the vertical limb of the diagonal band (VDB); gamma-aminobutyric acid of septal area is mainly found in the diagonal band nucleus(td); Dopamine is present in high levels in td and lateral septal nucleus(S1) of septal area; The S1 contain high densities enkephalin-containing neuronal cell bodies and terminals; In addition, substance P and norepinephrine are also high levels in the septal area. These substance above-mentioned have a relations with acupuncture analgesia of septal area. A large number of serotonin-containing neurons are found in the raphe nuclei. The serotonin play an important role in acupuncture analgesia. The serotonin-containing neurons in dorsal raphe nucleus project to S1. The fiber connections of the raphe nuclei with the td are reciprocation. The periaqueductal gray is a important structure on pain modulation. It projects to septal area and receives the fibers from S1. A number of adrenergic neurons are located within the locus coeruleus. The locus coeruleus participate pain modulation and acupuncture analgesia. The neuro-anatomy study demonstrated that locus coeruleus projects to septal area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of the septal area in acupuncture analgesia]. 169 24

Fischer-344 rat pups were injected with either 10 mg/kg delta 9-tetrahydrocannabinol (THC) or vehicle on postnatal days 4,6 and 8. Pups were then allowed to mature. On day 129 of age rats were exposed to a stress paradigm which consisted of inescapable electric foot-shock administered at 1 mA for 15 sec daily for 8 days. Analgesia induced by foot-shock was measured by tail withdrawal from 55 degree C water. On the 9th day rats were exposed to the shock environment only. Fifteen minutes following measurement of tail withdrawal, animals were sacrificed. Plasma corticosterone and prolactin were measured. Levels of norepinephrine, dopamine and 5-hydroxytryptamine and metabolites were determined in frontal cortex, hippocampus and hypothalamus. Neonatal exposure to THC produced an increase in baseline tail withdrawal latency. No effect of THC exposure was seen on acute stress-induced analgesia. Rats exposed to THC required a greater number of conditioning trials to develop conditioned analgesia than animals treated neonatally with vehicle. The conditioned stress increased plasma corticosterone without affecting prolactin. Stress increased hypothalamic 5HT and 5HIAA while decreasing 5HT turnover in this area. Dopamine and DOPAC levels in the hypothalamus and frontal cortex were increased by stress; dopamine turnover in the frontal cortex was elevated by stress. Neonatal THC and stress elevated norepinephrine above control levels in the hypothalamus, while increasing 5HT in the hippocampus and frontal cortex. The stress-induced increase in DOPAC in the frontal cortex was decreased by THC exposure. These data suggest that long-term neurochemical changes may occur with neonatal administration of THC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neonatal administration of delta-9-tetrahydrocannabinol (THC) alters the neurochemical response to stress in the adult Fischer-344 rat. 244 11

The cardiovascular effects of dopamine were studied before and during thoracic epidural analgesia (TEA) in eight patients prior to abdominal aortic surgery. Dopamine was infused at rates of 2, 4, and 8 micrograms X kg-1 X min-1. Mean plasma dopamine concentration increased proportionally to the infusion rate. Before TEA, dopamine 8 micrograms X kg-1 X min-1 decreased systemic vascular resistance 4 +/- 4 mmHg min X 1-1 (m +/- SD) (P less than 0.05), but increased mean arterial pressure 15 +/- 12 mmHg (P less than 0.01), cardiac output 1.9 +/- 1.0 1 X min-1 (P less than 0.01), heart rate 10 +/- 9 beats X min-1 (P less than 0.05), and plasma norepinephrine concentration 544 +/- 252 pg X ml-1 (P less than 0.01). After the induction of TEA, which extended above the T2 dermatome and below the L2 dermatome, saline and albumin were infused to maintain central venous and pulmonary capillary wedge pressures. TEA reduced mean arterial pressure from 96 +/- 18 to 55 +/- 8 mmHg (P less than 0.01), cardiac output from 4.7 +/- 0.9 to 3.9 +/- 0.9 1 X min-1 (P = 0.05), systemic vascular resistance from 21 +/- 6 to 14 +/- 3 mmHg min X 1-1 (P less than 0.05), and plasma norepinephrine concentration from 394 +/- 141 to 207 +/- 73 pg X ml-1 (P less than 0.01). The plasma epinephrine concentration was reduced 49% after the induction of TEA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of dopamine during thoracic epidural analgesia in man. 357 78

Adult male Fischer-344 rats were dosed sc with 1 or 2.5 mg/kg of triethyl lead chloride (TEL) for 5 consecutive days. One week after the last dose, TEL-exposed rats had decreased Met-enkephalin in the hypothalamus, septum, and frontal cortex, while substance P was decreased in the hippocampus and frontal cortex. Dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) in the caudate nucleus were not altered by TEL nor were serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in the caudate nucleus, hypothalamus, hippocampus, or frontal cortex. In a second experiment, rats were dosed with 1.75 mg/kg sc for 5 days. Subsequent assay of brain tissue indicated that TEL decreased met-enkephalin levels in the septum of rats one and seven days after cessation of dosing; effects on substance P were not observed. TEL-induced decreases in Met-enkephalin in the septum were temporally associated with increased hot plate latencies. One day after cessation of dosing with TEL, concentration of 5-HIAA in the caudate nucleus, hippocampus, frontal cortex, and brain stem, and 5-HT in the hippocampus and brain stem were increased. Biogenic amine concentrations were not affected in any other region or at any other time postdosing. A third experiment indicated that TEL-induced analgesia could be attenuated by 10 mg/kg chlordiazepoxide or 10 mg/kg of naloxone. The present results suggest that TEL-induced analgesia may be due to alterations in emotionality or reactivity to noxious stimuli, which may be associated with the alteration in delta opiate mechanism in the limbic system, such as the change of septal enkephalin neuronal activities.
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PMID:Correlation of neurochemical and behavioral effects of triethyl lead chloride in rats. 619 48

1. A single injection in rats of 250 microgram of 6-hydroxydopamine HCl (6-OHDA) into the subarachnoidal space of the spinal cord of rats resulted in a lasting, selective depletion of spinal noradrenaline. Dopamine levels in the spinal cord and catecholamine levels in various brain regions were not markedly affected. 2. When ether anesthesia was used spinal noradrenaline was found to be almost completely depleted by the administration of 6-OHDA. Only partial depletion was achieved when pentobarbitone anaesthesia or neuroleptic analgesia was used. 3. The blood pressure rise caused by electrical stimulation of the posterior hypothalamus was not affected by 6-OHDA treatment 7 days previously. 4. 6-OHDA administration did not influence the development of two-kidney Goldblatt hypertension. When 6-OHDA was administered 7 days before clipping, a slight delay of the development was observed, but this did not occur when 6-OHDA treatment was given 3--4 h before clipping. 5. It is concluded that intact spinal noradrenergic neurotransmission is neither a prerequisite for the development of two-kidney Goldblatt hypertension, nor for the pressor response to hypothalamic stimulation.
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PMID:Effect of depletion of spinal noradrenaline by 6-hydroxydopamine on the development of renal hypertension in rats. 747 22

Agonist interactions in antinociceptive effects between clonidine and opioids can be used to reduce opioid requirements in surgical patients. However, clonidine can cause marked sedation and associated respiratory dysfunction. Thus, the benefit of using clonidine to reduce opioid use on respiration is questionable. This double-blind randomized study compared the analgesic efficacy, arterial blood gases, and pharmacokinetics of an intravenous (IV) infusion of fentanyl 75 micrograms/h and a mixture of fentanyl 25 micrograms/h plus clonidine 0.3 micrograms.kg-1.h-1 in 32 healthy young adults after surgery for scoliosis correction. Oxygen saturation (FIO2: 0.21) and respiratory rate were monitored as well as supplemental analgesia demands (IV ketoprofen via a patient-controlled device), pain, sedation, and hemodynamics. Oxygen and naloxone (5 micrograms.kg-1.min-1) were administered, respectively, if more than three episodes of oxygen saturation less than 90% were observed within 10 min and if PaCO2 was higher than 50 mm Hg. Pain relief, sedation, and ketoprofen requirements were similar in both groups. The number of episodes of arterial desaturation less than 90% (> 20 s) was 106 for four patients in the fentanyl group (versus none in the clonidine-fentanyl group). Naloxone was required in six patients and oxygen in two patients of the fentanyl group (versus none in the group receiving clonidine). Dopamine, 10 micrograms.kg-1.min-1, was required in one patient of the clonidine-fentanyl group to correct hypotension. Mean arterial blood pressure, plasma clearance, and the elimination rate constant of fentanyl were lower in the clonidine-fentanyl group than in the fentanyl group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Balanced postoperative analgesia: effect of intravenous clonidine on blood gases and pharmacokinetics of intravenous fentanyl. 797 37

Dopamine is administered frequently in the operating theatre and intensive care unit patients undergoing mechanical ventilation with the aim of specifically enhancing renal blood flow. In an uncontrolled, open study, we administered sequentially different doses of dopamine (0, 2, 4, 8 and 0 microgram kg-1 min-1) during a 1-h period each. Systemic haemodynamic and renal haemodynamic variables were measured simultaneously using a pulmonary artery catheter and radiopharmaceuticals, respectively. We studied seven haemodynamically stable patients (mean age 66 yr), with a serum creatinine concentration < 160 mumol litre-1, after elective infrarenal abdominal aortic reconstruction. All patients received extradural analgesia with bupivacaine and sufentanil, and none had a previous history of heart failure. Dopamine induced a dose-dependent increase in cardiac index which returned to baseline after cessation of the dopamine infusion. Glomerular filtration rate (GFR) increased with all doses of dopamine, whereas renal blood flow (RBF) increased significantly only with the 2- and 4-microgram kg-1 min-1 doses. However, the ratio RBF/cardiac output remained unchanged with the 2- and 4-microgram kg-1 min-1 doses, but decreased with 8 micrograms kg-1 min-1 from 14 (1.5)% to 10 (1.3)%. We conclude that dopamine increased RBF and GFR as a result of an increase in cardiac output.
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PMID:Lack of specific renal haemodynamic effects of different doses of dopamine after infrarenal aortic surgery. 934 41

The present study was undertaken to investigate the antinarcotic effects of velvet antler water extract (VAWE) from Cervus elaphus on morphine. Morphine-induced analgesic action was measured by tail-flick method. Morphine-induced hyperactivity and reverse tolerance were evidenced by measuring the enhanced ambulatory activity using a tilting-type ambulometer. Dopamine (DA) receptor supersensitivity in mice displaying morphine-induced reverse tolerance was evidenced by the enhanced response in ambulatory activity to the DA agonist, apomorphine. The repeated administration of VAWE significantly inhibits the development of morphine-induced analgesic tolerance, physical dependence, reverse tolerance and postsynaptic DA receptor supersensitivity. But a single administration of VAWE did neither antagonize morphine-induced analgesia nor inhibit morphine-induced hyperactivity. From the above results, it is presumed that VAWE may be useful for prevention and therapy of the adverse actions of morphine caused by the repeated administration of morphine.
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PMID:Antinarcotic effects of the velvet antler water extract on morphine in mice. 1043 6


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