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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A multiple stimulus (secondary or repetitive stimulus) to the sensory nerve endings in the skin and in the connective subcutaneous tissue is exerted by acupuncture. Because of the tight interlacing of nerve endings, this stimulus affects simultaneously the sensory fibres of both the cerebrospinal nerve, the Sympathicus and the Parasympathicus. The slow conducting pain fibres (C-fibres) are inhibited in their function by the fast conducting Abeta-fibres and Adelta-fibres, which transmit pressure, vibration and electric currents (Foerster, Zottermann). In addition a secondary stimulus inhibits or modulates a peripheral pain stimulus (pain of operation) in various synapses on the sensory pathway to the cortex, especially in the substantia gelatinosa of the spinal cord. According to Keidel, Raich and Albrecht pain stimuli are masked up to 50% by vibration and other "rivaling" stimuli. Furthermore, acupuncture releases a higher level of Noradrenaline and Serotonine in the liquor of ventricles. These two biogenic amines effect also an analgesia such as demonstrated in animals by artificial injection in the ventricles. The author gives also a detailed review about the importance of the transmitters noradrenaline, serotonine and acteylcholine for the acupuntural analgesia.
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PMID:[On a neurophysiological interpretation of acupunctural analgesia in tonsillectomy and in extensive operations (author's transl)]. 12 4

Premature infants are capable of mounting physiologic and metabolic responses to pain. Systemic and local anesthesia reduce stress responses to major and minor surgical procedures. We evaluated the effects of local anesthesia (5 mg/kg lidocaine) preceded by either 1 mg/kg secobarbital (S) intravenously or by 2 micrograms/kg fentanyl (F) intravenously on the stress response to Broviac catheter placement. Twenty-nine premature infants ages 5 to 30 days, weighing between 650 and 1350 gm, were randomly assigned to either S or F groups. Age, birthweight, sex, race, and severity of illness were similar among S and F groups. Heart rate and blood pressure remained unchanged throughout the procedure. Oxygen saturation (O2sat) declined significantly in both groups during skin preparation and wound closure, but not during incision, dissection, or tunneling. In spite of fractional inspired oxygen adjustments made in 13 of 14 S- and 3 of 15 F-treated patients, decline in O2sat was more common and more pronounced (p less than 0.01) in S-treated babies. Hyperglycemic responses occurred in all S- and in none of the F-treated patients (p less than 0.001). Norepinephrine plasma concentrations did not change during Broviac catheter placement in either F or S group. Epinephrine concentrations were more elevated in S- than in F-treated patients, although these differences were not statistically significant. Low-dose fentanyl analgesia effectively complements local lidocaine anesthesia during Broviac catheter placement. Sedatives neither abolish metabolic responses to surgical stress nor prevent profound and persistent oxygen desaturation.
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PMID:Analgesia versus sedation during Broviac catheter placement. 174 75

The efficacy of intravenous (iv) and epidural infusions of alfentanil for postoperative pain relief was investigated in 24 patients (ASA physical status 1-2) who were scheduled for abdominal hysterectomy. The patients were allocated randomly to receive either epidural or iv alfentanil. In both groups, a loading dose of 15 micrograms.kg-1 was administered, followed by a constant rate infusion of 18 micrograms.kg-1.h-1 alfentanil for 20 h. Both routes provided similar degrees of analgesia; however, analgesia occurred earlier in the intravenously treated group (P less than 0.03). Mean plasma alfentanil concentrations (Cps) varied between 42 and 82 ng.ml-1 in the iv group and 23 and 68 ng.ml-1 in the epidural group, with higher concentrations in the iv group for the first 60 min only (P less than 0.01). Cps increased with infusion time, suggesting accumulation of alfentanil. After infusion ended, pain recurred at the same time in both groups, whereas the alfentanil Cps still were greater than 45 ng/ml. Postoperative epinephrine concentrations decreased after 60 min of infusion (P less than 0.02), whereas, after 6 h, cortisol levels decreased to preoperative values. Norepinephrine concentrations decreased only slightly. The only clinically meaningful effect on vital signs that occurred was an abrupt reduction of respiratory rate after the iv loading dose. PaCO2 increased to the same extent in both groups during the first 15 min only. The incidence of opioid-related side effects was similar in both groups. These results suggest that the iv and epidural routes were equally effective for providing postoperative pain control and controlling the postoperative response to surgical stress.
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PMID:Alfentanil infusion for postoperative pain: a comparison of epidural and intravenous routes. 173 10

This study demonstrates that pre-exposure to stress influences subsequent effects of stress on pain sensitivity (stress-induced analgesia) and on plasma corticosterone and brain catecholamine activity. Animals exposed to a 30 min shock session (S1 = 8, 5.0 s shocks) 10 days earlier showed a significant attenuation of shock-induced analgesia, as measured by increased latency of tail withdrawal from a hot water bath immediately after a 40 s, 1.6 mA footshock (S2). Animals exposed to shock 10 days before testing also exhibited a higher plasma corticosterone response to testing than did all other groups. Norepinephrine (NE) levels in the frontal cortex and dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) levels in the frontal cortex and nucleus accumbens were not altered in any group. However, the DOPAC/DA ratio in the frontal cortex was increased by analgesia testing, and this increase was enhanced only by the combination of shock 10 days before testing and shock immediately before the test (S1 + S2). These results are consistent with previous reports from this laboratory which indicate that an animal's acute response to stress is strongly influenced by its past history of stress.
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PMID:Prior stress attenuates the analgesic response but sensitizes the corticosterone and cortical dopamine responses to stress 10 days later. 250 60

Intrathecal (i.t.) pretreatment of rats with either theophylline (50 micrograms) or 8-phenyltheophylline (3 micrograms) antagonized antinociception produced by i.t. injection of morphine (0.3-3 micrograms) in the tailflick and hotplate tests, but had no effect on antinociception produced by i.t. injection of noradrenaline (10-30 micrograms). In other experiments designed to test whether morphine released adenosine from the spinal cord, adenosine release from synaptosomes was measured by high-performance liquid chromatography with fluorescence detection of etheno-adenosine. Depolarization with 24 mM K+ or 50 microM veratridine released 3 times as much adenosine from dorsal than from ventral spinal cord synaptosomes. K+ released primarily adenosine whereas veratridine released both adenosine and nucleotide(s). Morphine (1-100 microM) produced a Ca++-dependent release of endogenous adenosine, comparable to K+-evoked adenosine release, which was blocked by 1 microM naltrexone. Noradrenaline (5-500 microM) produced a Ca++-dependent release of a nucleotide which was subsequently degraded extracellularly to adenosine by ecto-5'-nucleotidase. This release was antagonized by 10 microM phentolamine and by 1 microM yohimbine. These results suggest that, within the spinal cord, morphine may act on opioid receptors to release adenosine which subsequently acts at adenosine receptors to produce spinal analgesia. Spinal analgesia produced by noradrenaline does not appear to involve adenosine release.
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PMID:Involvement of adenosine in the spinal antinociceptive effects of morphine and noradrenaline. 282 55

The acute effects of the 5-hydroxytryptamine agonist, 5-Methoxy-N,N-dimethyltryptamine (5-MeO-DMT), upon pain sensitivity, using shock titration, tail-flick and hot-plate methods, in noradrenaline- and 5-hydroxytryptamine-depleted rats were examined. Noradrenaline depletion, following the systemic administration of N-2-chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP4, 2 X 50 mg/kg, i.p.), caused a reversal of the analgesic effect of 5-MeO-DMT on shock-titration from hypo- to hypersensitivity, and a total blockade of the antinociceptive effect of 5-MeO-DMT upon pain responses in the hot-plate and tail-flick tests. Pretreatment with either p-chloroamphetamine (2 X 10 mg/kg) or p-chlorophenylalanine (200, 100, 100 mg/kg), that depletes central 5-hydroxytryptamine stores, failed to alter the analgesia caused by acute 5-MeO-DMT. Strong evidence is provided for the effect of central noradrenaline depletion upon the analgesic effect of the 5-HT agonist. These findings suggest an important tonic influence of the noradrenaline system upon the descending spinal 5-HT pathway in rats.
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PMID:Blockade and reversal of 5-methoxy-N,N-dimethyltryptamine-induced analgesia following noradrenaline depletion. 315 73

The antinociceptive effect of acute administration of 5-HT receptor agonists and agents releasing 5-HT from neuronal terminals was studied in rats by using the hot-plate, tail-flick and shock-titration tests. Noradrenaline depletion by the noradrenaline-neurotoxin N-2-chloroethyl-N-ethyl-2-bromo-benzylamine hydrochloride (DSP4, 2 X 50 mg/kg) blocked the analgesia induced by the 5-hydroxytryptamine (5-HT) receptor agonists 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and quipazine, as well as that induced by acute release of 5-HT by p-chloroamphetamine (PCA) and increased 5-HT synthesis by 5-hydroxytryptophan (5-HTP). Analgesia in the tail-flick test was partly blocked by both methergoline and mianserin, whereas the analgesic effects of 5-MeODMT in the hot-plate and shock-titration tests were unaffected by the 5-HT antagonists. In the shock-titration test it was found that the DSP4-pretreated animals were made hyperalgesic by acute 5-MeODMT, and this hyperalgesia was blocked by both mianserin and methergoline, implying that this effect was 5-HT receptor mediated. It is therefore concluded that a functional central noradrenergic system is required for eliciting 5-HT receptor mediated analgesia, and that these interactions, at least in part, are probably spinally located.
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PMID:Analgesia induced by 5-hydroxytryptamine receptor agonists is blocked or reversed by noradrenaline-depletion in rats. 348 88

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88

The objectives of this study were to investigate the duration of analgesia and the development of tolerance following continuous intrathecal administration of morphine and norepinephrine alone, and morphine followed by norepinephrine via mini-osmotic pumps in the rat. Analgesia was assessed by the tail-flick test. In single pump experiments morphine 1 microliter (10 micrograms)/h (7 days) and 0.5 microliter (10 micrograms)/h (14 days) produced analgesia with tolerance by days 5-7. Norepinephrine 1 microliter (15 micrograms)/h (7 days) produced analgesia equivalent to that of morphine with tolerance developing by day 3. Following continuous intrathecal morphine 1 microliter (10 micrograms)/h for 5 days, norepinephrine 1 microliter (15 micrograms)/h for 7 days failed to produce a significant increase in analgesia. This was in contrast to the increase in analgesia seen when the norepinephrine infusion followed a saline infusion. Determination of the norepinephrine concentration in the solution from the osmotic pumps verified that the norepinephrine is stable for the treatment period.
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PMID:Analgesia and tolerance to intrathecal morphine and norepinephrine infusion via implanted mini-osmotic pumps in the rat. 384 Feb 48

Timolol of 0.5% was applied in 6 eyes prior to cataract extraction, while 7 eyes were not treated. Aqueous humor was drawn after retrobulbar analgesia with 2% lidocaine and analyzed for epinephrine and norepinephrine using a radioenzymatic assay. Epinephrine levels averaged 15.8 +/- 16.2 and 19.3 +/- 27.5 pg/ml in the timolol treated group and controls respectively. The corresponding values for norepinephrine were 1.59 +/- 0.55 and 1.87 +/- 0.90 ng/ml. These differences were not statistically significant. Norepinephrine levels in this study were somewhat higher than in previous reports of catecholamine levels in human aqueous humor and considerably higher than plasma levels of norepinephrine. There was no significant correlation between aqueous humor norepinephrine levels and age in the two groups combined. The mean norepinephrine levels for men and women in the two groups combined were 1.73 +/- 0.89 and 1.76 +/- 0.56 ng/ml. The difference was not statistically significant. Timolol resulted in a decrease in the intraocular pressure.
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PMID:Human aqueous humor catecholamines. 408 54


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