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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The successful termination of 19 consecutive late 1st and 2nd trimester pregnancies using a combination of intravenous prostaglandin E2 (PGE2) and oxytocin (Syntocinon) is reported. PGE2 (5 mg in 500 ml of 5% glucose) was initially infused at the rate of 2.5 mcg/minute and then increased to 5 mcg/minute after half an hour. The infusion was increased to a maximum of 10 mcg/minute. Oxytocin was infused 2 hours after the PGE2 at a constant rate of 128 mU/minute. Mean total dose of PGE2 used was 5.9 mg at an overall rate of 6.1 mcg/minute. Average induction/delivery interval was 16 hours, with only 1 patient taking more than 24 hours. Abortion was complete in 13 cases (68%). Vomiting occurred in 13 women; pain was minor and was controlled by pethidine. Mild and transient thrombophlebitis was also reported. There were no reported cases of diarrhea and or cervical damage. Compared to the use of intravenous PG alone, PG given intraamniotically alone or with intravenous oxytocin, and PG given extraamniotically alone or with intravenous oxytocin, this study shows that a combination of intravenous PGE2 and oxytocin at the dose level described is closer to meeting all the desired criteria for the acceptability of any abortion method (ease and safety of administration, side effects, lengths of induction delivery interval, and effectiveness in terms of success rate and uterine evacuation).
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PMID:Letter: Intravenous prostaglandins and oxytocin for mid-trimester abortion. 4 97

In a clinical trial carried out in 34 pregnancy women Enzaprost F 4 (prostaglandin F2-alpha) was administered into the uterus to cause uterine contractions in the 2nd and 3rd trimesters. The indications for the treatment were: 1. membrane rupture in 20 cases between the 21st and 26th weeks of pregnancy; 2. fetal death in 12 cases between the 24th and 34th weeks of pregnancy, and 3. induced abortion for medical reasons in 2 cases of primiparae in the 2nd trimester. Enzaprost was administered in physiological salt solution in doses of 2-5 mg with a total dose of 9-22 mg (average 18.5 mg). Contractions appeared within 15-30 minutes in groups 1 and within 20-30 minutes in groups 2 and 3. Abortions in the three different groups began 10.2, 11.5, and 6.0 hours after administration in primiparae and 7.3 and 8.2 hours, respectively, after treatment in groups 1 and 2 in women other than primiparae. Oxytocin had to be administered additionally in 3 cases in groups 1 and 2. The method proved to be safe and effective, side effects occurred in 6 cases (17.6%) consisting of cardiac pain, nausea, tachycardia, and increased systolic pressure.
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PMID:[Induction of uterine contractions using Enzaprost F administered into the uterine cavity]. 346 46

A comparative study of prostaglandins F2 alpha induced abortion and hysterotomy is presented. The intraamniotic and extraamniotic procedures were employed, using doses of 40 mg and 2.5-5.0 mg of prostaglandin, respectively. Failure to abort by the intraamniotic method occurred in 8% of the cases (50 patients), whereas the failure rate with the extraamniotic method was 42% (51 patients). Oxytocin infusion was administered to 14 of the 30 successful cases in the extraamniotic group and to 16 of the 46 successful cases in the intraamniotic group. No severe side effects occurred except for 1 case of cervical rupture in the intraamniotic group. Nausea and vomiting were the most common side effects. Blood pressure fell significantly in 12 patients in the intraamniotic group, although the decrease was transitory. 14 patients in the intraamniotic group required analgesics for pain. The average hospital stay for intraamniotic patients was 4 days less than for hysterotomy patients.
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PMID:Comparison of abortion performed with prostaglandin F2 alpha and hysterotomy. 444 Oct 29

The hormonal changes in maternal serum during parturition induced by amniotomy and oxytocin (OXY) infusion or oral prostaglandin E2 (PGE2) medication have been compared in 68 patients (33 women in the PGE2 group, 35 in the oxytocin group). The effect of PGE2 differed from that of oxytocin. Thus the prostaglandin elicited increases in total estriol (p < 0.001) and decreases in prolactin (p < 0.01), TSH (p < 0.05) and HPL (p < 0.05) from the basal level to that immediately before parturition. Maternal serum cortisol levels rose to the same extent in both treatment groups (p < 0.001). The significant (p < 0.05) increase occurred earlier among women receiving PGE2 (two hours into therapy), even though labor pain was experienced later in this group. The serum estriol elevation in these patients was significant three hours after start of therapy (p < 0.05). A similar time course was noted for the decrease of serum prolactin in PGE2 treated patients. The drop in maternal serum levels of HPL and TSH in the PGE2 group was significant only immediately prior to partus. Neither PGE2 nor oxytocin induced changes in maternal serum levels of HCG or alpha-fetoprotein or estradiol. Oxytocin but not PGE2 lead to a decrease in maternal serum progesterone concentrations; this was significant (p < 0.05--p < 0.01) only late in labor. Mixed umbilical serum levels of the hormones mentioned above were the same regardless of method of induction. Hence the increased maternal estriol concentrations during PGE2 treatment were not reflected in fetal blood. It is suggested that increases in maternal estriol levels during PGE2 medication are due to effects on the maternal enterohepatic circulation rather than on the fetoplacental unit. Irrespective of maternal treatment umbilical serum from female newborns contained statistically higher (p < 0.05) levels of estradiol and HCG than serum from male children.
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PMID:Changes in serum hormone levels during labor induced by oral PGE2 or oxytocin infusion. 616 Jul 19

Recent neuroanatomical and behavioral evidence has indicated that vasopressin (VP) increases pain thresholds. In the present study intracerebroventricular (ICV) administration of both arginine VP (AVP: 75-500 ng) and 1-deamino-8-D-arginine vasopressin (DDAVP: 150-500 ng) elevated tail flick latencies. Oxytocin (OXY, ICV), also elevated tail-flick latencies (150-1000 ng); however this increase was accompanied by "barrel-roll" seizure activity. VP analgesia was eliminated by pretreatment with 1-deamino-penicillamine-2(O-methyl)tyrosine-AVP (dPTyr(me)AVP: 500 ng, ICV), a VP antagonist, but not naloxone (1 or 10 micrograms, ICV), suggesting that VP modulates nonciceptive thresholds through its own binding sites. Conversely, pretreatment with naloxone (1 micrograms, ICV) but not dPTyr(me)AVP (1 microgram, ICV) attenuated the analgesic efficacy of systemic morphine (10 mg/kg), further dissociating VP and central opiate analgesic processes. Finally, systemic pretreatment with dexamethasone potentiated VP analgesia. These data support the notion that VP is a specific non-opioid pain inhibitor.
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PMID:Vasopressin analgesia: specificity of action and non-opioid effects. 649 25

The aim of this progressive study is to clarify whether the pain-in-labour drugs Oxytocin and Prostaglandin E2 do have an influence on postpartum serumbilirubin concentrations of the neonates. Two groups of neonates in which labour was induced with Oxytocin or Prostaglandin E2 were compared with a control group without pain-in-labour stimulants. The three groups were comparable in respect of obstetrical anamnesis and risk factors. The serumbilirubin concentration of the neonates was controlled at very frequent intervals during the first 72 hours. In the three groups, no difference could be found in the serumbilirubin values during the 72 hours' duration of the study.
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PMID:[Influence of oxytocin and prostaglandin E2 on icterus neonatorum (author's transl)]. 721 66

The effect of systemically administered oxytocin and a specific oxytocin antagonist, 1-deamino-2-D-Tyr(OEt)-4-Thr-8-Orn-oxytocin, on heat pain sensitivity was examined in rats. Intraperitoneal (i.p.) oxytocin at 1 mg/kg, but not at 0.1 and 0.3 mg/kg, significantly increased response latencies on the hot-plate test. However, the rats displayed clear signs of sedation, motor impairment and vasoconstriction after 1 mg/kg oxytocin. Skin temperature on the plantar surface of the hind paws was also significantly decreased by this dose of oxytocin. The oxytocin antagonist (1 mg/kg i.p.) did not influence response latency. Since increased response latency was not the only behavioral effect of oxytocin, we conducted electrophysiological experiments to examine the effect of systemic oxytocin on the nociceptive flexor reflex in decerebrate, spinalized, unanesthetized rats. Oxytocin at 0.1 mg/kg i.p. did not influence flexor reflex magnitude, mean blood pressure or heart rate. Oxytocin at 0.3 and 1 mg/kg caused a gradual increase in blood pressure with stronger effect observed with 1 mg/kg. Neither 0.3 nor 1 mg/kg oxytocin significantly influenced the flexor reflex magnitude and heart rate. We thus conclude that systemic oxytocin did not produce analgesia in rats and the observed increase in response latency in the hot-plate test may result from the sedative and vasoconstrictive effects of this peptide. Furthermore, since the oxytocin antagonist did not significantly alter response latency on the hot-plate test, it is unlikely that endogenous oxytocin exerts a tonic effect on the pain threshold in rats.
Pain 1994 May
PMID:Is systemically administered oxytocin an analgesic in rats? 809 May 16

This study aimed to investigate if pregnancy-induced hypoalgesia occurs in the sow, and to examine the role of endogenous opioids which are known to be released in response to nociception. Sixteen Large White x Landrace multiparous sows were tested in straw bedded pens (2.5 x 2.5 m) during weeks 4, 8 and 12 of pregnancy and over the farrowing period. Testing involved thermal stimulation of eight areas on the rear-quarters of the sows with a CO2 infra-red laser until a physical response was seen (tail flick, leg move or muscle twitch) or for a maximum of 16 s. Over the farrowing period testing was more frequent, and at 3.75 h after the birth of the first piglet, half the sows received an injection (i.m.) of an opioid antagonist naloxone (N) (1 mg kg(-1) body weight) with the remainder receiving a control dose of saline (S). Responses were recorded 15 and 30 min post-injection. There was no significant difference between response times over weeks 4, 8 and 12 of pregnancy (P = 0.152), however a significant rise was seen from week 12 to 5 days before parturition (P = 0.002). Response times continued to rise until the birth of the first piglet by which time the majority of sows had stopped responding within 16 s (P < 0.001). Response times fell over days 1, 2 and 7 post-partum. After administration of naloxone response times fell compared to control animals at 15 min (P < 0.001) and 30 min (P < 0.01) post-injection. These results suggest that nociceptive threshold increases during late pregnancy in the sow, perhaps as an endogenous defence against labour pain, and that during parturition this change in nociceptive threshold is, at least in part, opioid-mediated. Oxytocin is known to be inhibited by endogenous opioids at parturition, thus future research should consider the potential role of increased nociception at birth as a negative feedback to oxytocin release.
Pain 1997 Aug
PMID:Opioid-mediated changes in nociceptive threshold during pregnancy and parturition in the sow. 927 99

Induction of labor has increased from 9% to 18% of all U.S. deliveries in recent years. Several useful oxytocin induction protocols are available, both from the ACOG Practice Bulletin #10 and institutional sources. Higher-dose protocols tend to result in fewer cesarean deliveries for dystocia but more "fetal distress." There is no consensus as to which protocol is best, and the clinician is advised to understand the trade-offs involved and how those trade-offs could relate to the clinician's local situation. Given the availability now of prostaglandin agents for induction with an unfavorable cervix, the advantage of less hyperstimulation in low-dose oxytocin protocols may become increasingly important. The most important risks include hyperstimulation (frequent but usually brief and well-tolerated), failed induction (occasional and important), and uterine rupture in some studies (rare but dangerous). Pain was not a sensitive indicator of uterine rupture in a large 1989 study. Fetal heart rate changes were much more likely to herald uterine rupture in that study. Oxytocin's greatest weakness is that some patients will not respond well to it, especially with marked cervical unfavorability. However, given an individual patient whose uterus will respond adequately to this drug, oxytocin has the advantage of short half-life and the option for prompt cessation if desired. Intrauterine pressure catheters with oxytocin usage are usually well-worth their minor risks. Current ACOG literature lists induction of labor in the setting of one or more previous low-transverse cesarean deliveries as necessitating "special attention" and "close patient monitoring." The well-informed clinician will be familiar with the issues involved.
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PMID:Oxytocin for labor induction. 1094 53

The release of adrenocorticotropin (ACTH) from the corticotrophs is controlled principally by vasopressin and corticotropin-releasing hormone (CRH). Oxytocin may augment the release of ACTH under certain conditions, whereas atrial natriuretic peptide acts as a corticotropin release-inhibiting factor to inhibit ACTH release by direct action on the pituitary. Glucocorticoids act on their receptors within the hypothalamus and anterior pituitary gland to suppress the release of vasopressin and CRH and the release of ACTH in response to these neuropeptides. CRH neurons in the paraventricular nucleus also project to the cerebral cortex and subcortical regions and to the locus ceruleus (LC) in the brain stem. Cortical influences via the limbic system and possibly the LC augment CRH release during emotional stress, whereas peripheral input by pain and other sensory impulses to the LC causes stimulation of the noradrenergic neurons located there that project their axons to the CRH neurons stimulating them by alpha-adrenergic receptors. A muscarinic cholinergic receptor is interposed between the alpha-receptors and nitric oxidergic interneurons which release nitric oxide that activates CRH release by activation of cyclic guanosine monophosphate, cyclooxygenase, lipoxygenase and epoxygenase. Vasopressin release during stress may be similarly mediated. Vasopressin augments the release of CRH from the hypothalamus and also augments the action of CRH on the pituitary. CRH exerts a positive ultrashort loop feedback to stimulate its own release during stress, possibly by stimulating the LC noradrenergic neurons whose axons project to the paraventricular nucleus to augment the release of CRH.
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PMID:Role of the hypothalamic pituitary adrenal axis in the control of the response to stress and infection. 1100 12


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