Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been demonstrated in animal model of somatic pain that hypothalamic paraventricular nucleus (PVN) participates in acupuncture analgesia, probably by mediation of vasopressin release. The role of PVN in acupuncture analgesia for experimental visceral pain in rats was further investigated in the present study. Experimental results demonstrated that electroacupuncture could inhibit the writhing response, produced by intraperitoneal injection of antimonium potassium tartrate and this inhibitory effect could be enhanced by electrical stimulation of PVN, but decreased by electrolytical lesion of PVN, intracerebroventricular injection of vasopressin antiserum (14 microliters) or the vasopressin antagonist, d(CH2)5Tyr(Me)-AVP (500 ng/5 microliters). Intraperitoneal administration of the latter drug (10 micrograms/kg), however, was ineffective. The above experimental results suggest that vasopressinergic neurons in PVN also participate in the inhibition of visceral pain by electroacupuncture.
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PMID:[Involvement of vasopressinergic neurons of paraventricular nucleus in the electroacupuncture-induced inhibition of experimental visceral pain in rats]. 129 59

The Asu-AVT (1,6-aminosuberic acid -8-arginine-vasotocin) in an analogue of 8-arginine-vasotocin (AVT) which is one of pineal hormones. The effect of Asu-AVT on the pain threshold and EA analgesia was studied in rats. An increase of 16.2-41.5% in pain threshold was observed within 70 min. after ivc of Asu-AVT (75ng), while the Asu-AVT injection in combination with EA produced a significant increase of 164.6-309.1% in pain threshold, which was much higher than that in the saline-EA group (p < 0.05-0.01). The effect of Atu-AVT is analogous to that of oxytocin and arginine-vasopressin. The data indicate ivc of ASu-AVT not only elevates the pain threshold, but also enhances the EA analgesia. These results suggest that the pineal hormone, AVT may play a role in the EA analgesia.
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PMID:[Effect of Asu-AVT on electroacupuncture (EA) analgesia]. 133 26

This work was to investigate the change of the contents of vasopressin and oxytocin during acupuncture in rat. Acupuncture could not only cause a change of immunoreactive arginine vasopressin, but also cause a change of immunoreactive oxytocin in many regions of rat brain. These results suggest that arginine vasopressin and oxytocin might be through the central nervous system to participate acupuncture analgesia.
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PMID:[Effect of acupuncture on the contents of vasopressin and oxytocin in the rat]. 133 32

Intraspinally administered alpha 2-adrenergic agonists are being examined for postoperative analgesia, yet their effects on the hemodynamic response to acute hemorrhage have not been examined. In this study chronically prepared conscious sheep received thoracic intrathecal saline or clonidine 300 micrograms followed in 15 min by rapid removal of 1,000 ml blood. In saline-treated ewes blood pressure was maintained and heart rate steadily increased during hemorrhage of up to 700 ml blood, with further blood removal resulting in rapid decreases in both variables. In contrast, heart rate never increased and blood pressure was maintained only up to 400 ml blood loss in animals receiving intrathecal clonidine. Compared to saline controls, clonidine did not alter blood pressure or heart rate at the end of hemorrhage or during blood pressure restitution during the next hour. Clonidine inhibited the increase in plasma epinephrine at the end of hemorrhage without altering plasma norepinephrine, vasopressin, renin, or atrial natriuretic factor. Intrathecal idazoxan, a specific alpha 2-adrenergic antagonist, reversed clonidine's effect on blood pressure during hemorrhage. Intravenous DG-5128, a poorly lipid-soluble alpha 2-adrenergic antagonist, also reversed clonidine's effect and additionally completely blocked any reduction in blood pressure and heart rate during hemorrhage. These data suggest that intrathecal clonidine interferes with maintenance of blood pressure during hemorrhage, likely because of a spinal sympatholytic effect, but does not affect the ultimate decrease in blood pressure after rapid removal of 1,000 ml blood. This difference in effect during the two phases of hemorrhage can be explained by the relative importance of the sympathetic nervous system in each.
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PMID:Intrathecal clonidine and the response to hemorrhage. 135 38

Pathophysiologic mechanisms of bradycardia during epidural anaesthesia (L3-L4 with 1% lidocaine, 38 ml) were evaluated by studying changes in selected cardiovascular and hormonal parameters. Six of eight subjects (analgesia to T8-T10) remained circulatory stable with no significant changes in heart rate (HR), mean arterial pressure (MAP) and thoracic impedance (TI). In one of two subjects MAP decreased after 25 min from 85 to 50 mmHg (11.3 to 6.7 kPa), HR from 80 to 45 beats.min-1 while thoracic impedance increased from 25.5 to 26.5 ohm. End-systolic diameter (ESD) and end-diastolic diameter (EDD) of the left ventricle determined with echocardiography were reduced from 3.8 to 3.2 cm (17%) and 5.6 to 5.0 cm (11%), respectively. In the other subject MAP decreased after 25 min from 75 to 50 mmHg (10.0 to 6.7 kPa) and HR from 82 to 60 beats.min-1 while thoracic impedance increased from 28.8 to 29.6 ohm. ESD was reduced from 3.8 to 3.3 cm (13%), and EDD from 5.6 to 5.0 cm (11%). Both subjects recovered after infusion of saline and being placed in the head-down position. There were no consistent changes in plasma catecholamines, whereas pancreatic polypeptide increased from 5 and 3 to 152 and 69 pmol.l-1, vasopressin from 3 and 2 to 152 and 46 pmol.l-1, and aldosterone from 282 and 229 to 383 and 485 pmol.l-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced left ventricular diameters at onset of bradycardia during epidural anaesthesia. 146 23

Recent evidence has indicated that vasopressin (VP) can increase the pain threshold. It is not clear whether the paraventricular nucleus (PVN) of hypothalamus, which is one of the main nuclei that secrete VP in brain, is involved in the acupuncture analgesia (AA). The present study was designed to examine the role of PVN in AA. Experiments were carried out on Wistar rats using tail stimulation vocalization test to measure the pain threshold. The acupoints "Renzhong" and "Chengjiang" were selected for electroacupuncture. Electrical stimulation of PVN could increase significantly the pain threshold and enhance the effect of AA. On the contrary, electrolytical lesion of PVN could decrease the effect of AA obviously, which could be recovered by cerebroventricular injection (ICV) of 300 ng of arginine VP. Pretreatment with AVP-antiserum (ICV) could attenuate the effect of AA. These data indicated that PVN plays an important role in pain modulation and in the effect of AA. This role might be mediated by the VP-containing neurons in PVN.
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PMID:[The role of paraventricular nucleus of hypothalamus in acupuncture analgesia in rats]. 187

The analgesic effect of electrical stimulation of the hypothalamic paraventricular nucleus (PVN) was studied. Additionally, the involvement of vasopressin and opioid peptides in this process was examined by comparing vasopressin-deficient (Brattleboro) and Long-Evans rats and by administering the opiate antagonist naloxone. Rats were chronically implanted with a stimulating electrode in the parvocellular (PVN-Pc) and magnocellular (PVN-Mg) divisions of the PVN. At least 10 days after surgery, the analgesic effects of PVN stimulation were examined in lightly anesthetized rats, using the tail-flick method, and in unanesthetized rats, using the hot-plate test. PVN stimulation produced marked analgesia in both tests. Current threshold for analgesia was lower from PVN-Pc than from PVN-Mg. Threshold did not differ significantly between Brattleboro and Long-Evans rats and was not affected by naloxone administration. The results indicate that the PVN is part of the brain's pain inhibitory system, and show that the analgesia induced by PVN stimulation is not mediated by either vasopressin or opioid peptides.
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PMID:Stimulation of the hypothalamic paraventricular nucleus produces analgesia not mediated by vasopressin or endogenous opioids. 198 39

Acute hypertensive states can produce antinociception, largely via unknown mechanisms. The aim of the present series of experiments was to examine potential hormonal and neural bases of analgesia induced by i.v. infusion of the pressor (hypertensive) agent phenylephrine. All rats were implanted with right jugular and left carotid cannulae for phenylephrine infusion and blood pressure/heart rate monitoring, respectively, and were tested approximately 24 h later in the unanesthetized state. The tail-flick test was used to measure responsivity prior to, during, and after phenylephrine infusion. Potential adrenal and pituitary contributions to phenylephrine-induced antinociception were examined, respectively, by physical disruption of adrenal blood flow and pharmacological suppression of pituitary activation. Acute block of all adrenal hormones, via closure at the time of testing of pre-implanted adrenal ligatures, did not block phenylephrine antinociception. However, pharmacological suppression of pituitary activation via pretreatment with the synthetic glucocorticoid dexamethasone abolished phenylephrine antinociception. Intriguingly, dexamethasone had no noticeable effect on urination prior to phenylephrine administration, yet only dexamethasone-treated rats exhibited copious urination during phenylephrine infusion. This suggests that the hypertensive agent phenylephrine releases vasopressin from the posterior pituitary terminals of the paraventricular hypothalamus (PVH) in a dexamethasone-suppressible manner, possibly via the known baroreceptor-nucleus tractus solitarius (NTS)-PVH link. Since (1) bilateral lesions of the spinal cord dorsolateral funiculus (DLF) were shown in the current study to abolish phenylephrine antinociception, (2) PVH is known to send vasopressinergic projections to the spinal cord via the DLF, and (3) intrathecal vasopressin produces antinociception via V1-like vasopressin receptors, the effect of an intrathecal V1 vasopressin antagonist was tested on phenylephrine-induced antinociception. The V1 vasopressin antagonist blocked phenylephrine antinociception, suggesting that phenylephrine antinociception may be mediated by a baroreceptor-NTS-PVH-DLF circuit leading to vasopressin release at spinal levels.
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PMID:Phenylephrine-induced antinociception: investigations of potential neural and endocrine bases. 227 28

Since the first paravertebral blockade was carried out by Sellheim in 1905, this method has proved effective for the isolated blockade of spinal nerves. The efficacy of preoperative intercostal blockade (ICB) in combination with neuroleptanalgesia (NLA) or Pentothal-pentazocine-N2O anesthesia (Pe-Pz) was studied (unilateral analgesia for cholecystectomy). Group 1: NLA; group 2: NLA with ICB; group 3: Pe-Pz; group 4: Pe-Pz with ICB. The analgesic requirement differed significantly between groups 1 (0.33 mg fentanyl) and 2 (0.15 mg fentanyl) and groups 3 (63.5 mg pentazocine) and 4 (31.5 mg pentazocine). There were also significant differences in circulatory responses. The maximum deviation from the initial value at the beginning of the operation in group 1 compared to group 2 was pulse rate + 28.7% vs + 2.4%, mean arterial pressure (Part) + 24.6% vs + 3.1%, and systolic pressure (Psyst) + 33% vs +/- 0%; group 3 compared to group 4: pulse rate + 16.4% vs + 3.2%, Part + 24.5% vs 0.0%, and Psyst + 26.5% vs + 196. The times of action of ICB extended from 7.54 h to 11.33 h for partial analgeisa, time to the first dose of analgesic from 12.3 h to 16.9 h (etidocaine 0.5% and 1% respectively without and with epinephrine). The mean blood levels after 100 mg bupivacaine-CO2 rose to 1.16 micrograms/ml after 5 min and reached a maximum after 15 min (1.29 micrograms/ml) as compared to 0.98 micrograms/ml after addition of ornithine-vasopressin. These values are very much higher than those after the use of bupivacaine-HCl solution. Etidocaine and bupivacaine-HCl have comparable durations of analgesia. Toxicologically, both substances can be applied safely with consideration of all pharmacological data for ICB. Of a total of 3,485 intercostal blockades, 2,775 were applied perioperatively (pre- and postoperatively); 265 were carried out for trauma patients (rib fractures) and 445 for therapeutic indications (herpes zoster neuralgia, tumor pain, costovertebral pain). In 8 blocks 10% ammonium sulfate, in 4 blocks absolute alcohol, and in 19 blocks 5% phenol were used for neurolysis. In 2 cases a marginal pneumothorax was seen, which was resorbed spontaneously (0.06%). Altogether 16,270 single intercostal nerves were blocked. Single-session intercostal blockade can be combined as unilateral analgesia with general anesthesia. This combination is characterized by stable circulatory conditions with avoidance of hypertensive reactions. The long-lasting analgesia allows early mobilization and physiotherapy both postoperatively and posttraumatically in patients with unilateral thoracic and abdominal pain.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The single intercostal block--surgical and therapeutic indications]. 264 21

Sufentanil (mean total dose 2 micrograms/kg) was compared with fentanyl (mean total dose 15 micrograms/kg) as a supplement to 60% N2O anesthesia in 30 adult patients undergoing general surgical procedures. Comparisons were made with respect to stability of hemodynamic variables (heart rate and systolic and diastolic blood pressure), changes in stress hormones (cortisol, antidiuretic hormone, epinephrine, norepinephrine, and dopamine), recovery of alertness and orientation, time to extubation, postoperative analgesia, and measures of respiratory depression (resting end-tidal carbon dioxide tension [PETCO2], CO2 response curve for minute ventilation [delta VE/delta PETCO2]). Hemodynamic variables remained stable and similar in both groups throughout the study. Plasma hormone levels remained similar to baseline in both groups until 1 h postoperatively when epinephrine levels were significantly elevated in both groups (P less than 0.05). Recovery times, including time to extubation, were similar in both groups. Patients given sufentanil had less pain 30 min postoperatively than those given fentanyl, although at 60 min postoperatively pain levels were similar in both groups. Small but significant elevations in resting PETCO2 were seen in both groups postoperatively (P less than 0.05), but postoperative delta VE/delta PETCO2 responses were significantly depressed only in patients receiving fentanyl (P less than 0.05). The results of this study demonstrate that sufentanil-N2O anesthesia is as effective as fentanyl-N2O in attenuating the hemodynamic and hormonal responses to the stress of general surgery. Because continuous intraoperative PETCO2 monitoring was not employed in this study, intraoperative hypocapnea cannot be strictly excluded as a possible influence on the postoperative measures of ventilatory drive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of sufentanil-N2O and fentanyl-N2O in patients without cardiac disease undergoing general surgery. 294 75


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