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)

Fifty patients with non-cardiac chest pain underwent 24 hour intraoesophageal pH and pressure recording and provocation tests to determine the relative value of both techniques in establishing the oesophageal origin of the chest pain. Twenty six patients (52%) had at least one positive provocation test: the acid perfusion test was positive related in 18 patients (36%), the edrophonium test in 16 patients (32%), the vasopressin test in five patients (10%), and the balloon distension test (performed in only 20 patients) in one (5%). The 24 hour pH and pressure recording correlated spontaneous chest pain attacks with abnormal motility or gastro-oesophageal reflux in 19 patients (38%). Fourteen of these patients also had at least one positive provocation test. Therefore, 24 hour pH and pressure recordings are only slightly better than a set of provocation tests in identifying the oesophagus as the cause of chest pain (10% diagnostic gain). In the case of oesophageal chest pain, however, 24 hour recording appeared to be the only way to identify the nature of the underlying oesophageal abnormality that caused the spontaneous pain attacks--for example, gastro-oesophageal reflux, motility disorders, or irritability of the oesophagus.
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PMID:Ambulatory 24 hour intraoesophageal pH and pressure recordings v provocation tests in the diagnosis of chest pain of oesophageal origin. 237 9

Surgical hypophysectomy performed in 18 cases with hormone-dependent carcinoma resulted in tumour regression in 38.8% of the cases, and pain relief in 88%. Neuroadenolysis performed 170 times on 130 cases resulted in pain relief in 94% with hormone-dependent carcinoma, and 70% with non-dependent carcinoma. The clinical investigations, following performance of neuroadenolysis, indicate suppressed pituitary function, significant increase of ACTH, thyrotropin-releasing hormone and vasopressin in the cerebrospinal fluid (CSF), delay of long latencies in somatosensory evoked potential and increased pain threshold of C-fibres. Increase of beta-endorphin in CSF was very brief. Though the exact physiological activity in pain sensation of those peptides other than endorphins still remains obscure, increase of the peptides which are mainly synthesized in the hypothalamopituitary axis, along with suppressed pituitary function, is considered to exert a long-lasting suppressive effect on the mediation and perception of cancer pain through C-fibres and the central nervous system.
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PMID:The pituitary as a target of antalgic treatment of chronic cancer pain: a possible mechanism of pain relief through pituitary neuroadenolysis. 243 39

In this study in conscious rats, we tested the hypothesis that substance P, a central pressor peptide and a potential transmitter substance of pain pathways, could be involved in the cardiovascular defense reaction that is typically associated with unpleasant sensory stimuli. The hemodynamic responses to centrally administered substance P were pharmacologically characterized. The increases in blood pressure and heart rate after intracerebroventricular injections of substance P were accompanied by mesenteric and renal vasoconstriction and hind limb vasodilation (pulsed-Doppler flow probes). The pressor and vasoconstrictor responses were attenuated by peripheral alpha 1-adrenoceptor blockade with prazosin but were not influenced by blockade of vascular vasopressin receptors with d(CH2)5Tyr(Me) arginine vasopressin (AVP). Cardiac beta 1-adrenoceptor blockade with metoprolol abolished the tachycardic and reduced the pressor responses. Substance P-induced hind limb vasodilation was not sensitive to intravenous atropine but was largely prevented by peripheral beta 2-adrenoceptor blockade with ICI 118,551. Thus, the substance P-induced pressor effects are mediated by alpha 1-adrenergic sympathetic vasoconstriction and beta 1-adrenergic cardiac stimulation, whereas the hind limb vasodilation is mainly due to beta 2-adrenergic stimulation. Substance P dose-dependently (0.01-10 micrograms i.c.v.) released oxytocin but not vasopressin or adrenocorticotropic hormone (ACTH) from the pituitary gland. High doses reduced basal ACTH levels. Together with the hemodynamic responses, a behavioral arousal reaction was observed, which included increased locomotion, grooming, scratching, and skin biting. Our results demonstrate that a neuropeptide can induce classic cardiovascular defense reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substance P induces a cardiovascular defense reaction in the rat: pharmacological characterization. 245 61

Mechanisms for the therapeutic effect of oral contraceptives in dysmenorrhea were studied by recording intrauterine pressure on the first day of menstrual bleeding in women with moderate to severe symptoms and after three weeks of oral contraceptive therapy (150 micrograms levonorgestrel + 30 micrograms ethinyl estradiol, daily). Spontaneous uterine activity and reactivity to intravenous injections of vasopressin (6 pmol/kg body weight; n = 8) or prostaglandin F2 alpha (12 nmol/kg body weight; n = 9) at the two sessions were compared. During the first recording when all women had dysmenorrhea, the uterine activity and reactivity to both agonists were pronounced. After therapy, when the women felt essentially no pain, a statistically significant decrease in spontaneous uterine activity in terms of total pressure area, frequency and amplitude of contractions was observed. The agonist injections induced less pain at the second recording, although the magnitude of responses, superimposed on the much smaller uterine activity at this time, were not significantly different from those at the first recording during dysmenorrhea. The mechanism of pain relief by oral contraception in dysmenorrhea could be a lesser impact of the decreased contractile activity on uterine blood flow, abolishing the local ischemia. A reduced uterine reactivity to agonists might also to some extent contribute to the therapeutic effect.
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PMID:Effect of an oral contraceptive in primary dysmenorrhea--changes in uterine activity and reactivity to agonists. 250 70

A review of current advances in anatomy, physiology and pharmacology of vasoactive intestinal polypeptide (VIP) is presented. VIP is a basic 28-aminoacid peptide of molecular weight 3300. Nerves immunoreactive to VIP are in the heart, lung, digestive and genitourinary tract, eye, skin, ovaries and thyroid gland. In the central nervous system VIP-ergic neurons are found primarily in telencephalic areas. Here, VIP provokes the excitation, vasodilatation and together with noradrenaline participates in the regulation of cortical energy metabolism. VIP-ergic neurons are mainly present in afferent pathways of the spinal cord with higher density in the sacral segments. Anatomic distribution of VIP-ergic neurons suggests involvement in pain transmission and integration of the sacral autonomic reflex pathways. The biologic effects of VIP in periphery are the vasodilatation, relaxation of smooth muscle and influence on exocrine glands secretion. In the endocrine system VIP stimulates the secretion of different hormones (prolaction, growth hormone, oxytocin, vasopressin, ovarial and thyroid hormones). VIP-ergic innervation is changed in some organs during the diseases of those organs. Practical exploatation of this knowledge is limited at present because effective, non-polypeptide agonists and antagonists are not available yet.
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PMID:[Vasoactive intestinal polypeptide: a potential neurotransmitter]. 257 79

The centrally induced effects of angiotensin II and substance P on the cardiovascular system and on neuronal efferent activity of the splanchnic, renal, and adrenal nerves were investigated in chronically instrumented conscious rats. The pressor responses to substance P injected into the lateral brain ventricle were accompanied by marked and short latency increases in heart rate, cardiac output, splanchnic, renal, and adrenal nerve activity, and a rise in plasma noradrenaline and adrenaline. Behaviorally, an arousal-type reaction was observed. In contrast, the pressor responses to intracerebroventricular angiotensin II were associated with initial decreases in heart rate, cardiac output, splanchnic, renal, and adrenal nerve activity, and a fall in plasma noradrenaline at the time of the maximal blood pressure increase. In some but not all animals, a second blood pressure peak associated with increases in heart rate and splanchnic nerve activity was observed after several minutes. Incomplete chronic sinoaortic baroreceptor deafferentiation prevented the angiotensin II-induced fall in heart rate but not the initial fall in splanchnic nerve activity. The decreases in splanchnic nerve activity also occurred in diabetes insipidus rats and persisted in Long Evans rats after vascular vasopressin receptor blockade with d(CH2)5AVP, despite marked reductions of the pressor responses in both groups. Peripheral alpha-adrenoceptor blockade with prazosin or ganglion blockade with hexamethonium inhibited the central angiotensin II pressor responses only in combination with vasopressin receptor blockade. On the other hand, either sympatholytic drug, alone, abolished the pressor responses in the diabetes insipidus rats. This indicates that in intact conscious rats the central pressor effects of angiotensin II are initiated by vasopressin release but become dependent on the sympathetic nervous system when vasopressin is absent or not effective. When rats were allowed to drink in response to angiotensin II, a further sharp rise in blood pressure occurred, together with increases in heart rate and splanchnic nerve activity. The results demonstrate fundamental differences in the mechanisms by which central pressor peptides can influence cardiovascular and autonomic function. It is conceivable that the distinct sympathetic response patterns to central angiotensin II and substance P receptor stimulation form part of a specific cardiovascular adjustment to the individual behavioral reactions, such as drinking, as in the case of angiotensin II, or arousal within the central processing of pain, as in the case of substance P.
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PMID:Differential effects of central angiotensin II and substance P on sympathetic nerve activity in conscious rats. Implications for cardiovascular adaptation to behavioral responses. 257 49

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

The French technique of anaesthesia by electrostimulation described in 1972 by Cara and coworkers, consists of transcranial electrostimulation by means of a high frequency current combined with administration of a neuroleptic drug, a benzodiazepine, a curare and nitrous oxide with oxygen. Fentanyl is also given by some authors. In order to assess the benefit of such electrostimulation, this study compared two randomized groups of ten patients, scheduled for abdominal and pelvic surgery. Both groups received the same drugs (i.e. droperidol, flunitrazepam, pancuronium and nitrous oxide with oxygen), whereas patients in group I were also submitted to electrostimulation. This study describes and discusses the clinical behaviour of patients and the hormonal reactions before, during and after surgery. In both groups, operative conditions were satisfactory. Recovery and onset of spontaneous ventilation were rapid and no patient had an unpleasant recall of the operation itself. However, most of them complained of postoperative pain. Electrostimulation did not reduce the quantity of drugs required during and after surgery. In both groups, circulatory activity was significantly increased. In group I, the arterial pressure and the heart rate were significantly higher than in group II during and after surgery. The hormonal reactions showed that in both groups adrenocorticotrophic hormone, growth hormone and antidiuretic hormone increased during surgery. Adrenocorticotrophic hormone concentration was higher in group I during the operation. The serum levels of cortisol decreased before surgery in group I and rose in both groups during and after laparotomy; prolactin increased before surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Electro-drug anesthesia. Clinical and hormonal effects of transcranial electrostimulation]. 299 Feb 60

Thirty two male patients undergoing coronary bypass surgery were given low (group A, 0.01 mg/kg bw) and high dose (group B, 0.035 mg/kg bw) fentanyl anaesthesia. Haemodynamic and hormone responses were investigated from the beginning of anaesthesia until extracorporeal circulation (ECC) (group A: n = 16; group B: n = 16). Significant changes in haemodynamics occurred only in group A including an increase in heart rate (36%) and systolic arterial pressure (21%). Plasma vasopressin (ADH) levels rose significantly in both groups after the beginning or surgical procedure which was markedly less pronounced in patients with high fentanyl (group B). In group A (low dose) a second dose of fentanyl was given after sternotomy, which was followed by a significant decrease in ADH (80% from previous value). No significant variations could be demonstrated in plasma levels of cortisol, ACTH, and human growth hormone (HGH). The data stress the importance of plasma-vasopressin-levels in determining the endocrine stress response following trauma and operation. On the other hand there was a lack of correlation between trauma and pain and frequently reported patterns of the endocrine-metabolic stress response.
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PMID:[Significance of endocrine parameters of stress]. 299 19


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