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At least 883 records · Page 49Linked to original sources
PubMed2001

Intravenous anesthetics inhibit nonadrenergic noncholinergic lower esophageal sphincter relaxation via nitric oxide-cyclic guanosine monophosphate pathway modulation in rabbits.

BACKGROUND: Nonadrenergic noncholinergic (NANC) nerves have important roles in the regulation of the lower esophageal sphincter (LES) motility and function. The effects of thiopental, ketamine, and midazolam on NANC LES relaxation were investigated. METHODS: The isometric tension of circular muscle strips from Japanese White rabbits was examined. The NANC relaxation was induced by KCl (30 mM) in the presence of atropine (3 x 10(-6) M) and guanethidine (3 x 10(-6) M). The modifications of the NANC and sodium nitroprusside (SNP; 10(-5) M)-induced relaxation by the anesthetics were examined. The content of 3',5'-cyclic guanosine monophosphate (cGMP) was measured by radioimmunoassay. RESULTS: The KCl-induced relaxation was abolished by pretreating with tetrodotoxin (10(-6) M). The NANC relaxation was inhibited in the presence of N(G)-nitro-L-arginine (L-NNA; 3 x 10(-5) M), methylene blue (10(-6) M), apamin (10(-7) M), and glibenclamide (10(-5) M). The SNP-induced relaxation was inhibited by methylene blue but was not affected by tetrodotoxin, L-NNA, apamin, or glibenclamide. Ketamine (EC50 = 8.8 x 10(-5) M) and midazolam (EC50 = 4.8 x 10(-6) M) suppressed the NANC response in a concentration-dependent manner, leaving SNP-induced response unchanged. Thiopental altered neither of the relaxations. cGMP content was decreased in the presence of ketamine and midazolam. CONCLUSION: The NANC relaxation was mediated by nitric oxide and by low-conductance calcium- and adenosine triphosphate-sensitive potassium channels of smooth muscle. The modulation of the nitric oxide-cGMP pathway was related, at least in part, to the inhibitory actions of ketamine and midazolam on the NANC LES relaxation.

Anesthetics, Intravenous↗
PubMed1987

Effect of in vivo nitroglycerin therapy on endothelium-dependent and independent vascular relaxation and cyclic GMP accumulation in rat aorta.

Vascular relaxation by the organic (nitroglycerin) and inorganic (sodium nitroprusside) nitrovasodilators and the endothelium-dependent vasodilators (acetylcholine and histamine) has been associated with cyclic GMP accumulation. Tolerance to vasodilation by nitroglycerin commonly occurs following prolonged exposure to nitroglycerin. This study investigates the effects of in vivo nitroglycerin therapy on vascular relaxation and cyclic GMP accumulation induced by the nitrovasodilators and the endothelium-dependent vasodilators. Rats were injected with nitroglycerin or the propylene glycol diluent control for 4-7 days. Thoracic aortas from the nitroglycerin-treated rats were 750-fold less sensitive to the relaxant effects of nitroglycerin. In contrast, these aortas were only threefold less sensitive to the relaxant effects of sodium nitroprusside, while the maximum relaxation to acetylcholine and histamine was depressed by 50 and 41%, respectively. Desensitization to relaxation was associated with reduced cyclic GMP elevations to all the vasodilators. Relaxation to 8-bromo cyclic GMP, dibutyryl cyclic AMP, or diltiazem was unaffected by nitroglycerin therapy. Tolerance was also associated with an increased sensitivity to the contractile effects of low concentrations of norepinephrine. This increased sensitivity to norepinephrine was associated with a decrease in cyclic GMP levels. The present results suggest that: (1) desensitization to nitroglycerin, sodium nitroprusside, acetylcholine, and histamine by nitroglycerin therapy may be at the level of cyclic GMP accumulation; (2) cyclic GMP is the common mediator of relaxation induced by the nitro- and endothelium-dependent vasodilators; (3) the mechanisms involved in the activation of guanylate cyclase and relaxation by sodium nitroprusside, acetylcholine, and histamine are probably different than those of nitroglycerin; and (4) cyclic GMP may be acting as a physiological negative feedback signal in agonist-induced contraction.

Acetylcholine↗
PubMed1991

Dual mechanism of the relaxing effect of nicorandil by stimulation of cyclic GMP formation and by hyperpolarization.

In addition to previous results from our laboratory showing that nicorandil relaxed vascular smooth muscle by increasing cyclic GMP levels, it was shown to activate K-channels as well, an effect that also leads to relaxation. In the present study, we attempted to differentiate quantitatively between these two effects in isolated bovine coronary artery strips with simultaneous isotonic measurement of length and radioimmunoassay (RIA) determination of cyclic GMP. When the strips were contracted by the thromboxane A2 analogue U 46619 (1 microM) with 10 microM methylene blue added, nicorandil produced 30-50% relaxation without significant changes in cyclic GMP. When in U 46619-contracted strips the hyperpolarizing effect of nicorandil was suppressed by increasing extracellular K+ to 80.4 mM (30-fold), nicorandil caused only 52% relaxation, whereas cyclic GMP increases were not significantly suppressed. Quantitative separation of both mechanisms of relaxation by nicorandil was further achieved through calculation of the cyclic GMP-mediated component from a correlation between increases in cyclic GMP and percentage of relaxation as produced by nicorandil under conditions of inhibited hyperpolarization, i.e., in strips contracted with 1 microM U 46619 or 26.8 mM K+ (10-fold) and exposed to either 30-fold K+ or 10 mM Ba2+. Under both conditions, similar correlations between cyclic GMP and relaxation were obtained. Because U 46619, in addition to its contractile effect, partially antagonized the relaxation by nicorandil without changing cyclic GMP, the correlation was corrected for this effect and indicated a participation of cyclic GMP in the overall relaxant response of approximately 30-40% at low and less than or equal to 80-90% at high concentrations of nicorandil.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Effects of some inorganic divalent cations and protein kinase C inhibitors on endothelium-dependent relaxation in rat isolated aorta and mesenteric arteries.

The effects of nitrendipine and several metal ions possessing Ca2+ antagonistic activity were examined on acetylcholine (ACh) and histamine-induced endothelium-dependent relaxations in norepinephrine (NE)-precontracted rat aortic rings and perfused mesenteric arteries. Nitrendipine (1 nM) profoundly attenuated ACh and histamine-induced relaxations of perfused mesenteric arteries but was ineffective against either agonist in aorta. The transition metal ions Co2+, Mn2+, and Ni2+, but not the nontransition ions (Cd2+, Sn2+, and Zn2+), markedly inhibited ACh and histamine relaxations in the aorta, whereas all metal ions antagonized KCl contractions. At the highest concentration devoid of effect on arterial perfusion pressure, none of the transition metal ions altered endothelium-dependent relaxations in the mesenteric arteries. Endothelium-independent relaxations induced by sodium nitroprusside (SNP) were attenuated by Mn2+ but not by Co2+ or Ni2+. Calmidazolium or W-7 inhibited ACh- and histamine-induced relaxations in both aorta and mesenteric arteries, whereas staurosporine and H-7 were ineffective against aortic relaxations; in mesenteric arteries, staurosporine but not H-7 attenuated both endothelium-dependent and -independent relaxations. We conclude (a) that the transition metal ions most likely inhibit endothelium-derived relaxing factor (EDRF) (NO) release in the aorta through endothelial receptor-operated Ca2+ channels; (b) that the effects of nitrendipine (shared by nifedipine) in mesenteric arteries result from an interaction with a site that may have structural similarities with, but is distinct from, the L-type Ca2+ channel; and (c) that the inhibitory effects of the calmodulin antagonists may reflect an action on endothelial NO synthase.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1995

Involvement of nitroxidergic and noradrenergic nerves in the relaxation of dog and monkey temporal veins.

We determined involvement of nitric oxide (NO) derived from perivascular nerve in venous relaxation. In helical strips of dog superficial temporal veins contracted with prostaglandin F2 alpha (PGF2 alpha) nicotine produced a contraction, which was reversed to a relaxation by prazosin. The relaxation was partially attenuated by timolol or metoprolol. The residual relaxation was not influenced by treatment with atropine or indomethacin and by endothelium denudation but was abolished by NG-nitro-L-arginine (L-NA), a NO synthase inhibitor, and hexamethonium. L- but not D-arginine reversed the inhibition induced by L-NA. Relaxations induced by NO were not influenced by L-NA. Similar results were also obtained in relaxations induced by transmural electrical stimulation that were sensitive to tetrodotoxin (TTX). In the monkey venous strips, relaxations induced by nicotine under treatment with prazosin were reduced by timolol. The relaxation observed with combined treatment with alpha- and beta-antagonists was abolished by L-NA, and L-arginine restored the response. The presence of nerve fibers containing NO synthase immunoreactivity or NADPH diaphorase in the adventitia of dog and monkey veins was determined histologically. The findings so far obtained strongly suggest the presence of perivascular nerves that mediate venodilation via a release of NO. Contractions of the temporal vein appear to be mediated by norepinephrine (NE) released from adrenergic nerves that stimulates alpha 1-adrenoceptors, whereas relaxations are mediated by neurogenic NE, acting possibly on the beta 1-adrenoceptor subtype, in addition to NO derived from nerves.

Adrenergic alpha-Antagonists↗
PubMed1997

Endothelium-dependent relaxation is not uniformly impaired in chronic heart failure.

Abnormalities of vasomotor tone are characteristic of heart failure. This study was designed to assess the effects of chronic heart failure on endothelium-dependent relaxation in both large conduit arteries and small resistance vessels and to determine whether or not impaired nitric oxide (NO) production is involved. Segments of pulmonary artery (PA), abdominal aorta (AA), and small mesenteric artery (MA) were harvested from rats with heart failure resulting from coronary artery ligation and from sham-operated controls. Organ-bath experiments done in the presence of indomethacin to avoid the influence of vasodilatory prostanoids demonstrated that relaxation to acetylcholine (ACh) was impaired in the PA but not the AA or MA of the group with heart failure. Endothelium-independent relaxation to nitroglycerin was not significantly affected by the development of heart failure. Constriction to prostaglandin (PG) F(2alpha) was enhanced in PA but not in AA or MA segments. Preincubation with N(omega)-nitro-L-arginine (NNA) to inhibit the production of NO increased baseline force in vessels from all three beds, but the effect was greatest in the PA. Although relaxation to ACh was significantly diminished by NNA in the PA, it was not completely abolished. Furthermore, ACh-mediated relaxation in the presence of NAA was still impaired in the group with heart failure compared with the sham-operated control group. NNA had only mild effects on ACh-mediated relaxation in MA. These results demonstrate that (a) the mediators of endothelium-dependent relaxation may vary throughout the arterial circulation, (b) the contribution of NO to endothelium-dependent relaxation is substantial in PA and minimal in mesenteric resistance vessels, (c) endothelium-dependent relaxation is not uniformly impaired throughout the arterial bed by the development of heart failure, and (d) although a defect in NO production may account for enchanced vasoconstriction seen in response to PGF(2alpha), it does not account for the diminished vasodilatory response to ACh in this experimental model of heart failure.

Acetylcholine↗
PubMed2000

Genistein potentiates the relaxation induced by beta1- and beta2-adrenoceptor activation in rat aortic rings.

In rat aortic rings, genistein, an inhibitor of tyrosine kinase, but not daidzein, an inactive analogue of genistein, potentiated the relaxation induced by isoproterenol. Atenolol, a beta1-adrenoceptor antagonist, or ICI-118,551, a beta2-adrenoceptor antagonist, inhibited the relaxation induced by isoproterenol. The potentiating effect of genistein on the relaxation induced by isoproterenol in the presence of ICI-118,551 was apparently greater than that in the presence of atenolol. In the presence of ICI-118,551, theophylline, an inhibitor of cyclic adenosine monophosphate (cAMP)-dependent phosphodiesterase (cAMP-PDE), markedly inhibited the potentiating effect of genistein on the isoproterenol-induced relaxation, whereas in the presence of atenolol, theophylline only partly inhibited the potentiating effect of genistein. The relaxation induced by forskolin, an activator of adenylyl cyclase, was potentiated by genistein or theophylline. In the presence of theophylline, the relaxation induced by forskolin was not further affected by genistein. Genistein also inhibited the activities of cAMP-PDE. In the presence of atenolol, but not ICI-118,551, iberiotoxin, an inhibitor of Ca-activated K channels, inhibited the relaxation induced by isoproterenol and the potentiating effect of genistein. In the presence of atenolol, quinacrine, an inhibitor of phospholipase A2, and metyrapone, an inhibitor of P-450 enzymes, but not alpha-naphthoflavone, an inhibitor of P-450 enzymes, indomethacin, a cyclooxygenase inhibitor, or AA861, a 5-lipoxygenase inhibitor, inhibited the potentiating effect of genistein. These results suggest that the potentiation of the beta1-adrenoceptor-induced relaxation by activation of genistein may mostly be due to inhibition of cAMP-PDE activities. In addition, the potentiation of the relaxation induced by activation of beta2-adrenoceptors by genistein may be related to the inhibition of arachidonic acid metabolism and cAMP-PDE activities.

Adrenergic beta-Agonists↗
PubMed2001

Relaxant effects of isoproterenol and selective beta3-adrenoceptor agonists on normal, low compliant and hyperreflexic human bladders.

PURPOSE: We compared the relaxant effects of the stimulation of beta-adrenoceptors with isoproterenol and of drugs selective for beta-adrenoceptor subtypes in detrusor preparations from patients with normal and neurogenic bladder, respectively. MATERIALS AND METHODS: We studied in vitro preparations of a cystometrically normal, low compliant and hyperreflexic bladder from 45, 26 and 7 patients, respectively. RESULTS: Isoproterenol relaxed concentration dependently and with the same potency as detrusor preparations obtained from normal and neurogenic bladders. In 37 normal detrusor, 25 low compliant and 7 hyperreflexic cases pD2 values were 6.36, 6. 25 and 6.38, respectively. Maximal relaxation did not differ significantly among the 3 groups (about 80% of 10-5 M. forskolin induced relaxation). Neither the beta1-/beta2-adrenoceptor agonist dobutamine nor the beta2-adrenoceptor agonist procaterol produced any significant relaxation of preparations from the 3 groups at a concentration of up to 10-5 M. At a concentration of 10-4 M. the preparations were relaxed but neither of these effects reached a maximum. BRL37344A and CL316243, selective beta3-adrenoceptor agonists and CGP-12177A (a selective beta3-adrenoceptor partial agonist and beta1-/beta2-adrenoceptor antagonist) relaxed detrusor preparations from the normal, low compliant and hyperreflexic groups when applied at concentrations greater than 10-6 M. For each agonist the pD2 value did not differ significantly among the 3 groups. CONCLUSIONS: beta-adrenoceptor stimulation is an effective way of relaxing the human detrusor and the effect is similar in normal and neurogenic bladders. A major portion of the relaxant effect of isoproterenol is mediated via beta3-adrenoceptor stimulation. Clinical trials may reveal whether this method is useful for treating bladder overactivity.

Adrenergic beta-Agonists↗
PubMed1982

Behavioral treatment of high blood pressure II. Acute and sustained effects of relaxation and systolic blood pressure biofeedback.

The effects on blood pressure of regular patient and professional monitoring of blood pressure, extensive patient-involved assessment of results, relaxation, and systolic blood pressure biofeedback are analyzed by comparisons of data from two 3-month treatment periods with results from a 1-month baseline period and by comparisons among control and treatment groups. Ninety borderline hypertensive patients completed the treatments. Major findings are: A Acute effects; 1) Both relaxation and systolic blood pressure biofeedback lowered blood pressure acutely. 2) Improvement in performance of relaxation and biofeedback with practice showed that they are learned skills. 3) Acutely, relaxation and biofeedback were equally effective for lowering systolic blood pressure, but relaxation lowered diastolic blood pressure more. B. Long-term effects; 1) Blood pressure declined for at least 6 months with regular monitoring and patient-involved assessment. 2) The greatest lowering of blood pressure by behavioral intervention occurred during periods when pressures tended to be highest. 3) A combination of relaxation and biofeedback, with biofeedback preceding relaxation, was better than either used alone and slightly, but not significantly, better than relaxation preceding biofeedback. 4) The long-term effects of biofeedback were slightly greater than those of relaxation. A staged, incremental behavioral treatment of borderline hypertension is proposed.

Behavior Therapy↗
PubMedDate not supplied

Effect of relaxation therapy on cardiac events after myocardial infarction: a 5-year follow-up study.

BACKGROUND: Evidence suggests that breathing and relaxation therapy may influence cardiac events in persons after acute myocardial infarction (MI). The authors studied the effects of breathing and relaxation therapy on rates of cardiac events and cost effectiveness in past MI patients. METHODS: Patients (n = 156) were chosen randomly to receive either exercise training plus relaxation therapy (relaxation group; n = 76) or exercise training only (control group; n = 80). The occurrence of major cardiac events and cardiac rehospitalizations in the two treatment groups was compared. RESULTS: At 5-year follow-up, 12 cardiac deaths had occurred, 5 in the relaxation group and 7 in the control group, reinfarction occurred in 10 and 12 patients, and cardiac surgery was performed in 2 and 11, respectively. In total, 15 (20%) and 26 (33%) patients, respectively, experienced at least one cardiac event (odds ratio [OR] for the relaxation group: 0.55, 95% confidence interval [CI] 0.29-1.05; adjusted for risk factors OR 0.52, 95% CI 0.28-0.99). Regarding all cardiac rehospitalizations, in the relaxation group, 30 patients (39%) had experienced 52 cardiac events, for which the patients were hospitalized for a total of 476 days. In the control group, 38 patients (48%) had experienced 78 cardiac events (OR 0.72; 95% CI 0.38-1.36), comprising 719 days of hospitalization. The total number of hospitalizations was reduced by 31% as a result of relaxation instruction. CONCLUSIONS: In the long-term, the disease course after myocardial infarction is influenced favorably by giving relaxation therapy in addition to cardiac rehabilitation. The extra costs of the therapy are compensated by a decrease in hospitalization for cardiac problems.

Angina, Unstable↗
PubMed2003

Muscle relaxants for nonspecific low back pain: a systematic review within the framework of the cochrane collaboration.

STUDY DESIGN: A systematic review of randomized and/or double-blinded controlled trials. SUMMARY OF BACKGROUND DATA: The use of muscle relaxants in the management of nonspecific low back pain is controversial. It is not clear if they are effective, and concerns have been raised about the potential adverse effects involved. OBJECTIVES: The aim of this review was to determine if muscle relaxants are effective in the treatment of nonspecific low back pain. METHODS: A computer-assisted search of the Cochrane Library (Issue 2, 2002), MEDLINE (1966 up to October 2001), and EMBASE (1988 up to October 2001) was carried out. These databases were searched using the algorithm recommended by the Cochrane Back Review Group. References cited in the identified articles and other relevant literature were screened. Randomized and/or double-blinded controlled trials, involving patients diagnosed with nonspecific low back pain, treated with muscle relaxants as monotherapy or in combination with other therapeutic methods, were included for review. Two reviewers independently carried out the methodologic quality assessment and data extraction of the trials. The analysis comprised not only a quantitative analysis (statistical pooling) but also a qualitative analysis ("best evidence synthesis"). This involved the appraisal of the strength of evidence for various conclusions using a rating system based on the quality and outcomes of the studies included. Evidence was classified as "strong," "moderate," "limited," "conflicting," or "no" evidence. RESULTS: Thirty trials met the inclusion criteria. Twenty-three trials (77%) were of high quality; 24 trials (80%) were on acute low back pain. Four trials studied benzodiazepines, 11 nonbenzodiazepines, and 2 antispasticity muscle relaxants in comparison with placebo. Results showed that there is strong evidence that any of these muscle relaxants are more effective than placebo for patients with acute low back pain on short-term pain relief. The pooled relative risk for nonbenzodiazepines versus placebo after 2 to 4 days was 0.80 (95% confidence interval: 0.71 to 0.89) for pain relief and 0.49 (95% confidence interval: 0.25 to 0.95) for global efficacy. Adverse events, however, with a relative risk of 1.50 (95% confidence interval: 1.14 to 1.98) were significantly more prevalent in patients receiving muscle relaxants and especially the central nervous system adverse effects (relative risk 2.04; 95% confidence interval: 1.23 to 3.37). The various muscle relaxants were found to be similar in performance. CONCLUSIONS: Muscle relaxants are effective in the management of nonspecific low back pain, but the adverse effects require that they be used with caution. Trials are needed that evaluate if muscle relaxants are more effective than analgesics or nonsteroidal anti-inflammatory drugs.

Controlled Clinical Trials as Topic↗
PubMed2006

Disturbed paraspinal reflex following prolonged flexion-relaxation and recovery.

STUDY DESIGN: Repeated measures experimental study of the effect of flexion-relaxation, recovery, and gender on paraspinal reflex dynamics. OBJECTIVE: To determine the effect of prolonged flexion-relaxation and recovery time on reflex behavior in human subjects. SUMMARY OF BACKGROUND DATA: Prolonged spinal flexion has been shown to disturb the paraspinal reflex activity in both animals and human beings. Laxity in passive tissues of the spine from flexion strain may contribute to desensitization of mechanoreceptors. Animal studies indicate that recovery of reflexes may take up to several hours. Little is known about human paraspinal reflex behavior following flexion tasks or the recovery of reflex behavior following the flexion tasks. METHODS: A total of 25 subjects performed static flexion-relaxation tasks. Paraspinal muscle reflexes were recorded before and immediately after flexion-relaxation and after a recovery period. Reflexes were quantified from systems identification analyses of electromyographic response in relation to pseudorandom force disturbances applied to the trunk. RESULTS: Trunk angle measured during flexion-relaxation postures was significantly higher following static flexion-relaxation tasks (P < 0.001), indicating creep deformation of passive supporting structures in the trunk. Reflex response was diminished following flexion-relaxation (P < 0.029) and failed to recover to baseline levels during 16 minutes of recovery. CONCLUSION: Reduced reflex may indicate that the spine is less stable following prolonged flexion-relaxation and, therefore, susceptible to injury. The absence of recovery in reflex after a substantial time indicates that increased low back pain risk from flexion-relaxation may persist after the end of the flexion task.

Adult↗
PubMed2005

Relaxant effects of beta-adrenergic agonists on porcine and human detrusor muscle.

AIM: Relaxant effects of different beta-adrenoceptor agonists on porcine and human detrusor were examined. Thus, the beta-adrenoceptor subtype mainly responsible for relaxation in the detrusor muscle of pigs was characterized. Additionally, different effects of several beta-agonists in both species were shown. METHODS: Experiments were performed on muscle strips of porcine and human detrusor suspended in a tissue bath. The relaxant effects of the non-selective beta-agonist isoprenaline, the selective beta2-agonists procaterol, salbutamol and the selective beta3-agonists BRL 37344, CL 316 243 and CGP 12177 on potassium-induced contraction were investigated. The inhibitory effect of different substances on the maximum contraction and the rank order of potency for endogenous catecholamines was determined in pigs. Furthermore, concentration-relaxation curves were performed for pigs and humans. RESULTS: Pigs: In the pre-treatment experiments isoprenaline and procaterol showed similar effects. The concentration-response experiments showed that the maximum relaxation induced by procaterol and salbutamol was more than 90%, not significantly different from isoprenaline, whereas the maximum relaxations of CL 316 243, BRL 37344 and CGP 12177 amounted to 68, 70 or 30%, respectively. Rank order of potencies was isoprenaline > or = adrenaline > noradrenaline. Humans: Isoprenaline, procaterol, salbutamol and CL 316 243 showed a maximum relaxation of 80, 41, 24 and 35% and pD2 values of 6.24, 5.65, 5.48 and 5.55, respectively. CONCLUSION: Beta2-receptors play a main functional role in mediating relaxation of porcine detrusor. Selective beta2- and beta3-agonists similarly relax the human detrusor. Effects were smaller compared with the pig.

Adrenergic beta-Agonists↗
PubMed2004

Systematic relaxation to relieve postoperative pain.

BACKGROUND: Unrelieved pain after surgery can lead to complications, prolonged hospital stay, and delayed recovery. Because of side effects from opioids and differences in response, it is important to use non-pharmacological methods in addition to analgesics to decrease patient discomfort and anxiety. AIMS: We examined the effects of a systematic method of relaxing the body on the sensory and affective components of postoperative pain, anxiety, and opioid intake after initial ambulation. DESIGN: A randomized controlled trial with relaxation and control groups was used. METHOD: The convenience sample of 102 adults underwent abdominal surgery at a large hospital in Thailand. Systematic relaxation was used for 15 minutes during recovery from the first ambulation after surgery. Pain was measured with 100 mm Visual Analogue Sensation and Distress of Pain Scales before and after the intervention. State anxiety was measured before surgery and after the intervention; opioid intake was recorded 6 hours later. RESULTS: The relaxation group had less post-test sensation and distress of pain (26 and 25 mm less, respectively) than the control group (P = 0.001). Relaxation did not result in significantly less anxiety or 6-hour opioid intake. However, group differences in state anxiety were in the expected direction and fewer participants in the relaxation group requested opioids. Nearly all reported that systematic relaxation reduced their pain and increased their sense of control. CONCLUSION: Substantial reductions in the sensation and distress of pain were found when postoperative patients used systematic relaxation. Although tested in Thailand, we recommend that nurses in other countries try systematic relaxation with postoperative patients, in addition to analgesic medication, measuring pain scores and asking about cultural acceptance.

Abdomen↗
PubMed2006

Involvement of M(2) muscarinic receptors in relaxant response of circular muscle of mouse gastric antrum.

Our previous study showed that atropine significantly inhibited the sustained relaxation induced by electrical field stimulation (EFS) in the circular muscle strips prepared from the mouse antrum, and that pituitary adenylate cyclase activating peptide (PACAP) partially mediated the sustained relaxation. The muscarinic receptor subtype associated with the sustained relaxation was examined in the present study by using each muscarinic receptor subtype of knockout (KO) mice. EFS-induced sustained relaxation in the antrum prepared from M(2) receptor KO mice was significantly less than that of wild-type mice. Atropine failed to inhibit this relaxation. On the other hand, similar sustained relaxation and inhibitory effects of atropine to those of wild-type mice were observed in M(1), M(3) and M(4) receptor KO mice. Exogenously added PACAP-27 relaxed the antral strips of wild-type and M(2) receptor KO mice to a similar extent. Immunohistochemical study revealed that M(2) receptor immunoreactivity was localized with PACAP-immunoreactivity in enteric neurons within the antrum of wild-type mice. In contrast, atropine did not affect the EFS-induced sustained relaxation in the gastric fundus. These results suggest that M(2) receptors modulate the sustained relaxation, probably through the regulation of PACAP release, in the mouse antrum.

Animals↗
PubMed1993

Mediators of nicotine-induced relaxations of the rat gastric fundus.

1. Relaxations of strips of rat gastric fundus were elicited with nicotine (100 mumol/L), nitric oxide (NO; 30 mumol/L), sodium nitroprusside (SNP; 100 nmol/L) and vasoactive intestinal polypeptide (VIP; 1 nmol/L). 2. Methylene blue (30 mumol/L), an inhibitor of soluble guanylate cyclase, reduced relaxations elicited by NO and nicotine, but not those elicited by VIP. 3. Chymotrypsin (1 U/mL) abolished VIP-induced relaxations and reduced nicotine-induced relaxations, but had no effect on SNP-induced relaxations. 4. NG-nitro-L-arginine methyl ester (L-NAME; 100 mumol/L), an inhibitor of NO synthase, reduced relaxations elicited by nicotine, but not those elicited by SNP or VIP. 5. When nicotine-induced relaxations had been reduced by either L-NAME or chymotrypsin, the addition of the other agent produced a greater reduction. However, the relaxations were not abolished. 6. Nicotine-induced relaxations were abolished by tetrodotoxin (1 mumol/L) or hexamethonium (100 mumol/L), indicating that they were due to activation of neuronal nicotinic receptors. Their reduction by methylene blue and L-NAME indicates that an NO-like mediator was involved. Their reduction by chymotrypsin indicates that a VIP-like peptide was involved. However, since they were not abolished by a combination of L-NAME and chymotrypsin, it appears that at least one more as yet unidentified mediator may be involved.

Animals↗
PubMed1994

Differences in endothelium-dependent relaxation in various arteries from Watanabe heritable hyperlipidaemic rabbits with increasing age.

1. Endothelium-dependent relaxation in response to acetylcholine (ACh) and the calcium ionophore A23187 was examined in aorta, coronary, basilar and renal arteries isolated from Watanabe heritable hyperlipidaemic (WHHL) rabbits of 2, 6 and 12 months of age, with normolipidaemic heterozygous WHHL rabbits as controls. 2. In the rings of WHHL rabbit aortae and coronary arteries preconstricted with vasoconstrictors, endothelium-dependent relaxation in response to ACh was attenuated with age compared to the heterozygous WHHL rabbits. A significant negative correlation was found between the total cholesterol content and the relaxation response to ACh in the aortae or coronary arteries from 6 and 12 month old WHHL rabbits. 3. In the rings of basilar arteries, endothelium-dependent relaxations to ACh were not modified with age. Similarly, in the rings of renal arteries, the relaxation response to ACh was not changed with age, but in the 6 and 12 month preparations, after the age of 6 months, a contraction following the relaxation appeared at higher concentrations of ACh (10(-7) to 10(-6) mol/L). The contraction was endothelium-dependent and inhibited by indomethacin. 4. A23187-induced endothelium-dependent relaxations were also markedly attenuated in the aorta and significantly in the coronary artery with age. 5. Endothelium-independent relaxation to sodium nitroprusside was not changed in all arteries from WHHL rabbits of different ages. 6. These findings indicate that in the aorta and coronary artery of the WHHL rabbit, the endothelium-dependent relaxation to ACh and A23187 becomes impaired with increasing age (i.e., with the progression of cholesterol deposition in the arterial wall) but is preserved in the basilar and renal artery.

Acetylcholine↗
PubMed1995

Nitric oxide and cyclic GMP formation following relaxant nerve stimulation in isolated human corpus cavernosum.

OBJECTIVE: To investigate further the role of the nitric oxide (NO)-cyclic GMP pathway as the mediator of relaxant neurotransmission in human corpus cavernosum and to establish whether impaired activity of this pathway contributes to the pathophysiology of impotence. PATIENTS AND METHODS: Samples of cavernosal tissue were obtained from 59 men undergoing penile operations. The controls comprised four men with penile carcinoma and 17 with Peyronie's disease. Of the impotent men, 35 had clinical evidence of penile vascular disease on pre-operative investigation, whilst three had non-vascular impotence. Each biopsy was divided into two strips which were then suspended under tension in organ bath chambers. The relaxant innervation of one strip of each pair was stimulated electrically whilst the other strip was left unstimulated. The formation of NO and cyclic GMP was calculated by comparing their respective tissue content in the stimulated and unstimulated strips. RESULTS: Overall, stimulation of the relaxant innervation produced significant increases in the tissue content of both NO and cyclic GMP. Incubation with an inhibitor of NO biosynthesis abolished the mechanical relaxant response and the formation of both NO and cyclic GMP. The magnitude of relaxant response and the formation of NO was diminished in tissue from men with vascular impotence compared to controls. The increase in cyclic GMP content was similar in both these groups. Relaxant response, NO formation and cyclic GMP formation in tissue from men with non-vascular impotence was similar to controls. CONCLUSIONS: This study provides further evidence that the NO-cyclic GMP pathway acts as the mediator of nerve-evoked smooth muscle relaxation in human corpus cavernosum. Diminished NO formation following relaxant nerve stimulation may account for impaired relaxant responses found in tissue from men with vascular impotence and may contribute to the cause of their erectile dysfunction.

Adult↗