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PubMed2002

Closed-form expressions for level-averaged electron spin relaxation times outside the Zeeman limit: application to paramagnetic NMR relaxation.

Paramagnetic enhancement of NMR relaxation (NMR-PRE) depends on thermal relaxation of the electron spin system. Most previous analyses of experimental NMR-PRE data have relied on Bloembergen--Morgan (B--M) theory to describe the magnetic field dependence of electron spin relaxation in liquid samples. However, B--M theory assumes a Zeeman-limit situation and is not physically appropriate to the common case of S > or = 1 transition metal ions which possess a permanent zero-field splitting (zfs) that is comparable to or larger than the Zeeman splitting. Theory has been needed which (1) includes the effects of the zfs interaction, thus providing a realistic description of the magnetic field dependence of the NMR-PRE outside the Zeeman limit, and (2) describes electron spin relaxation phenomena at a comparable level of complexity to that of B--M theory, i.e., with two magnetic field-dependent electron spin relaxation times, tau(S1) and tau(S2), defined in the laboratory coordinate frame. Theory of this kind is developed. Expressions derived in a previous study (R. R. Sharp and L. L. Lohr, J. Chem. Phys. 115, 5005 (2001).) for level-specific relaxation rates have been averaged over spin eigenstates to give level-averaged quantities, tau(S1,2). This kind of averaging leads to a great simplification in the mathematical form of the results. Simple zfs-limit molecular-frame and laboratory-frame expressions are given for electron spin S=1, 3/2, 2, and 5/2. General expressions, valid for S > or = 1 and for arbitrary magnitudes of the Zeeman and zfs energies, are derived for level-averaged electron spin relaxation times defined in both the laboratory- and the molecule-fixed coordinate frames. The new theory coincides with B--M theory in the Zeeman limit.

Journal Article↗
PubMed1982

Mechanics of myocardial relaxation: application of a model to isometric and isotonic relaxation of rat myocardium.

Using a simple model for cardiac muscle relaxation which takes into account muscle length, activation, elasticity and a rate constant for the decay of activation, we are able to use easily measured mechanical parameters to assess the state of the cardiac relaxing system. In isolated trabeculae carneae from the left ventricle of the rat, performing physiologically sequenced contractions, observations have been made (1) at varying preloads and afterloads, (2) with changes in temperature from 23 degrees to 33 degrees C, (3) with changes in bath Ca2+ concentration and (4) with the addition of isoproterenol. During isometric relaxation, the slope (SIM) of the curve relating maximum rate of decline of force (-dF/dtmax) to end-systolic muscle length is load-independent and sensitive to interventions which directly affect the cardiac relaxing system (e.g., temperature, isoproterenol); it is only slightly sensitive to bath calcium concentration. During isotonic relaxation, the maximum velocity of lengthening (+dL/dtmax) is in negative linear proportion to muscle shortening at a given preload, the slope (SIT) of the curve relating +dL/dtmax to end-systolic length is sensitive to the interventions which directly affect the cardiac relaxing system but insensitive to calcium-mediated inotropic interventions. The model provides a theoretical basis for the use of SIM and SIT as measures of the relaxation process.

Animals↗
PubMed1995

Spin-lattice relaxation and magnetization transfer in intracranial tumors in vivo: effects of Gd-DTPA on relaxation parameters.

Spin-lattice relaxation time T1 and relaxation parameters in magnetization transfer (MT) imaging were measured in 11 intracranial tumors before and after injection of Gd-DTPA at 0.1 T by using the inversion recovery method and the saturation transfer technique, respectively. Preinjection T1 relaxation times of the tumors were longer than those of white matter, but after Gd-enhancement the relaxation times of most tumors were in the same range as those of white matter. Gd-DTPA shortened the apparent relaxation time in the presence of off-resonance saturation pulse (T1a) due to marked shortening of the relaxation time of mobile water (T1w). Gd-DTPA decreased the magnetization transfer contrast (MTC) but did not influence on the magnetization transfer rate (Rwm). The parameters MTC and Rwm differed clearly between Gd-enhanced tumors and normal brain, whereas the relaxation time T1a was in many Gd-enhanced tumors in the same range as in normal brain.

Brain Neoplasms↗
PubMed2005

Electromyographic assessment of the activity of the masticatory using the agonist contract-antagonist relax technique (AC) and contract-relax technique (CR).

Proprioceptive neuromuscular facilitation (PNF) techniques are a group of therapeutic procedures that may be used to cause relaxation of muscles. Studies have found controversial results when applying these techniques. The aim of the present study was to evaluate the effectiveness of masticatory muscle relaxation through the use of the contract-relax technique (CR) when compared with the agonist contract-antagonist relax technique (AC). A convenience sample of 30 students was recruited for this study. The CR and the AC techniques were applied to the subjects in order to cause relaxation of the masticatory muscles. Electromyography activity of all muscles was registered. Two way ANOVA with repeated measures analysis demonstrated that both the AC technique and the CR technique did not decrease the EMG activity of masticatory muscles (P>0.05). Instead, both techniques caused an increase in electromyographic activity of the masticatory muscles. Based on the results obtained from this study, both the CR and the AC techniques were not effective in causing relaxation of the masticatory muscles. The purported physiological mechanisms of PNF techniques, which stated that they act through reciprocal inhibition and autogenic inhibition causing muscular relaxation, are not supported by this study.

Adult↗
PubMed2006

The molecular origins of nonlinear response in solute energy relaxation: the example of high-energy rotational relaxation.

A key step in solution-phase chemical reactions is often the removal of excess internal energy from the product. Yet, the way one typically studies this process is to follow the relaxation of a solute that has been excited into some distribution of excited states quite different from that produced by any reaction of interest. That the effects of these different excitations can frequently be ignored is a consequence of the near universality of linear-response behavior, the idea that relaxation dynamics is determined by the solvent fluctuations (which may not be all that different for different kinds of solute excitation). Nonetheless, there are some clear examples of linear-response breakdowns seen in solute relaxation, including a recent theoretical and experimental study of rapidly rotating diatomics in liquids. In this paper we use this rotational relaxation example to carry out a theoretical exploration of the conditions that lead to linear-response failure. Some features common to all of the linear-response breakdowns studied to date, including our example, are that the initial solute preparation is far from equilibrium, that the subsequent relaxation promotes a significant rearrangement of the liquid structure, and that the nonequilibrium response is nonstationary. However, we show that none of these phenomena is enough to guarantee a nonlinear response. One also needs a sufficient separation between the solute time scale and that of the solvent geometry evolution. We illustrate these points by demonstrating precisely how our relaxation rate is tied to our liquid-structural evolution, how we can quantitatively account for the initial nonstationarity of our effective rotational friction, and how one can tune our rotational relaxation into and out of linear response.

Journal Article↗
PubMed1992

Bradykinin-induced, N omega-nitro-L-arginine-insensitive endothelium-dependent relaxation of porcine coronary arteries is not mediated by bioassayable relaxing substances.

The effect of the arginine analogue, N omega-nitro-L-arginine (L-NNA) was studied on bradykinin-induced relaxation in porcine coronary arteries. In the presence of indomethacin (3 x 10(-6) M) and captopril (10(-6) M), treatment with L-NNA (10(-4) M) had no effect on the bradykinin-induced (10(-10)-10(-7) M) relaxations in strips contracted with U-46619. In contrast to the findings in organ chamber experiments, bradykinin-induced release of endothelium-derived relaxing factor(s) (EDRFs) was abolished after 45 min of treatment of perfused porcine coronary artery segments with L-NNA (10(-4) M) in a superfusion bioassay system. These results show that, in addition to the release of nitric oxide, endothelium-dependent relaxation of porcine coronary arteries to bradykinin involves an alternative mechanism(s), which accounts for the relaxation in the presence of L-NNA. Since the release of a relaxing mediator could not be detected from L-NNA-treated porcine coronary artery segments under bioassay conditions, it is postulated that either no diffusible factor(s) is involved in the L-NNA-insensitive endothelium-dependent relaxation, or it is mediated by an extremely labile endothelium-derived substance(s).

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Lysophosphatidylcholine-induced vascular relaxation and production of cGMP are mediated by endothelium-derived relaxing factor.

Endothelial cells produce powerful vasorelaxant substances, among them an endothelium-derived relaxing factor that is believed to be nitric oxide. It relaxes vascular smooth muscle via activation of guanylate cyclase and a subsequent rise in cyclic GMP level. Lysophosphatidylcholine is a potent endothelium-dependent vascular smooth muscle relaxant. Its action, similar to that of endothelium-derived relaxing factor, mediates an increase of cGMP in smooth muscle cells. The experiments reported here demonstrate that inhibitors of nitric oxide formation, such as N-omega-nitro-L-arginine and its methyl ester, inhibit relaxation and cyclic GMP formation by lysophosphatidylcholine in bovine pulmonary artery strips with intact endothelium in a dose-dependent manner. N-omega-Nitro-D-arginine methyl ester does not inhibit relaxation; L-arginine, but not D-arginine, reverses the effect of N-omega-nitro-L-arginine and its methyl ester. It is concluded that lysophosphatidylcholine-induced endothelium-dependent vasorelaxation is endothelium-derived relaxing factor-mediated.

Animals↗
PubMed1993

Inhibition by sulfhydryl compounds of vascular relaxation induced by nitric oxide and endothelium-derived relaxing factor.

On rings of rabbit thoracic aorta precontracted with phenylephrine, L-cysteine (Cys) and dithiothreitol (DTT) (1-100 microM), but not glutathione (GSH), produced dose-dependent augmentation of contraction in endothelium-intact, but not in endothelium-denuded rings. The augmentation appeared to be due to inhibition of basally released endothelium-derived relaxing factor (EDRF), and was abolished by pretreatment with superoxide dismutase (SOD, 15 U/ml). At a high dose (1 mM), Cys and GSH produced transient, and DTT produced sustained endothelium-independent relaxation, not influenced by SOD. Cys and DTT (10 microM), but not GSH, produced a small but significant inhibition of acetylcholine-induced endothelium-dependent relaxation, and this inhibition was prevented by SOD. In a perfusion-bioassay system in which EDRF was released by acetylcholine from endothelium of a perfused segment of rabbit aorta, Cys and DTT (20 microM), but not GSH, infused into the perfusate between the segment and an endothelium-denuded bioassay ring, partially inhibited relaxation by the EDRF, but not when SOD was present. In organ chamber experiments, the large transient relaxation of endothelium-denuded rings produced by 75 nM nitric oxide (NO) was partially inhibited in a concentration-dependent manner by Cys, DTT and GSH (0.1-100 microM). Moderate relaxation by 15 nM NO was almost completely inhibited by each compound at 10 microM. The order of potency was Cys > DTT > GSH. Cystine, glutathione disulfide and alanine did not inhibit. Inhibition of NO-induced relaxation was largely attenuated by SOD.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed2004

Progressive muscle relaxation, yoga stretching, and ABC relaxation theory.

This study compared the psychological effects of progressive muscle relaxation (PMR) and yoga stretching (hatha) exercises. Forty participants were randomly divided into two groups and taught PMR or yoga stretching exercises. Both groups practiced once a week for five weeks and were given the Smith Relaxation States Inventory before and after each session. As hypothesized, practitioners of PMR displayed higher levels of relaxation states (R-States) Physical Relaxation and Disengagement at Week 4 and higher levels of Mental Quiet and Joy as a posttraining aftereffect at Week 5. Contrary to what was hypothesized, groups did not display different levels of R-States Energized or Aware. Results suggest the value of supplementing traditional somatic conceptualizations of relaxation with the psychological approach embodied in ABC relaxation theory. Clinical and research implications are discussed.

Adaptation, Psychological↗
PubMed1985

Characteristics of subjects experiencing relaxation and relaxation-induced anxiety.

The purpose of this study was to determine the psychological characteristics of people who show a paradoxical increase in anxiety during relaxation training. Thirty-eight subjects who reported being anxious 50% or more of the day, were divided into two groups based on their scores on the Tellegen and Atkinson absorption scale. Half of each group was given progressive muscle relaxation training; the other half a meditational procedure. Separate regression analyses for each group showed that during meditational procedure 32% of the change in heart rate and 42% of the change in a subjective response measured by changes in the position of an "anxiety lever", could be predicted by the subjects' scores on the Tellegen absorption scale, the cognitive component of the state version of the Cognitive-Somatic Anxiety Questionnaire, and other psychological tests. Similarly, 49% of the heart rate changes during progressive muscle relaxation training were predicted by these and other measures. The multiple R for anxiety lever during progressive muscle relaxation training was not significant, however. Three of 18 meditational procedure subjects and two of 20 progressive muscle relaxation subjects showed increased heart rates during relaxation training. Two of the three meditational procedure subjects also showed an increase in subjective tension as measured by the anxiety lever.

Adolescent↗
PubMed1989

Vascular relaxation mediated by hydroxylamines and oximes: their conversion to nitrites and mechanism of endothelium dependent vascular relaxation.

Hydroxylamines (R-NHOH) and oximes (R = NOH) relax rat aortic rings independent of the presence of the endothelium. The relaxation is inhibited by methylene blue, an inhibitor of soluble guanylate cyclase and by hemoglobin, an inhibitor of the endothelium dependent relaxing factor (EDRF). Both the oximes and hydroxylamines generate NO/NO2- ions on treatment with iodine in glacial acetic acid. However, there is no correlation between relaxation and NO/NO2- formation. Compared to hydroxylamines, the oximes are less potent relaxing agents and not efficiently converted to NO/NO2- ions. We suggest that endothelium dependent relaxation is associated with a hydroxylamine like compound and is not directly related to NO.

Animals↗
PubMed1997

Influence of cytochrome P-450 inhibitors on endothelium-dependent nitro-L-arginine-resistant relaxation and cromakalim-induced relaxation in rat mesenteric arteries.

In several blood vessels, endothelium-dependent vasorelaxation is in part mediated by an endothelium-derived hyperpolarizing factor (EDHF), the nature of which is as yet unknown. However, some evidence suggests that EDHF might be a cytochrome P-450-dependent monooxygenase metabolite of arachidonic acid. By using isometric tension measurements on rat main mesenteric arteries, the influence of four structurally and mechanistically different cytochrome P-450 inhibitors (proadifen, miconazole, 1-amino-benzotriazole, and 17-octadecynoic acid) was investigated on relaxations elicited by EDHF, assessed as the nitro-L-arginine-resistant component of acetylcholine-induced relaxation, and on relaxations provoked by the endothelium-independent potassium channel opener cromakalim. Proadifen (30 microM) inhibited the EDHF- as well as the cromakalim-induced relaxation, but not that elicited by nitroprusside. Also miconazole (30 microM) inhibited both the EDHF and the cromakalim-induced relaxation. On the other hand, 17-octadecynoic acid (5 microM) had no influence, and 1-aminobenzotriazole (1 mM) even potentiated EDHF- and cromakalim-induced relaxations. We conclude that the EDHF, released from the rat mesenteric artery by acetylcholine, is unlikely to be a cytochrome P-450-dependent monooxygenase metabolite of arachidonic acid and that proadifen and miconazole interfere with the action of cromakalim.

Acetylcholine↗
PubMed1987

Selective inhibition by gossypol of endothelium-dependent relaxations augments relaxations to glyceryl trinitrate in rabbit coeliac artery.

1 Acetylcholine, substance P, prostaglandin E1 and the nitrovasodilator glyceryl trinitrate induced concentration-dependent relaxations of endothelium-intact strips of rabbit coeliac artery precontracted with noradrenaline. 2 Endothelium-denuded strip preparations contracted to acetylcholine and showed no response to substance P. The relaxant response to prostaglandin E1 was unimpaired after removal of endothelium, whereas the response to glyceryl trinitrate was increased. 3 A 20 min exposure of endothelium-intact strips to gossypol, an irreversible inhibitor of the production and/or release of endothelium-derived relaxing factor, abolished vasodilatation in response to the endothelium-dependent agents acetylcholine and substance P, did not change relaxations to prostaglandin E1, but significantly enhanced relaxations in response to glyceryl trinitrate. 4 In view of the assumed common mechanism of action of endothelium-derived relaxing factor and nitrovasodilators, these results suggest an interference of the two active principles at the level of the vascular smooth muscle cell.

Acetylcholine↗
PubMed1990

Recurrent tension headache in adolescents treated with self-help relaxation training and a muscle relaxant drug.

Forty-eight adolescents suffering from recurrent tension headache participated in a controlled trial conducted in a high school setting. During the first treatment phase self-help relaxation training was compared with a waiting-list group. Following this phase a pharmacological regimen consisting of a muscle relaxant (chlormezanone) and placebo was superimposed on relaxation therapy in a double-blind crossover design. Each treatment phase encompassed a 5-week period. In addition to the evaluation of headache complaints, psychological distress among students was measured with respect to their experience of somatic complaints, depressive, anxiety and stress symptoms. Although self-help relaxation training significantly decreased the severity and annoyance of adolescents' headache besides their somatic complaints, the clinical improvement of headache was modest. The addition of chlormezanone did not help those who were nonresponders to self-help relaxation training. Finally, a set of pretreatment variables consisting of baseline headache severity and annoyance, experience of anxiety and daily life stress among adolescents could predict outcome of self-help relaxation therapy.

Adolescent↗
PubMed1998

Monkey corpus cavernosum relaxation mediated by NO and other relaxing factor derived from nerves.

Isolated monkey corpus cavernosum muscle strips contracted with prostaglandin F2 alpha and treated with prazosin responded to transmural electrical stimulation with frequency-related relaxations that were abolished by tetrodotoxin. The nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA) significantly attenuated but did not abolish the response; L-arginine reversed the inhibition. The neurogenic relaxation was not influenced in the strips treated with atropine or calcitonin gene-related peptide (CGRP)-(8-37), a CGRP-receptor antagonist, and those desensitized to vasoactive intestinal polypeptide (VIP) or pituitary adenylate cyclase-activating polypeptide (PACAP). Nerve fibers containing NADPH diaphorase were histochemically demonstrated in cavernous tissues. The relaxant response resistant to the NO synthase inhibitor was abolished by high K+ and tetrabutylammonium but was unaffected by glibenclamide, charybdotoxin, apamin, ouabain, SKF-525a, a cytochrome P-450 inhibitor, and oxyhemoglobin. It is concluded that neurogenic relaxations of monkey corpus cavernosum muscle is associated partly with NO released as a neurotransmitter and that other relaxing factor(s) possibly responsible for K+ channel opening also participates; however, the type of K+ channel involved is not determined. Acetylcholine, VIP, CGRP, PACAP, and the Na+ pump do not seem to be involved in the neurogenic relaxation.

Animals↗
PubMed1987

Nature of endothelium-derived relaxing factor: are there two relaxing mediators?

The role of arachidonic acid in forming endothelium-derived relaxing factor remains controversial. This controversy may be explained if more than one factor exists. To test this hypothesis, the effects of various inhibitors of arachidonic acid metabolism were studied. The perfusate from canine femoral arteries with endothelium was bioassayed with coronary artery rings without endothelium. Treatment of the perfused segment (but not the bioassay ring) with inhibitors of phospholipase A2 (quinacrine) or cytochrome P450 (metyrapone) had no effect on the basal relaxing activity of the effluent; treatment with the inhibitor of lipoxygenase, nordihydroguaiaretic acid, significantly depressed it. With increasing concentrations of acetylcholine, a biphasic concentration-relaxation curve was obtained; the enzyme inhibitors depressed or prevented the first phase but did not affect the second phase. Infusion of arachidonic acid or soybean lipoxidase directly on the bioassay ring did not cause relaxation; together, they evoked concentration-dependent relaxations. These data suggest that acetylcholine can trigger the release of two chemically different relaxing mediators from the endothelium of the canine femoral artery. One factor may be a product of lipoxygenase (or epoxigenase). The second factor is not a metabolite of arachidonic acid and may be released under basal conditions. The existence of two (or more) chemically different endothelium-derived mediators may help to explain the controversial data regarding the nature of the factor(s).

Acetylcholine↗
PubMed1993

[Comparative study of the psychophysiologic relaxation effects of an optic-acoustic mind machine with relaxation music].

The present study was designed to test the effectiveness of an optical-acoustic mind machine (brain machine) in inducing relaxation. The mind machine used in this study stimulates the user with flickers of light and pulsating sounds. During the treatment the stimulation decreases from 10 to 2 hertz and increases again at half time. No other relaxation inducing effects were used. Sixteen subjects received two or three sessions of instruction with the mind machine. Afterwards the parameters listed below were continuously recorded during one session with the mind machine and one session with the presentation of relaxing environmental sounds, which was conducted one week later: Frontal EMG, SCL on the left hand, heart rate. Pre- and posttreatment samples of saliva were collected and assessed for salivary IgA (S-IgA) and salivary cortisol (S-cortisol). Changes in the subjects' self-report were measured with a bipolar adjective list. ANCOVA with repeated measures revealed a decrease for all electrophysiological parameters during the mind machine session. S-cortisol concentration decreases as S-IgA increases. The mind machine made the subjects feel warmer and calmer. The results of this with in design revealed no reliable differences between the mind machine and the relaxing sounds of nature on the physiological and self-esteem parameters. The significantly greater decrease of SCL during the mind machine session was due to the elevated baseline of this parameter. The results lead to the conclusion that the mind machine seems to be useful in inducing relaxation, but is no more effective than the relaxing nature sounds used in this study.

Acoustic Stimulation↗
PubMed2001

Explanation of the crystallization rate of amorphous nifedipine and phenobarbital from their molecular mobility as measured by (13)C nuclear magnetic resonance relaxation time and the relaxation time obtained from the heating rate dependence of the glass transition temperature.

To gain further insight into the effect of molecular mobility on the crystallization rate of amorphous drugs, the mean relaxation times of amorphous nifedipine and phenobarbital were calculated based on the Adam-Gibbs-Vogel (AGV) equation, using the parameters D, T(0), and T(f), derived from the heating rate dependence of the glass transition temperature (T(g)) of the amorphous drugs and heat capacity of the drugs in the amorphous and crystalline states. These relaxation times were compared with the crystallization rate of amorphous nifedipine and phenobarbital reported previously. The spin-lattice relaxation time (T(1)) and the spin-lattice relaxation time in the rotating frame (T(1rho)) of phenobarbital and nifedipine carbons were also determined. The temperature dependence of the crystallization rate of nifedipine and phenobarbital on the T(g) was coincident with that of the mean relaxation time calculated according to the AGV equation within experimental error, indicating that the crystallization of nifedipine and phenobarbital is largely correlated with molecular mobility at the temperatures studied. A (13)C nuclear magnetic resonance relaxation study indicated that the molecular motion of nifedipine and phenobarbital in the mid-kHz frequency range became significant at temperatures higher than T(g)-20 and T(g), respectively.

Calcium Channel Blockers↗