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PubMed2001

Zen meditation and ABC relaxation theory: an exploration of relaxation states, beliefs, dispositions, and motivations.

This study is an attempt to rigorously map the psychological effects of Zen meditation among experienced practitioners. Fifty-nine Zen meditators with at least six years of experience practiced an hour of traditional Zazen seated meditation. A control group of 24 college students spent 60 min silently reading popular magazines. Before relaxation, all participants took the Smith Relaxation States Inventory (SRSI), the Smith Relaxation Dispositions/Motivations Inventory (SRD/MI), and the Smith Relaxation Beliefs Inventory (SRBI). After practice, participants again took the SRSI. Analyses revealed that meditators are less likely to believe in God, more likely to believe in Inner Wisdom, and more likely to display the relaxation dispositions Mental Quiet, Mental Relaxation, and Timeless/Boundless/Infinite. Pre- and postsession analyses revealed that meditators showed greater increments in the relaxation states Mental Quiet, Love and Thankfulness, and Prayerfulness, as well as reduced Worry. Results support Smith's ABC Relaxation Theory.

Buddhism↗
PubMed2005

Relaxation of canine corporal smooth muscle relaxation by ginsenoside saponin Rg3 is independent from eNOS activation.

It has been reported that nitric oxide (NO) is involved in the relaxation mechanism of ginsenoside saponin in various smooth muscle in experimental animals. Although ginsenoside Rg(3) showed both endothelium-dependent and -independent component relaxation in vascular smooth muscle, the action mechanism of the relaxation of corporal muscle is not clear. We, thus, investigated the relaxation mechanism of ginsenoside Rg(3) using isolated canine corpus cavernosum. Ginsenoside Rg(3) concentration-dependently relaxed the canine corpus cavernosum that had been contracted by phenylephrine (PE), in which IC(50) was 1.68 x 10(-5) g/ml. Ginsenoside Rg(3) significantly (P < 0.05) potentiated acetylcholine (ACh)-induced relaxation in endothelium intact corpus cavernosum. Methylene blue (MB) but not N(omega)-nitro-L-arginine methylester (L-NAME) or ODQ (1H-[1,2,4]oxadiazol-[4,3-]quinoxsalin-1-one) modified the dose-response curve of ginsenoside Rg(3). Ginsenoside Rg(3) also significantly potentiated relaxation response to UV light in the presence of streptozotocin (STZ), which was almost completely (P < 0.01) blocked by ODQ. Ginsenoside Rg(3) concentration-dependently inhibited corporal phosphodiesterases (PDE), which resulted in increase of cyclic adenosine monophosphate (cAMP) as well as cyclic guanosine monophosphate (cGMP) contents in corporal smooth muscles. MB inhibited the accumulation of cGMP but not cAMP by ginsenoside Rg(3). These results indicate that mechanism responsible for the relaxation by ginsenoside Rg(3) is not by stimulating endothelial nitric oxide synthase (eNOS) of the canine corporal smooth muscle but by increasing cyclic nucleotide levels through PDE inhibition.

Animals↗
PubMed1992

Isometric squeeze relaxation (progressive relaxation) vs meditation: absorption and focusing as predictors of state effects.

We taught isometric squeeze relaxation (a variant of progressive relaxation) or meditation to 52 anxious subjects (16 men, 36 women). For meditation, pretreatment high absorption correlated with reductions in state cognitive and somatic anxiety as well as increments in state focusing. For isometric squeeze relaxation, pretreatment low state focusing correlated with reductions in somatic anxiety and increments in focusing. Results suggest that isometric squeeze relaxation (and progressive relaxation) may be more appropriate for individuals who have difficulty focusing, and meditation for those who already possess well-developed relaxation skills at a trait level. The results appear more consistent with Smith's cognitive-behavioral model of relaxation than with Benson's relaxation response or Davidson and Schwartz's specific effects models.

Adult↗
PubMed1992

Highly potent beta-2 sympathomimetics convert to less potent partial agonists as relaxants of guinea pig tracheae maximally contracted by carbachol. Comparison of relaxation with receptor binding and adenylate cyclase stimulation.

Beta-adrenergic agonists are among to the most potent dilators of airway smooth muscle available and act as functional antagonists of a variety of contractile stimuli. In order to elucidate their loss of relaxant potency in dependence on antagonistic stimuli tracheal relaxation by the beta-2 sympathomimetics (+/-)-salbutamol (+/-)-fenoterol, and (+/-)-formoterol was compared to (-)-isoprenaline in guinea pig tracheae partially and maximally precontracted by carbachol. In partially precontracted tracheae, salbutamol, fenoterol and formoterol exerted maximum relaxation with low EC50 of 20, 5.6 and 0.29 nmol/l, respectively. In maximally precontracted tracheae, however, salbutamol, fenoterol and formoterol were only partial agonists for relaxation with different intrinsic activities (0.62, 0.62 and 0.77, respectively) and increased EC50 (120, 50 and 3.6 nmol/l, respectively). A reduction of relaxant potency by increased muscarinic stimuli was also observed for beta-1 adrenoceptors stimulated by (-)-noradrenaline after blockade of beta-2 adrenoceptors. In order to investigate if the reduced relaxant potency of beta-2 sympathomimetics was caused by a reduced spare receptor capacity or a reduced intrinsic activity for stimulation of adenylate cyclase (AC), we performed experiments in membranes from lung and tracheal cells. In radioligand binding, beta-2 sympathomimetics recognized the high-affinity state (57%) of the beta-2 adrenoceptor with a lower effectiveness than (-)-isoprenaline, which exhibited a 100-fold higher affinity for high over low-affinity states. Dissociation constants for the low-affinity state matched EC50 for AC stimulation. Intrinsic activities (%) for AC stimulation were significantly lower for salbutamol (67%), fenoterol (67%) and formoterol (89%) than for (-)-isoprenaline (100%), indicating that the reduced relaxation potency of the beta-2 sympathomimetics of maximally precontracted tracheae is caused by a reduced intrinsic activity for AC stimulation. It might be speculated that formoterol could improve drug therapy of asthma due to its high binding affinity and its high intrinsic activity for relaxation.

Adenylyl Cyclases↗
PubMed1983

Endothelium-dependent relaxation of rabbit aorta. II. Inhibition of relaxation stimulated by methacholine and A23187 with antagonists of arachidonic acid metabolism.

Methacholine, A23187 and arachidonic acid (AA) relax segments of rabbit thoracic aorta via mechanisms which are dependent on an intact endothelium. Relaxation stimulated by AA was previously found by us to be antagonized by eicosatetraynoic acid and nordihydroguaiaretic acid, but not indomethacin. The purpose of the present investigation was to determine the effects of several inhibitors of AA metabolism on endothelium-dependent relaxation stimulated by methacholine and A23187 in rings of rabbit thoracic aorta. Relaxation in response to methacholine and A23187 was: 1) not affected by indomethacin pretreatment (20 microM, 30 min); 2) inhibited by 50 microM eicosatetraynoic acid pretreatment, 53 and 33%, respectively; and 3) inhibited in a dose-dependent manner by nordihydroguaiaretic acid (10-50 microM) with complete inhibition occurring after 25 and 50 microM pretreatment, respectively. Methacholine-induced relaxation was completely blocked by 10 microM quinacrine (QUIN), whereas A23187-stimulated responses were not significantly affected. QUIN (10 microM) antagonized methacholine-stimulated contractile responses in a noncompetitive manner in rings devoid of endothelium. QUIN may interfere with activation via muscarinic receptors, complicating interpretation of its inhibitory effects. Eicosatetraynoic acid (50 microM), nordihydroguairetic acid (50 microM) and QUIN (10 microM) do not exert significant inhibitory effects at the level of smooth muscle relaxation mechanisms as isoproterenol-induced relaxation was resistant to inhibition by these agents. We conclude that methacholine and A23187 relax rabbit aorta by mechanisms which require intact endothelium and involve noncyclooxygenase metabolites of AA.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed2000

Relationship between the crystallization rates of amorphous nifedipine, phenobarbital, and flopropione, and their molecular mobility as measured by their enthalpy relaxation and (1)H NMR relaxation times.

Isothermal crystallization of amorphous nifedipine, phenobarbital, and flopropione was studied at temperatures above and below their glass transition temperatures (T(g)). A sharp decrease in the crystallization rate with decreasing temperature was observed for phenobarbital and flopropione, such that no crystallization was observed at temperatures 20-30 degrees C lower than their T(g) within ordinary experimental time periods. In contrast, the crystallization rate of nifedipine decreased moderately with decreasing temperature, and considerable crystallization was observed at 40 degrees C below its T(g) within 4 months. The molecular mobility of these amorphous drugs was assessed by enthalpy relaxation and (1)H-NMR relaxation measurements. The enthalpy relaxation time of nifedipine was smaller than that of phenobarbital or flopropinone at the same T - T(g) values, suggesting higher molecular mobility of nifedipine. The spin-lattice relaxation time in the rotating frame (T(1rho)) decreased markedly at temperature above T(g). The slope of the Arrhenius type plot of the T(1rho) for nifedipine protons changed at about 10 degrees C below the T(g), whereas the slope for phenobarbital protons became discontinuous at about 10 degrees C above the T(g). Even at temperatures below its T(g), the spin-spin relaxation process of nifedipine could be described by the sum of its Gaussian relaxation, which is characteristic of solid protons, and its Lorentzian relaxation, which is characteristic of protons with higher mobility. In contrast, no Lorentzian relaxation was observed for phenobarbital or flopropione at temperatures below their T(g). These results also suggest that nifedipine has higher molecular mobility than phenobarbital and flopropione at temperatures below T(g). The faster crystallization of nifedipine than that of phenobarbital or flopropione observed at temperatures below its T(g) may be partly ascribed to its higher molecular mobility at these temperatures.

Crystallization↗
PubMed1992

Formoterol, fenoterol, and salbutamol as partial agonists for relaxation of maximally contracted guinea pig tracheae: comparison of relaxation with receptor binding.

In severe asthma attacks beta 2-sympathomimetics lose part of their therapeutic efficiency. To elucidate this loss of efficiency in an experimental model we compared the relaxant potency of salbutamol (SAL), fenoterol (FEN), formoterol (FOR), and (-)-isoprenaline (ISO) in guinea pig tracheae partially and maximally precontracted by 0.1 and 60 mumol/L carbachol, respectively. In partially precontracted tracheae the beta 2-sympathomimetics exerted maximum relaxation in comparison with ISO and low EC50S (nmol/L) for relaxation (SAL, 20; FEN, 5.6; FOR, 0.28; and ISO, 2.5). In maximally precontracted tracheae, however, the beta 2-sympathomimetics were only partial agonists for relaxation with reduced intrinsic activities (%) in comparison to ISO (SAL, 59%; FEN, 61%; FOR, 76%) and significantly increased EC50S (nmol/L) for relaxation (SAL, 130; FEN, 57; FOR, 3.0; ISO, 37). To investigate if the high relaxant potency of FOR is correlated with a higher binding affinity and/or a higher intrinsic activity for adenylate cyclase stimulation than for FEN and SAL, we performed experiments in receptor membranes from guinea pig lung. Binding competition of SAL, FEN, and FOR with [3H]ICI 118,551 for lung beta 2-adrenoceptors yielded dissociation constants (KD) of 320 (SAL), 120 (FEN), and 7.6 (FOR) nmol/L, which exhibited the same ranking as EC50S for relaxation. Concentrations of SAL, FEN, and FOR equivalent to 100 KD of the respective dissociation constants stimulated beta 2-adrenoceptor-coupled adenylate cyclase with different intrinsic activities (%) incomparison to ISO (SAL, 61%; FEN, 63%; FOR, 89%) matching intrinsic activities for relaxation. From these experiments it may be concluded that FOR might improve drug therapy of severe asthma not only due to its long mode of action discovered in clinical studies but also due to its high intrinsic activity and receptor affinity.

Adenylyl Cyclases↗
PubMed2005

Do theories of the glass transition, in which the structural relaxation time does not define the dispersion of the structural relaxation, need revision?

Upon decreasing temperature or increasing pressure, a noncrystallizing liquid will vitrify; that is, the structural relaxation time, taualpha, becomes so long that the system cannot attain an equilibrium configuration in the available time. Theories, including the well-known free volume and configurational entropy models, explain the glass transition by invoking a single quantity that governs the structural relaxation time. The dispersion of the structural relaxation (i.e., the structural relaxation function) is either not addressed or is derived as a parallel consequence (or afterthought) and thus is independent of taualpha. In these models the time dependence of the relaxation bears no fundamental relationship to the value of taualpha or other dynamic properties. Such approaches appear to be incompatible with a general experimental fact recently discovered in glass-formers: for a given material at a fixed value of taualpha, the dispersion is constant, independent of thermodynamic conditions (T and P); that is, the shape of the alpha-relaxation function depends only on the relaxation time. If derived independently of taualpha, it is an unlikely result that the dispersion of the structural relaxation would be uniquely defined by taualpha.

Journal Article↗
PubMed2005

A study of molecular vibrational relaxation mechanism in condensed phase based upon mixed quantum-classical molecular dynamics. II. Noncollisional mechanism for the relaxation of a polar solute in supercritical water.

Mixed quantum-classical molecular dynamics method has been applied to vibrational relaxation of a hydrophilic model NO in supercritical water at various densities along an isotherm above the critical temperature. The relaxation rate was determined based on Fermi's golden rule at each state point and showed an inverse S-shaped curve as a function of bulk density. The hydration number was also calculated as a function of bulk density based on the calculated radial distribution function, which showed a good correlation with the relaxation rate. Change of the survival probability of the solute vibrational state was analyzed as a function of time together with the trajectory of the solvent water and the interaction with it. We will show that the solvent molecule resides near the solute molecule for a while and the solvent contributes to the relaxation by the random-noiselike Coulombic interaction only when it stays near the solute. After the solvent leaves the solute, it shows no contribution to the relaxation. The relaxation mechanism for this system is significantly different from the collisional one found for a nonpolar solute in nonpolar solvent in Paper I. Then, the relaxation rate is determined, on average, by the hydration number or local density of the solvent. Thus, the density dependence of the relaxation rate for the polar solute in supercritical water is apparently similar to that found for the nonpolar solute in nonpolar solvent, although the molecular process is quite different from each other.

Journal Article↗
PubMed2006

Evidence against alpha-adrenoceptors mediating relaxation in rat thoracic aortae: alpha-agonists relaxation depends on interaction with alpha-adrenoceptors.

In rat aorta, the presence of functional alpha(2)-adrenoceptors (alpha(2)-AR) was investigated in ring preparations preconstricted with alpha(1)-adrenergic and non- alpha(1)-adrenergic agonists. Particularly, the hypothetical interference of alpha(2)-AR agonists with alpha(1)-AR-mediated vasoconstriction was evaluated. Relaxant and contractile responses to alpha(2)-AR agonists were obtained. In endothelium-intact and endothelium-denuded aortic rings preconstricted with phenylephrine (1 x 10(-6) m), the imidazoline derivatives, clonidine and UK14304, induced relaxations with similar order of potencies (-log EC(50)) and maxima relaxant effects respectively. Pretreatment with the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) had no effect on the relaxant responses to clonidine and UK14304. In phenylephrine-constricted rings with endothelium, relaxations to clonidine and UK 14304 were not antagonized by the selective alpha(2)-AR antagonist, rauwolscine (< or =1 x 10(-6) m). Clonidine and UK 14304 induced only contractions on endothelium-intact and endothelium-denuded aortic rings contracted with prostaglandin F(2alpha) (3 x 10(-7) m). Moreover, clonidine and UK 14304-induced relaxation of endothelium-denuded arteries precontracted with methoxamine but not with serotonin. Finally, the concentration-contraction curves to clonidine and UK 14304 in endothelium-denuded aortic rings were significantly shifted to the right by the alpha(1D)-AR selective antagonist, BMY 7378, and rauwolscine. The pA(2) and pK(B) values for BMY 7378 and rauwolscine, respectively, against endothelium-independent actions of clonidine and UK 14304 were characteristic of an effect on the alpha(1D)-AR. The other selective alpha(2)-AR agonist tested BHT 933 (an azepine derivative), lacks considerable relaxant and contractile effects in rat aorta. The results provide no evidence for the presence of functional alpha(2)-AR in rat aorta. Respectively, the relaxant and contractile effects of the imidazoline derivatives, clonidine and UK 14304, may be due to an adjustable (in relation to the agonist-dependent active state of the alpha(1)-AR), inhibitory and excitatory, interaction with alpha(1)-ARs.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Endothelium-dependent relaxation of canine basilar arteries. Part 1: Difference between acetylcholine- and A23187-induced relaxation and involvement of lipoxygenase metabolite(s).

Vascular responses to acetylcholine (ACh) and the calcium ionophore A23187 were studied in rings of canine basilar arteries. In preparations that were precontracted to a stable plateau by 3 X 10(-6) M prostaglandin F2 alpha (PGF2 alpha), 10(-9) to 10(-7) M A23187 elicited significant relaxation of the basilar arteries if the endothelium was intact. Judging from histologic findings, the ability of a ring to relax in this manner is due to the presence of the endothelium. The same concentration of A23187 did not relax vascular tissues in which the endothelium was purposely disrupted. Although 10(-7) to 10(-3) M ACh did not sufficiently produce endothelium-dependent relaxation of canine basilar artery rings, ACh in the same concentration did produce significant relaxation in canine femoral rings. Our results suggest that the sensitivity of the muscarinic receptor of cerebral arteries appears to be appreciably different from that of peripheral (femoral) arteries. Pretreatment with 1.5 X 10(-5) M indomethacin, a cyclooxygenase inhibitor, potentiated the contractile responses produced by PGF2 alpha in intact rings. Preincubation with the lipoxygenase inhibitors nordihydroguaiaretic acid at (NDGA) at 1.5 X 10(-5) M or AA861 at 10(-5) M prevented A23187-induced relaxation. The same concentration of NDGA and AA861 did not affect endothelium-independent relaxation induced by glyceryl trinitrate. We suggest that endothelium-dependent relaxation of the canine basilar artery by A23187 may be mediated by noncyclooxygenase metabolite(s).

Acetylcholine↗
PubMedDate not supplied

When does relaxation actually begin? The early phases of relaxation.

Exact timing of relaxation within the cardiac cycle was carried out by aid of polygrams consisting of epicardial segmental length curves, contractile force, left ventricular, left atrial and aortic pressures, indirect carotid curves, apex cardiogram, their derivatives and ECG reference tracings in the open-chest dog heart. The relaxation starts in late systole before aortic valve closure, at the nadir of the epicardial segmental length curve and at the climax of the contractile force curve. Onset of relaxation is indicated by the late systolic knee of the left ventricular pressure curve and, by the apex cardiogram as well as by the start of the downstroke of the negative phase on their first derivatives. The earliest phase of relaxation, from its beginning to the isovolumic relaxation period (IVRP), is proposed to be named "auxobaric relaxation period" (ABRP). Considerable lengthening was found during both ABRP and IVRP. This lengthening may provide an explanation for pre-inflow volume increments. The higher the frequency the longer the ABRP and the shorter the IVRP. In the more severe form of ischemia there is a sudden lengthening during ABRP and IVRP (late systolic bulging) whereas in the less severe form only onset of the relaxation is postponed within the cardiac cycle. The data suggest that ischemia leads to alterations in the early phase of relaxation even before involvement of the contraction phase (hypokinesis, akinesis, dyskinesis).

Animals↗
PubMed1987

Maintenance of relaxation-induced blood pressure reductions: the importance of continued relaxation practice.

This study examined the long-term importance of continued relaxation practice in the maintenance of relaxation-induced blood pressure reductions. An ABAB withdrawal-reinstatement design was employed with two hypertensive subjects. An objective, unobtrusive measure of home relaxation practice was used to monitor compliance. Subject 1 showed substantial reductions in systolic and diastolic blood pressure during 3 months of relaxation practice, followed by a 60% return to baseline during withdrawal, and a subsequent decrease with reinstatement of relaxation. Subject 2 showed a pattern similar to that of Subject 1 for systolic blood pressure, though the trend for diastolic pressure was unclear owing to a marginal treatment response. These preliminary data suggest that continued relaxation practice may be an important factor in the maintenance of relaxation-induced blood pressure reductions.

Adult↗
PubMed2003

Distinct hyperpolarizing and relaxant roles for gap junctions and endothelium-derived H2O2 in NO-independent relaxations of rabbit arteries.

We have compared the contributions of gap junctional communication and chemical signaling via H2O2 to NO-independent relaxations evoked by the Ca2+ ionophore A23187 and acetylcholine (ACh) in rabbit ilio-femoral arteries. Immunostaining confirmed the presence of connexins (Cxs) 37 and 40 in the endothelium and Cxs 40 and 43 in smooth muscle. Maximal endothelium-dependent subintimal smooth muscle hyperpolarizations evoked by A23187 and ACh were equivalent (approximately 20 mV) and almost abolished by an inhibitory peptide combination targeted against Cxs 37, 40, and 43. However, maximal NO-independent relaxations evoked by A23187 were unaffected by such peptides, whereas those evoked by ACh were depressed by approximately 70%. By contrast, the enzyme catalase, which destroys H2O2, attenuated A23187-induced relaxations over a broad range of concentrations, but only minimally depressed the maximum response to ACh. Catalase did not affect A23187- or ACh-evoked hyperpolarizations. After loading with an H2O2-sensitive probe, A23187 caused a marked increase in endothelial fluorescence that correlated temporally with relaxation, whereas only a weak delayed increase was observed with ACh. In arteries without endothelium, the H2O2-generating system xanthine/xanthine oxidase induced a catalase-sensitive relaxation that mimicked the gap junction-independent response to A23187 as it was maximally equivalent to approximately 80% of induced tone, but associated with a smooth muscle hyperpolarization <5 mV. We conclude that myoendothelial gap junctions underpin smooth muscle hyperpolarizations evoked by A23187 and ACh, but that A23187-induced relaxation is dominated by extracellular release of H2O2. Endothelium-derived H2O2 may thus be regarded as a relaxing factor, but not a hyperpolarizing factor, in rabbit arteries.

Acetylcholine↗
PubMed1983

Mechanism of relaxant action of papaverine. III. Comparison of sodium ion dependencies on the relaxant effects of papaverine, Aspaminol and benactyzine in guinea-pig taenia coli.

The role of sodium ion on the relaxant action of papaverine in guinea-pig taenia coli contracted by hypertonic 40 mM KCl were studied by manipulating the external sodium ion concentration and compared with those of its allied antispasmodics, Aspaminol and benactyzine. Whereas all of the three antispasmodics relaxed the taenia in all media used herein, their relaxant activities were declined by eliminating sodium ion from the bathing media. The declined relaxant activities were restored by re-introducing sodium ion to the solution depending on the amount of sodium ion but sodium ion dependencies of the restoration were not equal for each. In a solution containing 20 mM sodium ion, almost complete restoration was encountered with papaverine, while displayed only a slight restoration with Aspaminol and benactyzine. When a small amount of sodium ion was applied to the taenia before or after the treatment with the antispasmodics, the relaxation in response to papaverine was augmented, but those in response to Aspaminol and benactyzine were not affected. All of the three antispasmodics inhibited the cellular 45Ca-uptake in all media. While, their inhibitory activities were reduced by eliminating sodium ion from the media and were not restored so markedly by re-introducing 20 mM sodium ion to the solution. From these findings, it is suggested that papaverine may induce the smooth muscle relaxation not only by inhibiting the Ca-influx independently of the presence of sodium ion but also by other mechanisms sensitive to sodium ion, by contrast, Aspaminol and benactyzine may evoke the relaxation through mechanisms less sensitive to the presence of sodium ion, which include the inhibition of Ca-influx.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Idiosyncratic reality claims, relaxation dispositions, and ABC relaxation theory: happiness, literal christianity, miraculous powers, metaphysics, and the paranormal.

This study examined idiosyncratic reality claims, that is, irrational or paranormal beliefs often claimed to enhance relaxation and happiness and reduce stress. The Smith Idiosyncratic Reality Claims Inventory and the Smith Relaxation Dispositions Inventory (which measures relaxation and stress dispositions, or enduring states of mind frequently associated with relaxation or stress) were given to 310 junior college student volunteers. Principal components factor analysis with varimax rotation identified five idiosyncratic reality claim factors: belief in Literal Christianity; Magic; Space Aliens: After Death experiences; and Miraculous Powers of Meditation, Prayer, and Belief. No factor correlated with increased relaxation dispositions Peace, Energy, or Joy, or reduced dispositional somatic stress, worry, or negative emotion on the Smith Relaxation Dispositions Inventory. It was concluded that idiosyncratic reality claims may not be associated with reported relaxation, happiness, or stress. In contrast, previous research strongly supported self-affirming beliefs with few paranormal assumptions display such an association.

Adult↗
PubMed1993

Effect of denervation on endothelium-derived relaxing factor-dependent relaxation in the rat cremaster muscle.

Endothelium-derived relaxation mediated primarily by endothelium-derived relaxing factor/nitric oxide (EDRF/NO) is essential in the maintenance of vascular tone. However, little is known about the effects of denervation on EDRF-mediated relaxation in the microcirculation after reimplantation. Using intravital videomicroscopy in the rat cremaster model, this study assessed the effect of acute and chronic denervation of the muscle, produced by severing the genitofemoral nerve, on EDRF-mediated vasorelaxation. The results demonstrated that acetylcholine-induced EDRF relaxation (10(-6)M) significantly relieved norepinephrine-induced vasoconstriction in small arteries (40-80 microns diameter) in both the acute and chronic denervated muscles. There was no significant difference in the relaxant response between the denervated or innervated controls in each group or between the acute or chronic groups. This relaxation was prevented by methylene blue (10(-4) M). These findings suggest that EDRF-mediated relaxation in the microcirculation is not dependent on tissue innervation. Thus the use of potent endothelial dependent agonists may be of use in cases of vasospasm postreimplantation.

Acetylcholine↗
PubMed1990

Quantitative studies of hydrodynamic effects and cross-relaxation in protein solutions and tissues with proton and deuteron longitudinal relaxation times.

Longitudinal relaxation times T1 of water protons were measured in 5% protein solutions at different static magnetic fields (0.47, 2, and 7 T), for proteins with molecular weight ranging between 1.4 and 480 kDa and in solvents of varying degrees of deuteration. T1 values were also obtained for rat liver soaked with Krebs-Ringer solutions of varying degrees of deuteration at the above fields. For the samples containing D2O, T1 for deuterium was also measured at fields 2 and 7 T. The deuterium measurements were used to estimate water rotational correlation times which were in turn used to estimate the contribution of so-called "hydrodynamic effects" of macromolecules to proton relaxation. The proton relaxation rates at full deuteration were compared with those in protonated solvent (water) to obtain a second, direct measurement of this effect. Both measurements provide quantitation of the hydrodynamic effects, free from the contributions of other effects that are transparent to deuteration, and results from both measurements agree with each other reasonably well. The cross-relaxation rate between solute and solvent protons, and the contribution of paramagnetic impurities in the samples were also obtained from the proton T1 studies. The experimental results show that the hydrodynamic effects (intramolecular and intermolecular water-water interactions) are about the same magnitude in all the proteins studied as well as in rat liver. However, the cross-relaxation rate generally increases with increasing protein molecular weight. Measurements in soaked rat liver indicate that the cross-relaxation rate per unit mass of solute is much higher in tissues than in simple solutions of proteins of similar mean molecular weight. The results challenge the prevailing concept that the relaxation properties of biological tissues may be treated as a simple superposition of the properties of their constituents.

Animals↗