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At least 19 recordsLinked to original sources
PubMed1986

Thimerosal induces endothelium-dependent vascular smooth muscle relaxations by interacting with thiol groups. Relaxations are likely to be mediated by endothelium-derived relaxing factor (EDRF).

The sulfhydryl reagent thimerosal, as well as acetylcholine and Ca2+-ionophore A23187, produced concentration-dependent relaxations of intact rabbit aortic strips. The ability of strips to relax in response to these agents was dependent on the presence of vascular endothelium. Purposely removing the endothelium led to a complete loss of the relaxation responses. Thimerosal was at least as efficacious as A23187 in inducing endothelium-dependent relaxations, but its relaxations developed much slower than those induced by A23187 or acetylcholine. A small concentration of thimerosal that had no appreciable effect by itself, potentiated the relaxing response to acetylcholine in endothelium-intact preparations. Endothelium-dependent relaxations induced by larger concentrations of thimerosal, as well as relaxations produced by acetylcholine, were inhibited by the antioxidant and lipoxygenase inhibitor nordihydroguaiaretic acid, by haemoglobin, and by the inhibitor of soluble guanylate cyclase methylene blue. Indomethacin had no effect on these relaxations. The thiol compounds glutathione, 2-mercaptoethanol and a low concentration of dithiothreitol prevented (and reversed) relaxations induced by thimerosal, but had little or no effect on ACh relaxations. A high concentration of dithiothreitol also markedly inhibited the ACh relaxation. These results are consistent with the hypothesis that thimerosal stimulates endothelial cells to produce a relaxing substance whose properties are similar or the same as those of the endothelium-derived relaxing factor (EDRF) released in response to acetylcholine or A23187. The biochemical mechanism by which thimerosal induces the formation and/or release of this relaxing substance is likely to be different from ACh.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed2000

ABC relaxation theory and the factor structure of relaxation states, recalled relaxation activities, dispositions, and motivations.

ABC Relaxation Theory proposes 15 psychological relaxation-related states (R-States): Sleepiness, Disengagement, Physical Relaxation, Mental Quiet, Rested/Refreshed, At Ease/At Peace, Energized, Aware, Joy, Thankfulness and Love, Prayerfulness, Childlike Innocence, Awe and Wonder, Mystery, and Timeless/Boundless/Infinite. The present study summarizes the results of 13 separate factor analyses of immediate relaxation-related states, states associated with recalled relaxation activities, relaxation dispositions, and relaxation motivations on a combined sample of 1,904 individuals (group average ages ranged from 28-40 yr.). Four exploratory factor analyses of Smith Relaxation Inventories yielded 15 items that most consistently and exclusively load (generally at least .70) on six replicated factors. These items included happy, joyful, energized, rested, at peace, warm, limp, silent, quiet, dozing, drowsy, prayerful, mystery, distant, and indifferent. Subsequent factor analyses restricted to these items and specifying six factors were performed on 13 different data sets. Each yielded the same six-factor solution: Factor 1: Centered Positive Affect, Factor 2: Sleepiness, Factor 3: Disengagement, Factor 4: Physical Relaxation, Factor 5: Mental Quiet, and Factor 6: Spiritual. Implications for ABC Relaxation Theory are discussed.

Adult↗
PubMed2001

Measuring the longitudinal NMR relaxation rates of fast relaxing nuclei using a signal eliminating relaxation filter.

A new experiment for selective determination of the relaxation rates of fast relaxing NMR signals is presented. The experiment is derived from the conventional inversion recovery experiment by substituting the 180 degrees inversion pulse of this experiment with a signal eliminating relaxation filter (SERF) consisting of three 180 degrees pulses separated by two variable delays, Delta1 and Delta2. The SERF experiment allows a selective suppression of signals with relaxation rates below a given limit while monitoring the relaxation of faster relaxing signals. The experiment was tested on a sample of 20% oxidized plastocyanin from Anabaena variabilis, where the fast exchange of an electron between the reduced (diamagnetic) and the oxidized (paramagnetic) form results in a series of average signals with widely different relaxation rates. To ensure an optimum extraction of information from the experimental data, the relaxation rates were obtained from the SERF experiment by a simultaneous analysis of all the FIDs of the experiment using a fast linear prediction model method developed previously. The reliability of the relaxation rates obtained from the SERF experiment was confirmed by a comparison of the rates with the corresponding rates obtained from a conventional inversion recovery experiment.

Anabaena↗
PubMed2000

Music assisted progressive muscle relaxation, progressive muscle relaxation, music listening, and silence: a comparison of relaxation techniques.

The purpose of this study was to compare the effects of music assisted progressive muscle relaxation (M + PMR), progressive muscle relaxation (PMR), music listening, and silence/suggestion on measures of anxiety and perceived relaxation. The study also examined participant responses to a posttreatment questionnaire to identify relationships between musical and nonmusical elements in relaxation techniques. Sixty university students participated in the study. Fifteen participants were randomly assigned to each treatment condition. Subjects were tested individually using the same relaxation script for M + PMR and PMR conditions. One-way analyses of covariance were computed to compare pre and posttest differences among groups. Results of the ANCOVA revealed no differences among groups for the State Trait Anxiety Inventory (STAI) or the Visual Analog Scale (VAS). Analysis of variance, however, revealed each treatment condition to be equally effective in producing significant changes in anxiety and perceived relaxation from the pre to posttest period. Additionally, mean score differences revealed decreases for all conditions with M + PMR eliciting the greatest amount of change. A content analysis of posttreatment questionnaire items revealed detailed information about each participant's relaxation experience, state of mind, and use of self-generated relaxation techniques.

Adult↗
PubMed1990

Assessment of left ventricular relaxation by Doppler echocardiography. Comparison of isovolumic relaxation time and transmitral flow velocities with time constant of isovolumic relaxation.

Isovolumic relaxation time (IVRT) and events of early transmitral flow measured by Doppler echocardiography were validated against the time constant of left ventricular relaxation (tau) in open-chest dogs. During increased inotropy (by isoproterenol infusion) at constant preload, enhancement of relaxation was indicated by a decrease in tau from 48 +/- 12 (mean +/- SD) to 33 +/- 5 msec (p = 0.04) with a concomitant decrease in IVRT from 74 +/- 18 to 38 +/- 8 msec (p = 0.03). During decreased inotropy (by propranolol infusion) at constant preload, slowing of relaxation was indicated by an increase in tau from 40 +/- 8 to 51 +/- 13 msec (p = 0.02) with a concomitant increase in IVRT from 71 +/- 15 to 83 +/- 21 msec (p less than 0.05). A significant correlation between changes in tau and changes in IVRT was found (r = 0.66, p less than 0.001). In contrast, when left ventricular end-diastolic pressure was increased from 7 +/- 2 to 24 +/- 4 mm Hg at constant inotropy, tau increased from 47 +/- 14 to 64 +/- 25 msec (p = 0.03), whereas no change in IVRT was observed (76 +/- 19 and 71 +/- 19 msec, respectively). Aortic pressure was not significantly changed during any intervention, and heart rate was kept constant by pacing. Peak early transmitral velocity was unchanged by propranolol but increased during isoproterenol and saline infusion (p less than 0.001 and p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Phosphodiesterase inhibitors induce endothelium-dependent relaxation of rat and rabbit aorta by potentiating the effects of spontaneously released endothelium-derived relaxing factor.

The selective cyclic GMP phosphodiesterase inhibitor M&B 22948 and the less selective phosphodiesterase inhibitors papaverine and isobutylmethylxanthine (IBMX) each induced a component of relaxation of rat aortic rings that was endothelium-dependent. The most selective agent at inducing endothelium-dependent relaxation was M&B 22948, which caused little relaxation of endothelium-denuded rings at concentrations that produced almost complete relaxation of endothelium-containing rings. Although endothelium-dependent components of relaxation induced by papaverine and IBMX were clearly present, they were less well separated from the endothelium-independent components of relaxation. In the aorta of the rabbit, M&B 22948 and papaverine were less affective at inducing an endothelium-dependent component of relaxation than in the aorta of the rat, and IBMX produced no discernible endothelium-dependent component. The endothelium-dependent components of relaxation induced by M&B 22948, papaverine and IBMX on rat and rabbit aorta were probably dependent on endothelium-derived relaxing factor (EDRF), because they were associated with concomitant endothelium-dependent rises in cyclic GMP, and these components of relaxation as well as the rises in cyclic GMP were completely blocked by the EDRF-blocking agent hemoglobin. The action of hemoglobin was entirely specific, as none of the endothelium-independent components of relaxation induced by any of the phosphodiesterase inhibitors was affected by this hemoprotein. It is likely that the phosphodiesterase inhibitors induce their endothelium-dependent components of relaxation by inhibiting the hydrolysis of cyclic GMP formed in response to EDRF released spontaneously from endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed2000

Effects of progressive relaxation and classical music on measurements of attention, relaxation, and stress responses.

The present experiment examined relaxation using different experimental conditions to test whether the effects of individual elements of relaxation could be measured, whether specific effects were revealed, or whether relaxation resulted from a generalized "relaxation response." Sixty-seven normal, male volunteers were exposed to a stress manipulation and then to one of two relaxation (Progressive Relaxation, Music) or control (Attention Control, Silence) conditions. Measurements of attention, relaxation, and stress responses were obtained during each phase of the experiment. All four groups exhibited similar performance on behavioral measures of attention that suggested a reduction in physiological arousal following their relaxation or control condition, as well as a decreased heart rate. Progressive Relaxation, however, resulted in the greatest effects on behavioral and self-report measures of relaxation, suggesting that cognitive cues provided by stress management techniques contribute to relaxation.

Adolescent↗
PubMed1994

Relaxation of the bovine retractor penis muscle by a small K+ excess and the role of K+ in its neurogenic relaxation.

The mechanism of the relaxation of the bovine retractor penis muscle induced by 6.7 mM K+ as well as the role of K+ in the neurogenic relaxation of this muscle induced by nicotine, acetylcholine or electrical field stimulation, was studied. The relaxation induced by 6.7 mM K+ was, contrary to that induced by nicotine or electrical field stimulation, abolished by 10(-7) M ouabain. 15 min exposure to 10(-5) M NG-nitro-L-arginine, 3.2 x 10(-6) M tetrodotoxin, 5.0 x 10(-4) M hexamethonium, 5.3 x 10(-4) M methylene blue or hypoxia, all known to inhibit the neurogenic relaxation, did not affect the relaxation induced by 6.7 mM K+, which was also unaffected by 10(-5) M apamin, 3 x 10(-3) M 4-aminopyridine, 2.6 x 10(-2) M tetraethylammonium and 7.3 x 10(-4) M Ba2+. Exposure to K(+)-free solution reversibly abolished the neurogenic relaxations. The relaxations caused by 5.0 x 10(-7) M cromakalim and 2.0 x 10(-6) M pinacidil were totally blocked by 10(-5) M glibenclamide. Glibenclamide and apamin did not affect the tone of the muscle or its neurogenic relaxations. 4-Aminopyridine 4.0 x 10(-5) to 3.0 x 10(-3) M and tetraethylammonium 10(-4) to 2.6 x 10(-2) M raised the tone and enhanced the relaxations elicited by electrical field stimulation. The results indicate that the relaxation induced by 6.7 mM K+ is partly mediated by activation of Na(+)-K(+) ATPase and that its mechanism is thoroughly different from that of the neurogenic relaxations.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1975

Relaxation complexes of poasmid DNA and protein. III. Association of protein with the 5' terminus of the broken DNA strand in the relaxed complex of plasmid ColE1.

The location of the protein in the open circular DNA form of the ColE1 DNA-protein relaxation complex, induced by treatment with sodium dodecyl sulfate, has been studied using several enzymes of DNA metabolism. Escherichia coli exonucleases I and III are able to degrade extensively the nicked strand of the relaxed complex from the 3' end. DNA polymerase I can initiate synthesis using the relaxed complex as template-primer and specifically extends the 3' end of the nicked strand. The 5' end of the sodium dodecyl sulfate-relaxed complex, however, is blocked to the 5'-3' hydrolitic action T7 exonuclease. This block remains after trypsin treatment of the sodium dodecyl sulfate-relaxed complex but is removed by Pronase treatment. T4 DNA ligase is unable to seal either the sodium dodecyl sulfate-relaxed complex or the Pronase-treated relaxed complex even after pretreatment of the relaxed complex with T4 DNA polymerase and polynucleotide kinase. However, pretreatment with DNA polymerase I and the four deoxyribonucleoside triphosphates facilitates ligase closure of the Pronase-treated relaxed complex but not the sodium dodecyl sulfate-relaxed complex. These studies indicate that the protein in the relaxed ColE1 complex is located at or near the 5' end of the nicked strand.

Bacterial Proteins↗
PubMed1999

Pranidipine enhances relaxation produced by endothelium-derived relaxing factor in carotid artery.

The effects of pranidipine, a novel dihydropyridine-type Ca(2+)-channel antagonist, on acetylcholine-induced endothelium-dependent relaxation were investigated in isolated carotid artery of the guinea-pig. In arteries contracted with high-K(+) solution ([K(+)](0)=28.8 mM) containing noradrenaline, the relaxation was inhibited by N(omega)-nitro-L-arginine, indicating an involvement of endothelium-derived relaxing factor. Pranidipine (10(-9)-10(-7) M) augmented the relaxation in a concentration-dependent manner. Sodium nitroprusside produced a relaxation in arteries contracted with high-K(+) solution containing noradrenaline, in an endothelium-independent manner, and the relaxation was enhanced by pranidipine. 1H-[1,2,4] oxadiazolo [4, 3-a] quinoxalin-l-one (ODQ), an inhibitor of nitric oxide-sensitive guanylate cyclase, attenuated the relaxation produced by acetylcholine or sodium nitroprusside. In the presence of ODQ, pranidipine did not enhance the acetylcholine-induced relaxation. The relaxation produced by endothelium-derived hyperpolarizing factor was inhibited by pranidipine, with no alteration of the hyperpolarization. Thus, pranidipine augments the nitric oxide-induced relaxation, possibly by enhancing the mechanisms related to cyclic GMP.

Acetylcholine↗
PubMed1988

Lysolecithins as endothelium-dependent vascular smooth muscle relaxants that differ from endothelium-derived relaxing factor (nitric oxide)

The effects of lysolecithin (lysophosphatidylcholine) derived from egg yolk as well as of synthetic lysolecithins with different aliphatic chain lengths on tension development of rabbit aortic strips were investigated. Lysolecithins caused slowly progressing, dose-dependent relaxation that was inhibited by hemoglobin, methylene blue, and nordihydroguiaretic acid. Indomethacin caused no inhibition of relaxation. The degree of relaxation was endothelium-dependent and appeared to be related to the activation of guanylate cyclase [GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2]. Superoxide dismutase failed to influence relaxation. Lysolecithins with the longest aliphatic chain were the most potent relaxants of aortic strips. The experiments suggest a role of lysolecithins through their weak detergent action on membrane dynamics of endothelial cells, resulting in the production of cyclic GMP and the relaxation of arterial smooth muscle. Lysolecithins differ in several respects from endothelium-derived relaxing factor. Endothelium-derived relaxing factor is an unstable humoral substance released from endothelium and is identical to nitric oxide, itself a labile substance causing vascular relaxation and cyclic GMP accumulation. Lysolecithins may represent a different type of endothelium-dependent muscle relaxant.

Acetylcholine↗
PubMed1994

Pharmacological reactivity of human epicardial coronary arteries: characterization of relaxation responses to endothelium-derived relaxing factor.

1. Human epicardial coronary artery rings, freshly obtained from cardiac transplant patients, were examined for their responses to endothelium-derived relaxing factor (EDRF)-releasing agents. 2. Functional antagonism profoundly influenced relaxation responses in this tissue. Increasing force with concentrations of U46619 above 3 nM (40% of maximum contraction response) resulted in a reduction of the maximum response to four vasorelaxants which relax vascular smooth muscle via different mechanisms: the EDRF-releasing agents, substance P and bradykinin; the endothelium-independent nitro-vasodilator, sodium nitroprusside (SNP); and the beta-adrenoceptor agonist, isoprenaline. 3. Substance P, histamine, bradykinin and the Ca2+ ionophores ionomycin and A23187 all caused concentration- and endothelium-dependent relaxation in vessels pre-contracted with the thromboxane A2-mimetic, U46619 (3 nM) to an active force optimal for relaxation responses. Nifedipine (0.1 microM), added to prevent spontaneous contractions, had no effect or relaxation responses to substance P, bradykinin and histamine. 4. Substance P was the most potent of the EDRF-releasing agents examined and all agents except for bradykinin caused near-maximal relaxation. Bradykinin caused only 46.2% +/- 7.3% relaxation. Responses were abolished when the endothelium was removed and, except for histamine, were not significantly affected by indomethacin (3-10 microM, P > 0.05). Histamine (0.1-10 microM) caused a concentration-dependent contraction of arterial rings without endothelium. 5. The L-arginine analogues NG-nitro-L-arginine (L-NOARG, 0.1 mM) and NG-monomethyl-L-arginine (L-NMMA, 0.1 mM) both caused no further contraction in arteries precontracted with U46619 (3 nM) and were in general, poor inhibitors of responses to EDRF agonists. L-NMMA, but not L-NOARG,caused small but significant decreases in the maximum responses to substance P, bradykinin (18.5 +/- 6.9% and 27.6 +/- 10.9% relaxation with L-NMMA and L-NOARG, respectively), histamine and A23187 (P<0.05). The analogues had no effect on SNP responses.6. In conclusion, EDRF release in human isolated coronary artery is only poorly antagonized by the nitric oxide synthase inhibitors L-NOARG and L-NMMA. These results indicate that either the nitricoxide transduction pathway present in human coronary artery is different from that in other tissues or that another factor(s) (e.g. endothelium-derived hyperpolarizing factor) is also released in response to EDRF-releasing agents and augments the relaxation to nitric oxide.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1984

A controlled study of the effects of applied relaxation and applied relaxation plus operant procedures in the regulation of chronic pain.

Chronic back/joint pain patients participated in a comparative study of relaxation and operant therapies for chronic pain. Patients were randomly assigned to: (1) a waiting-list control, or to either (2) an applied relaxation, or (3) an applied relaxation plus operant conditioning treatment programme. Waiting patients were subsequently randomly assigned to active treatment. The results indicated that the treatment groups tended to do significantly better than the waiting-list control group for pain, medicine use, activity, and depression, but there were few clear differences between the treatment groups. Applied relaxation plus the operant programme was significantly better than relaxation for medicine reduction, and applied relaxation was better than relaxation and operant conditioning for a patient evaluation of reaching treatment goals. Within-group and single-subject analyses indicated that there were significant improvements between pre- and post-tests for the treatment groups, but not for the waiting-list control group. Follow-up data indicated maintenance, and that applied relaxation had significantly lower pain ratings than applied relaxation plus operant conditioning. Taken as a whole, the results show that applied relaxation can produce significant decreases in pain, and that the addition of an operant programme does not improve pain reductions, but does tend to improve results with activity and especially medicine intake variables.

Adult↗
PubMed1983

Mechanism of relaxant action of papaverine. II. Differences between modes of relaxant effects of papaverine and amytal in guinea-pig taenia coli.

Mode of relaxant effect of papaverine on guinea-pig taenia coli was compared with that of amytal, especially in regard to their actions on the calcium movements. The present results provided evidence that the mode of relaxant effect of papaverine differs from that of amytal. Papaverine relaxed the taenia coli even in the Na-free solution although its relaxant activity was markedly reduced, while amytal failed to reveal relaxant activity in the same condition. Reintroduction of a small amount of sodium ion to the Na-free solution restored the relaxant activities of papaverine and amytal but their sodium ion dependencies of the restoration were not equal. Amytal was more sensitive to sodium ion than papaverine. Papaverine induced the muscle relaxation with synchronous acceleration of 45Ca-efflux, while the relaxation in response to amytal was not accompanied by acceleration of 45Ca-efflux. The cellular 45Ca-uptake was inhibited by papaverine, but not by amytal. In these experiments, both papaverine and amytal were used at sufficient doses to inhibit the mitochondrial respiration. From these findings, it is concluded that papaverine relaxes the smooth muscle through different mechanism from that of amytal and thus the relaxant effect of papaverine may not be related to its inhibitory action on the mitochondrial respiration.

Amobarbital↗
PubMed1987

Endothelium-derived relaxing factor is a selective relaxant of vascular smooth muscle.

The present study examines the relaxant selectivity of endothelium-derived relaxing factor (EDRF) released from cultured endothelial cells. Endothelial cells from bovine pulmonary artery (CCL-209) in culture were grown on Cytodex-3 microcarrier beads, packed into a column and superfused to release EDRF. EDRF response was estimated by its ability to relax phenylephrine-contracted rings of rabbit aorta. Bradykinin and A23187 (10(-10) to 10(-6) M) caused dose-dependent release of EDRF from cultured bovine pulmonary artery endothelial cells. The release was dependent on endothelial cell number. A23187 caused a larger and longer-lasting release of EDRF than bradykinin. EDRF relaxation was selective for blood vessels. EDRF relaxed rabbit aortic rings, but it did not relax histamine-contracted guinea pig tracheal, rabbit taenia coli strips or oxytocin-contracted guinea pig uterine rings. These nonvascular smooth muscles were, however, relaxed by isoproterenol (10(-4) M) and sodium nitroprusside (SNP, 10(-5) M). The sensitivity of guinea pig aortic rings and tracheal strips to SNP were compared. The IC50 values for SNP (10(-9) to 10(-5) M) were 0.07 and 0.3 microM for aortic rings and tracheal strips, respectively. Although the tracheal strips were about 4-fold less sensitive than the aorta toward SNP, a complete relaxation was achieved. These results suggest that EDRF relaxes vascular smooth muscles but not respiratory, Gl or reproductive smooth muscles. Thus, EDRF may be a selective relaxant of vascular smooth muscle.

Animals↗
PubMed1996

Magnetization exchange in capillaries by microcirculation affects diffusion-controlled spin-relaxation: a model which describes the effect of perfusion on relaxation enhancement by intravascular contrast agents.

The effect of perfusion on relaxation time in tissue has only been considered for first-pass kinetics of NMR-signal after application of contrast agents. The importance of perfusion on relaxation has not yet been studied for steady state conditions, i.e., when the intravascular relaxation rate is constant in time. The aim of this study is to develop a model in which T1 relaxation is derived as a function of perfusion and intracapillary volume fraction (regional blood volume). Tissue is considered to be two-compartment system, which consists of intracapillary and extravascular space. Intracapillary relaxation differs from relaxation in the arterial system due to diffusion-exchange of magnetization from extravascular to intracapillary space. Perfusion tends to attenuate this difference and thus counteracts the effect on intracapillary relaxation. Relaxation in the extravascular and intracapillary magnetization are linked by diffusion. This dependence is presented in analytical form and a generic equation is derived. AT1 experiment is considered in which all spins of tissue and blood are inverted at the beginning. Calculations are performed for the fast exchange model of tissue. Perfusion increases relaxation enhancement of intravascular contrast agents. This effect is considerable in highly perfused tissue like myocardium. The dependence of relaxation on perfusion implies an overestimation of the regional blood volume when the calculation of the latter is based on tissue models that neglect perfusion. The model presented here is applied to predict the effect of perfusion on T1 imaging with FLASH-pulse sequences because this technique has been proven to be a powerful method to obtain T1 maps within a short time interval. For the fast exchange model, two algorithms are suggested that determine perfusion and regional blood volume from T1 imaging in the presence and absence of intravascular contrast agents.

Blood Volume↗
PubMed1996

A comparative study of endothelium-derived relaxing factor-mediated relaxation and smooth muscle cell function in arterial and venous vein bypass grafts.

The development of intimal hyperplasia in reversed vein grafts is associated with altered endothelial and vasomotor function. This study examines the effect of surgery on the morphology and vasomotor function of experimental arterial and venous vein bypass grafts. Twelve reversed vein grafts, 12 in situ vein grafts and 12 venovenous grafts were placed in 24 New Zealand White rabbits. All grafts remained patent and were harvested after 28 days. Isometric contraction to norepinephrine, histamine, bradykinin, serotonin and relaxation to acetylcholine and sodium nitroprusside following pre-contraction with prostaglandin F(2 alpha) were determined on the grafts and on contralateral jugular veins. Compared to the contralateral jugular veins, norepinephrine supersensitivity was induced in the reversed vein grafts, and venovenous vein grafts but not in the in situ vein grafts. Decrease in histamine sensitivity occurred in all grafted vessels. Bradykinin responses were significantly reduced in the in situ vein grafts and reversed vein grafts. Contractile responses to serotonin developed in the in situ vein grafts and reversed vein grafts only. Acetylcholine-induced endothelium-derived relaxing factor-mediated relaxation of the contralateral jugular veins was preserved in both venovenous grafts and in situ vein grafts but was lost in reversed vein grafts. All tissues relaxed to sodium nitroprusside in dose-dependent manner. The data suggest that norepinephrine supersensitivity in reversed vein grafts results from excision of the vessel. Attenuation of bradykinin responses and the enhanced contractile responses to serotonin appear predominantly to result from arterialization. Decreases in histamine sensitivity appear related both to excision and to arterialization. Neither the excision of the vein nor arterialization individually influences the alterations in endothelium-derived relaxing factor-mediated relaxation. However, a combination of excision and arterialization results in the altered endothelium-derived relaxing factor-mediated relaxation. This study suggests that the surgical preparation of the vein and the surgical procedure used have significantly different effects on endothelium-derived relaxing factor-mediated relaxation and smooth muscle contractility in vein grafts.

Acetylcholine↗
PubMed1999

Differentiation of abnormal relaxation pattern with aging from abnormal relaxation pattern with coronary artery disease in transmitral flow with the use of tissue Doppler imaging of the mitral annulus.

An abnormal relaxation pattern in transmitral flow velocity waveforms has been observed in older healthy subjects as well as in patients with heart disease. Accordingly, we investigated whether the hemodynamic differences between patients with coronary artery disease (CAD) with an abnormal relaxation pattern in transmitral flow (ratio of E-wave to A-wave velocities < 1.0) and healthy older subjects with an abnormal relaxation pattern can be distinguished with the use of mitral annular velocity (MAV) during early diastole. We measured MAV in the longitudinal direction of the heart during early diastole by M-mode color tissue Doppler imaging in 24 patients with atypical chest pain (defined as healthy subjects in this study) and 70 patients with CAD who underwent cardiac catheterization. In all patients a time constant of left ventricular pressure decay (tau) and the left ventricular (LV) end-systolic volume index were also measured. Twenty-one healthy subjects and 59 patients with CAD had an abnormal relaxation pattern in their transmitral flow. The age, heart rate, mean blood pressure, and ratio of E-wave to A-wave velocities were not different between the two groups. However, the tau was longer and the LV end-systolic volume index was greater in patients who had an abnormal relaxation pattern with CAD than in healthy subjects with an abnormal relaxation pattern. The MAV during early diastole was lower in the former than in the latter (5.8 +/- 1. 9 vs 9.8 +/- 1.9 cm/s, P <.001). Mitral annular velocity during early diastole by M-mode color tissue Doppler imaging can detect the differences in LV relaxation and LV systolic performance between the abnormal relaxation pattern with CAD and the physiologically abnormal relaxation pattern with aging, providing further information regarding the meaning of an LV abnormal relaxation pattern.

Aging↗