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PubMed1999

Reactive oxygen species: role in the relaxation induced by bradykinin or arachidonic acid via EDHF in isolated porcine coronary arteries.

Although endothelium-derived hyperpolarizing factor (EDHF) is thought to be a cytochrome P-450 product (arachidonic acid metabolite) in some tissues, in porcine coronary arteries (PCAs) its nature remains unclear. Because phospholipase A2 and C are involved in the synthesis and/or release of EDHF in the PCA, the arachidonic acid (AA) pathway may be involved. In the presence of the cyclooxygenase inhibitor indomethacin (10(-5) M) and the NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME; 10(-4) M), both bradykinin (BK; 10(-9)-10(-6) M) and AA (10(-7)-10(-4) M) induced dose-dependent relaxation of PGF2alpha-contracted PCA rings, which was blocked by a high extracellular concentration of KCl (30 mM) or pretreatment with ouabain, a Na+/K+-adenosine triphosphatase (ATPase) inhibitor (5 x 10(-7) M). Eicosatetraynoic acid (ETYA; 20 microM), which inhibits all AA pathways, slightly affected the response to BK and AA; however, lipoxygenase or cytochrome P-450 inhibitors had no effect, suggesting that relaxation is independent of these enzymatic pathways. Because endothelial cells can generate reactive oxygen species (ROS) via metabolism of AA and independent of cyclooxygenase activity, we also studied (a) whether ROS can relax the PCA, as well as the mechanism(s) involved, and (b) the role of ROS in BK- and AA-induced relaxation. Xanthine (X; 100 microM) plus xanthine oxidase (XO; 0.02 U/ml) induced time-dependent relaxation of PGF2alpha-contracted PCA rings in the presence of indomethacin and L-NAME. Dilatation was not affected by superoxide dismutase (SOD; 500 U/ml) but was abolished by catalase (300 U/ml), suggesting that hydrogen peroxide (H2O2) is involved. When rings were contracted by depolarizing them with 30 mM KCl, X/XO failed to elicit relaxation. Ouabain abolished the response to X/XO, suggesting that X/XO may induce relaxation by hyperpolarizing vascular smooth muscle cells via stimulation of the Na+/K+-ATPase pump. We therefore questioned whether ROS might be involved in BK- and AA-induced relaxation. Because catalase combined with SOD had little or no effect, we concluded that in the PCA, the relaxation induced by BK via EDHF involves some mechanism independent of NO, AA metabolism, or ROS.

Animals↗
PubMed2001

Different contribution of endothelial nitric oxide in the relaxation of human coronary arteries of ischemic and dilated cardiomyopathic hearts.

Coronary artery disease and congestive heart failure (CHF) have been associated with a reduction in nitric oxide (NO) release or bioavailability from the vascular endothelium. The objectives of this study were to compare the role of NO in human coronary vessels isolated from nonischemic dilated (DCM) (n = 10) and ischemic (ICM) (n = 12) cardiomyopathic hearts. Segments were mounted on a wire myograph to record changes in isometric tension. All experiments were performed in the presence of indomethacin (10 microM). Contractions induced by angiotensin II (0.1 microM) or a depolarizing physiologic solution containing 40 mM KCl, were of similar amplitude in DCM and ICM. In vessels precontracted with angiotensin II, acetylcholine (1 microM) caused an endothelium-dependent relaxation of rings from DCM but a paradoxical contraction of rings from ICM; NO synthase inhibition with Nomega-nitro-L-arginine (L-NNA, 100 microM) did not affect acetylcholine-induced relaxation or contraction of DCM or ICM vessels, respectively. By contrast, substance P (0.1 microM) induced an endothelium-dependent relaxation in both groups of vessels; this relaxation was prevented (p < 0.05) by L-NNA in vessels from ICM hearts but only reduced (p < 0.05) by L-NNA in vessels from DCM hearts. In depolarized conditions, acetylcholine contracted (p < 0.05) whereas substance P induced a complete relaxation (p < 0.05) of vessels from both groups: substance P-induced relaxation was abolished (p < 0.05) by L-NNA. Our data suggest that in the presence of indomethacin, NO does not contribute to acetylcholine-induced relaxation of human epicardial coronary arteries isolated from DCM hearts. Furthermore, whereas NO and a secondary endothelium-derived relaxing factor sensitive to high K+ contribute to substance P-induced relaxation of rings from DCM hearts, only NO is involved in ICM hearts.

Acetylcholine↗
PubMed2004

The use of muscle relaxant medications in acute low back pain.

STUDY DESIGN: Prospective cohort study. OBJECTIVES: To determine the characteristics of patients who take muscle relaxants for back pain after seeking care and to determine the relationship of muscle relaxant use with recovery from the episode of low back pain. SUMMARY OF BACKGROUND DATA: Low back pain is a common condition with a generally favorable short-term prognosis. Physicians in the acute setting commonly prescribe muscle relaxants. The indications for use and outcomes are not clear. METHODS: We performed a secondary data analysis of a cohort of 1633 patients who sought care from a variety of practitioners (primary care, physician of chiropractic, orthopedic surgeon, Health Maintenance Organization) for low back pain. Patients were enrolled in the physician's office and interviewed at baseline, 2, 4, 8, 12, and 24 weeks. Pain, functional status, medication use, health care utilization, and satisfaction with care were assessed. RESULTS: Muscle relaxants were used by 49% of patients; among those who sought care from doctors, 64% used muscle relaxants. Muscle relaxant users were more impaired at baseline. Over time, among patients with greater functional status impairment (Roland disability score > 12) at baseline, muscle relaxant users had somewhat slower recovery from the episode of back pain. This finding persisted after controlling for baseline functional status, age, worker's compensation status, and use of nonsteroidal inflammatory agents. CONCLUSIONS: Use of muscle relaxants was very common among patients with acute low back pain. Muscle relaxant use was not associated with more rapid functional recovery.

Acute Disease↗
PubMed2006

Relaxivity of Gadopentetate Dimeglumine (Magnevist), Gadobutrol (Gadovist), and Gadobenate Dimeglumine (MultiHance) in human blood plasma at 0.2, 1.5, and 3 Tesla.

OBJECTIVES: We sought to determine the relaxivity and accurate relaxation rates of Gd-DTPA, Gd-BT-DO3A, and Gd-BOPTA at 0.2, 1.5, and 3 T in human blood plasma. MATERIALS AND METHODS: Contrast media concentrations between 0.01 and 16 mM in human plasma were used for relaxation measurements. The R1 and R2 relaxation rates and r1 and r2 relaxivities were determined. RESULTS: Gd-BOPTA produced the highest relaxation rates and relaxivities at all field strengths. The r1 and r2 values for Gd-BOPTA were 107-131% and 91-244% higher than for Gd-DTPA, respectively, and 72-98% and 82-166% higher than for Gd-BT-DO3A. Higher field strengths resulted in lower values of R1, R2, and r1 for all contrast agents tested and of r2 for Gd-DTPA and Gd-BT-DO3A. A linear dependence of R1 and R2 on concentration was found for Gd-DTPA and Gd-BT-DO3A and a nonlinear dependence for Gd-BOPTA for concentrations larger than 1 mM. The r1 and r2 relaxivity of Gd-BOPTA increased with decreasing concentration. CONCLUSIONS: Gd-BOPTA demonstrates the highest longitudinal r1 at all field strengths, which is ascribable to weak protein interaction. The R2/R1 ratio increases at higher field strength only for Gd-BOPTA, hence very short echo times are required for Gd-BOPTA to benefit from the higher longitudinal relaxivity.

Contrast Media↗
PubMed1999

Slow algebraic relaxation in quartic potentials and related results.

We present a detailed report [see S. Sen et al., Phys. Rev. Lett. 77, 4855 (1996)] of our numerical and analytical studies on the relaxation of a classical particle in the potentials V(x)= +/-x(2)/2+x(4)/4. Both of the approaches confirm that at all temperatures, the relaxation functions (e.g., velocity relaxation function and position relaxation function) decay asymptotically in time t as sin(omega(0)t)/t. Numerically calculated power spectra of the relaxation functions show a gradual transition with increasing temperature from a single sharp peak located at the harmonic frequency omega(0) to a broad continuous band. The 1/t relaxation is also found when V(x) is a polynomial in powers of x(2) with a nonvanishing coefficient accompanying the x(4) term in V(x). Numerical calculations show that in the cases in which the leading term in V(x) behaves as x(2n) with integer n, the asymptotic relaxation exhibits 1/t(phi) decay where phi =1/(n-1). We briefly discuss the analytical approaches to relaxation studies in these strongly anharmonic systems using direct solution of the equation of motion and using the continued fraction formalism approach for relaxation studies. We show that the study of the dynamics of strongly anharmonic oscillators poses unique difficulties when studied via the continued fraction or any other time-series construction based approaches. We close with comments on the physical processes in which the insights presented in this work may be applicable.

Journal Article↗
PubMed1971

The effect of auxin on stress relaxation in isolated Avena coleoptiles.

In order to characterize further the mechanical properties of coleoptile cell walls, stress relaxation measurements were made on methanol-boiled sections of Avena coleoptiles. Relaxation was measured both in mechanically conditioned specimens and in specimens which had not been previously extended. In both cases the relaxation was proportional to log time. Mechanical conditioning increased the relaxation modules and decreased the relative rate of relaxation. In contrast, pretreatment of the live coleoptiles with indoleacetic acid reduced the relaxation modulus and the absolute rate of relaxation but did not affect the relative rate of relaxation. Essentially similar pictures of the mechanical properties of coleoptile walls are obtained from stress relaxation and creep tests; the wall behaves as a nonlinear viscoelastic material.

Journal Article↗
PubMed1975

Isolation and partial characterisation of the relaxation protein from nuclei of cultured mouse and human cells.

A protein, called relaxation protein because of its ability to remove superhelical turns in closed-circular DNA, has been isolated and partially characterized from the nuclei of LA9 mouse and HeLa cells. The purification was facilitated by an assay method, with PM2 DNA, which used the fluorescence enhancement of the intercalating dye ethidium bromide upon binding to the closed-circular DNA. The amount of dye bound depends upon the degree of the superhelix density of the DNA. The relaxation products were analysed by the buoyant separation method in CsCl containing ethidium bromide and were shown to be completely relaxed. The purification resulted in a single band in a dodecylsulfate gel electrophoresis with an apparent molecular weight of 37000. The pH optimum is 7.0 and the optimal salt concentration is 0.2 M NaCl. The relaxation protein removes negative as well as positive supercoils, the latter generated by the interaction of ethidium bromide with closed-circular DNA. Relaxation of positive supercoils results, after removal of the dye, in the formation of molecules with superhelix densities exceeding that of native PM2 DNA (0.054). The highest negative superhelix density observed was -0.098 +/- 0.001. The corresponding positive superhelix density has been calculated to be + 0.023. A nicking--swivelling--closing mechanism is postulated, but nicked intermediates have so far not been demonstrated. The relaxation protein is not inhibited by known mammalian endonuclease I inhibitors, except for denatured DNA, and does not possess a conventional polynucleotide ligase activity. The relaxation activity was found to be predominantly in the nuclei, with only small amounts present in the cytoplasm and mitochondria. The biological function of transient swivels induced by the relaxation protein is not known. However, transient swivels are considered necessary or useful in the replication of closed-circular DNA or long linear DNA, respectively. Relaxation protein could replace the combined action of an endonuclease and a ligase ahead of the replication fork. Alternatively, transient swivels could be involved in the transcription process.

Animals↗
PubMedDate not supplied

Effects of fluvastatin on endothelium-derived hyperpolarizing factor- and nitric oxide-mediated relaxations in arteries of hypertensive rats.

Endothelial cells release endothelium-derived hyperpolarizing factor (EDHF), as well as nitric oxide (NO). It has recently been suggested that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) improve NO-mediated endothelial function, partially independently of their cholesterol-lowering effects. It is, however, unclear whether statins improve EDHF-mediated responses. Eight-month-old stroke-prone spontaneously hypertensive rats (SHRSP) were treated with fluvastatin (10 mg/kg per day) for 1 month. Age-matched, normotensive Wistar Kyoto (WKY) rats served as controls. Both EDHF- and NO-mediated relaxations were impaired in SHRSP compared with WKY rats. Fluvastatin treatment did not affect blood pressure and serum total cholesterol. The acetylcholine (ACh)-induced, EDHF-mediated hyperpolarization in mesenteric arteries did not significantly differ between fluvastatin-treated SHRSP and untreated SHRSP and the responses in both groups were significantly smaller compared with those of WKY rats. Endothelium-derived hyperpolarizing factor-mediated relaxations, as assessed by the relaxation to ACh in mesenteric arteries contracted with noradrenaline in the presence of N(G)-nitro-l-arginine and indomethacin, were virtually absent and similar in both SHRSP groups. In contrast, NO-mediated relaxation, as assessed by the relaxation in response to ACh in rings contracted with 77 mmol/L KCl, was improved in fluvastatin-treated SHRSP compared with untreated SHRSP (maximum relaxation in control and fluvastatin groups 42.0 +/- 5.2 and 61.2 +/- 3.8%, respectively; P < 0.05). Hyperpolarization and relaxation in response to levcromakalim, an ATP-sensitive K(+) channel opener, were similar between the two SHRSP groups. These findings suggest that fluvastatin improves NO-mediated relaxation, but not EDHF-mediated hyperpolarization and relaxation, in SHRSP. Thus, the beneficial effects of the statin on endothelial function may be mainly ascribed to an improvement in the NO pathway, but not EDHF.

Acetylcholine↗
PubMed1995

Influence of age on the relaxation induced by nifedipine in aorta from spontaneously hypertensive and Wistar Kyoto rats.

1. Nifedipine induces relaxation in aortic segments from Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) of 5-week-, 3-month-, 6-month- and 1.5-year-old precontracted with 50 mM K+ or 0.1 microM noradrenaline (NA). 2. In WKY rat segments precontracted with K+, nifedipine relaxation was reduced at 1.5 years. However, in SHR segments, the greatest relaxation was observed at 1.5 years. The relaxation elicited by nifedipine in segments from WKY of 6-month and 1.5-year-old precontracted with NA was higher than that reached at 5-week- and 3-month-old. However, the relaxation induced in SHR of 6-month and 1.5-year-old was only higher than that obtained at 5-week-old. 3. Relaxations elicited by nifedipine in segments from WKY precontracted with K+ were smaller than those observed in age-matched SHR segments. 4. The endothelium positively and negatively modulates the relaxation to nifedipine in segments from SHR and WKY rats of different ages precontracted with K+, respectively. However, in segments of both strain precontracted with NA, endothelium removal did not alter the relaxations obtained at different ages. 5. These results suggest that the relaxation elicited by nifedipine: (1) depends on the strain, with a tendency to be greater in the hypertensive strain; (2) is negatively and positively modulated by endothelium in WKY and SHR, respectively, and (3) is influenced by age, and this influence depends on both the contractile agent and the strain.

Aging↗
PubMed1986

Mechanisms of intrinsic tone in bullfrog lung: relaxant effects of indomethacin, ouabain and potassium.

Bullfrog hemilungs showed minimal relaxation (9 +/- 2% of the maximal relaxant effect of theophylline, Imax) after a 16 h incubation in 10(-5) M indomethacin, indicating that prostaglandin synthesis plays little or no role in the high intrinsic tone characteristic of this preparation. A higher concentration of indomethacin (10(-4) M) produced greater relaxation (23 +/- 3% of Imax), but also markedly potentiated isoprenaline-induced relaxation. The interaction with isoprenaline was similar to that previously found for papaverine, a phosphodiesterase inhibitor. Ouabain (10(-5) and 10(-4) M) produced an initial contraction followed by marked relaxation (50% of Imax), indicating that a ouabain-sensitive mechanism is of major importance in the maintenance of intrinsic tone. Ouabain-treated hemilungs showed reversal (relaxation) of the normal contractile response to 26 mM potassium and marked impairment of the contractile response to calcium in calcium-depleted preparations. These effects suggest that ouabain-induced relaxation reflects a drug action on calcium movements. The marked relaxation (30 to 40% of Imax) produced by 26 mM potassium in ouabain-treated hemilungs is of particular interest in that it indicates a mechanism of potassium-induced relaxation distinct from stimulation of sodium-potassium ATPase.

Animals↗
PubMed1993

Lack of effect of sumatriptan and UK-14,304 on capsaicin-induced relaxation of guinea-pig isolated basilar artery.

1. The objectives of this study were to assess the effects of sensory neuropeptide antagonists and presynaptically acting receptor agonists on capsaicin-induced relaxations of guinea-pig isolated basilar artery (GPBA). 2. Capsaicin, human alpha-calcitonin gene-related peptide (CGRP) and substance P (SP) caused concentration-related relaxations of GPBA which had been pre-contracted with prostaglandin F2 alpha (PGF2 alpha). Responses to capsaicin were not modified by the peptidase inhibitors, phosphoramidon (1 microM) and bestatin (100 microM). 3. The relaxant responses to capsaicin were blocked in a selective manner by ruthenium red (3 microM) and by the CGRP antagonist, CGRP8-37 (1 microM). CGRP8-37 also selectively inhibited the relaxant effects of CGRP. 4. The selective NK1 receptor antagonist, GR82334 (10 microM), inhibited SP-induced relaxations but had little effect on capsaicin-induced relaxations. 5. The 5-HT1 receptor agonist, sumatriptan, produced small contractions of GPBA under conditions of resting tone. In the presence of PGF2 alpha, sumatriptan had no further contractile effect. Sumatriptan (0.3 and 3 microM) did not modify capsaicin-induced relaxations of GPBA. 6. The alpha 2-adrenoceptor agonist, UK-14,304 (0.1 microM), had no effect on basal or PGF2 alpha-induced tone. UK-14,304 did not modify capsaicin-induced relaxations. 7. These results suggest that capsaicin causes relaxation of GPBA via a release of CGRP. This process is amenable to blockade by CGRP8-37 and ruthenium red, but not to modulation by either sumatriptan or UK-14,304.

Animals↗
PubMed1994

Cyclic GMP-independent relaxation and hyperpolarization with acetylcholine in guinea-pig coronary artery.

1. The effects of acetylcholine (ACh) on membrane potential, relaxation and cyclic GMP levels were compared to the NO donor L-nitrosocysteine (Cys-NO) in segments of guinea-pig coronary artery. 2. ACh and Cys-NO produced concentration-dependent relaxations of muscles contracted with the H1 receptor agonist, 2-(2-aminoethyl)pyridine (AEP, 0.35 mM). The relaxation to ACh was unchanged in the presence of NG-monomethyl-L-arginine (L-NMMA; 350 microM) or indomethacin (3 microM). 3. Oxyhaemoglobin (HbO; 20 microM) alone or in combination with L-NMMA increased the EC50 for ACh-induced relaxation whereas relaxation with Cys-NO was almost completely abolished with HbO. 4. Scorpion venom (SV; 8.7 micrograms ml-1) increased the EC50 for relaxation with ACh but not Cys-NO. Combined L-NMMA, HbO and SV produced nearly complete abolition of ACh-induced relaxations. 5. Basal cyclic GMP levels (i.e., 20 pmol mg-1 protein) were significantly increased following addition of either ACh (190 pmol mg-1 protein) or Cys-NO (240 pmol mg-1 protein). L-NMMA significantly reduced the rise of cyclic GMP with ACh but not Cys-NO. In contrast, SV did not significantly reduce the rise in cyclic GMP produced with ACh. In the combined presence of L-NMMA and HbO neither ACh nor Cys-NO produced a significant increase in cyclic GMP levels. 6. ACh gave rise to significantly greater membrane hyperpolarization than Cys-NO both in the presence and absence of AEP. Combined L-NMMA and HbO did not reduce the amplitude of hyperpolarization with ACh. 7. These data indicate that some but not all of the actions of ACh in the coronary artery can be mimicked by the NO donor, Cys-NO, suggesting that ACh releases NO as well as a second hyperpolarizing factor (i.e., EDHF). Release of NO results in a large increase in tissue cyclic GMP levels and minimal change in membrane potential whereas release of EDHF results in a large membrane hyperpolarization which is independent of changes in tissue cyclic GMP levels. Both of these pathways appear to contribute to relaxation throughout the entire ACh concentration-relaxation relationship.

Acetylcholine↗
PubMed1994

Effect of cyclopiazonic acid, an inhibitor of sarcoplasmic reticulum Ca(2+)-ATPase, on the frequency-dependence of the contraction-relaxation cycle of the guinea-pig isolated atrium.

1. The relevance of a functional sarcoplasmic reticulum (SR) membrane system to the contraction-relaxation cycle and to the force-frequency relationship of guinea-pig atrial tissue was investigated. Cyclopiazonic acid (CPA) was used to inhibit selectively the activity of the SR Ca(2+)-ATPase. IC50 values of 0.2 microM or 1.0 microM were measured in guinea-pig isolated SR membranes in the absence or presence of millimolar ATP, respectively. CPA (0.3-30 microM) did not inhibit the activity of the sarcolemmal Na(+)-Ca(2+)-exchanger as measured in isolated cardiac cell membrane preparations. 2. In guinea-pig isolated left atrium paced at 2.5 Hz (30 degrees C), CPA (1-100 microM) produced a concentration-dependent reduction in developed tension and a fall in the maximum rate of tension increase (+dT/dtmax) and decrease (-dT/dtmax). The twitch duration was markedly increased due to a prolongation of the time to peak tension, and in particular, the relaxation phase. 3. The contraction-relaxation cycle of the left atrium showed a marked dependence on the frequency of stimulation. The developed tension and +dT/dtmax showed a progressive increase from 0.5 Hz, reaching peak values at a stimulation rate of 1.5-2.5 Hz, the positive staircase phenomenon. Higher frequencies of stimulation caused a fall in these parameters. Resting tension was unaffected. The time-course of the contraction-relaxation cycle was also frequency-dependent, with both time to peak tension and relaxation time showing a progressive fall from 2.0-3.5 Hz. 4. The addition of CPA (30 microM) caused marked alterations in the frequency-dependence of the contraction-relaxation cycle. The frequency-dependence of developed tension, + dr/dtmax and dT/dt max was shifted downwards, particularly at higher frequencies, and the frequency at which peak values of+ dT/dtmax and - dT/dtmax were reached was shifted leftwards. The resting tension of the tissues in the presence of 30 micro M CPA was increased markedly at frequencies greater than 2 Hz. The time-course of the contraction-relaxation cycle was markedly prolonged between 1.0 and 3.5 Hz, due to an effect on both time to peak tension and relaxation time.5. In conclusion, these results show that CPA is a highly selective inhibitor of the cardiac SR Ca2+-ATPase, without effect on the sarcolemmal Na+-Ca2+-exchanger, and suggest that a functional SR Ca2+-ATPase is necessary for the normal contraction-relaxation cycle of guinea-pig cardiac tissue.Additionally, the results suggest an increasing dependence of tension development on SR Ca2+-ATPase with increasing frequency, which may reflect either a frequency-dependent activation of this enzyme or the diminished contribution of the Na+-Ca2+ exchanger. These results also provide novel support for the mechanism of the depressed force-frequency relation found in cardiac tissue of heart failure patients, in which there is a reduced expression of Ca2+-ATPase.

Animals↗
PubMed1999

Combined measurements of hippocampal N-acetyl-aspartate and T2 relaxation time in the evaluation of mesial temporal lobe epilepsy: correlation with clinical severity and memory performances.

PURPOSE: In this study we tried to find a correlation between the clinical severity and memory performances, by comparing proton magnetic resonance (MR) spectroscopy and T2 relaxation time measurements in the hippocampi, in a homogeneous group of 27 patients with unilateral mesial temporal lobe epilepsy with ipsilateral hippocampal sclerosis on MR imaging, with a view to answer the following questions: (a) how sensitive is this approach for the assessment of the apparently normal contralateral hippocampus, (b) do the results relate to the clinical severity, and (c) does it allow evaluation of the degree of hippocampal dysfunction. METHODS: Volume-selective proton MR spectroscopy of the head of both hippocampi was performed at 3 T, by using the PRESS sequence, with an echo time of 135 ms, to estimate NAA/(Cho + Cr) ratios. The relaxation times were measured at 0.28 T, by using a conventional Carr-Purcell-Meiboom-Gill sequence, with a repetition time of 2,000 ms, an echo time of 15 ms, and 48 echoes. RESULTS: The combination of NAA/(Cho + Cr) ratio and T2 relaxation time values was allowed to classify contralateral hippocampus abnormalities in two groups: first, decreased NAA/(Cho + Cr) ratio with strongly increased T2 relaxation time values corresponding to abnormalities observed in sclerotic ipsilateral hippocampi; and second, decreased NAA/(Cho + Cr) ratio with normal or slightly increased T2 relaxation time values. Whereas the NAA/(Cho + Cr) ratio or T2 relaxation time value alone was not correlated with memory performances, their association shows that left hippocampal injury evaluated both by NAA and T2 relaxation time measurements was clearly correlated with verbal memory scores, and right hippocampal injury, with visual memory scores. On the other hand, the maximal seizure frequency reported by the patients was correlated with ipsilateral NAA/(Cho + Cr) ratio and T2 relaxation time values but not with contralateral results. CONCLUSIONS: We showed that the combination of NAA and T2 relaxation time measurements can be used to examine the degree of ipsi- and contralateral hippocampal dysfunction or injuries and their relations with memory performances in the presurgical evaluation of patients.

Adult↗
PubMed1992

Hyperpolarization as a mechanism for endothelium-dependent relaxations in the porcine coronary artery.

1. The nature of endothelium-dependent relaxations resistant to nitro-L-arginine was investigated in porcine coronary arteries by measuring isometric force and membrane potential in the presence of indomethacin. 2. Bradykinin induced concentration- and endothelium-dependent relaxations and hyperpolarization in tissues contracted with prostaglandin F2 alpha. Nitro-L-arginine did not affect either the relaxations or the hyperpolarization induced by bradykinin. The threshold concentration of bradykinin was the same for the nitro-L-arginine-resistant relaxations and the membrane hyperpolarization. 3. Nitro-L-arginine-resistant relaxations were evoked by several agents (A23187, thrombin and UK 14304) in addition to bradykinin. The amplitude of membrane hyperpolarizations observed with all agents was proportional to that of nitro-L-arginine-resistant relaxations. 4. Thrombin caused more transient relaxations and hyperpolarizations than bradykinin in the presence of nitro-L-arginine. 5. In tissues contracted with high K+ or tetrabutylammonium (a non-selective K(+)-channel blocker), bradykinin inhibited the contractions in a concentration-dependent manner, whereas membrane hyperpolarization was not observed. The relaxations evoked by the kinin were abolished by nitro-L-arginine. 6. These results suggest that endothelium-dependent relaxations which are resistant to nitro-L-arginine are mediated by membrane hyperpolarization in the porcine coronary artery.

Animals↗
PubMed1982

Relaxant responses to transmural stimulation and nicotine of dog and monkey cerebral arteries.

In helical strips of dog and monkey cerebral arteries contracted with prostaglandin F2 alpha, transmural stimulation and nicotine produced relaxations that were abolished by tetrodotoxin and hexamethonium, respectively. These responses were attenuated by quinidine, whereas relaxations of dog coronary arteries to transmural stimulation and isoproterenol were unaffected. Treatment with vasoactive intestinal polypeptide (VIP) and substance P (SP) abolished the relaxant response of cerebral arteries to repeated applications of VIP and SP, respectively; however, after VIP or SP, a normal relaxant response to transmural stimulation or nicotine was produced. Aminophylline suppressed relaxations induced by ATP but not by nerve stimulation. VIP, SP, and adenosine 5'-triphosphate (ATP) relaxed dog cerebral arteries; the responses were unaffected by quinidine. However, only VIP and ATP relaxed monkey cerebral arteries, and SP contracted the arteries. Acetylcholine contracted monkey arteries, in which transmural stimulation produced a relaxation. It may be concluded that nerves innervating the cerebrospinal wall are stimulated electrically and chemically by nicotine, resulting in the arterial relaxation. However, a vasodilator transmitter was not identified. Quinidine appears to selectively antagonize the action of the transmitters on cerebroarterial smooth muscle.

Animals↗
PubMed1989

Is nitric oxide the only endothelium-derived relaxing factor in canine femoral veins?

Nitric oxide may be an endothelium-derived relaxing factor in systemic arteries and pulmonary veins. The endothelium-derived relaxing factor of systemic veins has not been characterized. Experiments were designed to determine whether the endothelium-derived relaxing factor of systemic veins shared chemical properties and mechanisms of action with nitric oxide. Rings of the canine femoral vein with and without endothelium were suspended in organ chambers for the measurement of isometric force. In rings without endothelium, relaxations to nitric oxide were augmented by superoxide dismutase plus catalase and were inhibited by hemoglobin, methylene blue, and LY 83583. The endothelium-dependent relaxations to acetylcholine and A23187 were not augmented by superoxide dismutase plus catalase but were inhibited by hemoglobin and only moderately reduced by either methylene blue or LY 83583. Relaxations to sodium nitroprusside were not inhibited by methylene blue and LY 83583. Relaxations to sodium nitroprusside were inhibited by ouabain and K+-free solution; those to nitric oxide were not. These results indicate that although the endothelium-derived relaxing factor released from canine systemic veins shares some chemical properties with nitric oxide, the mechanism by which relaxations are induced by the two differ. A factor dissimilar to nitric oxide but acting like sodium nitroprusside may be released by the endothelium of canine systemic veins.

Acetylcholine↗
PubMed1990

Impaired endothelium-dependent relaxations in hypertensive resistance arteries involve cyclooxygenase pathway.

Endothelial cells modulate vascular tone by releasing endothelium-derived relaxing (EDRF) and contracting factors. An imbalance of these factors in hypertension could contribute to increased peripheral vascular resistance. Mesenteric resistance arteries of Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were suspended in a myograph filled with physiological salt solution (37 degrees C; 95% O2-5% CO2). In WKY rings contracted with norepinephrine, acetylcholine (10(-9)-10(-4) M) evoked endothelium-dependent relaxations (88 +/- 2%, IC50 7.3 +/- 0.1; n = 31). Hemoglobin (10(-5) M) but not meclofenamate (10(-5) M) reversed the relaxations delineating EDRF as the mediator. Nitric oxide (3 X 10(-9)-10(-5) M) induced comparable relaxations as acetylcholine. In SHRSP, relaxations to acetylcholine but not those to nitric oxide were impaired (61 +/- 5%, IC50 greater than 6.6 +/- 0.4; n = 24; P less than 0.005). In SHRSP, meclofenamate but not the thromboxane synthetase inhibitor CGS 13080 normalized endothelium-dependent relaxations. Relaxations to sodium nitroprusside were enhanced in SHRSP both in rings with and without endothelium. Thus our results are compatible with the concept that endothelium-dependent relaxations in resistance arteries are mediated by nitric oxide. In SHRSP, endothelium-dependent relaxations are impaired because of a cyclooxygenase-dependent substance interfering with the release and/or action of EDRF.

Animals↗