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PubMed1985

Strategies and tactics in NMR imaging relaxation time measurements. I. Minimizing relaxation time errors due to image noise--the ideal case.

The effect of NMR image noise on errors in calculated values of relaxation times is quantitatively assessed by use of relaxation time noise figures, which are derived on the basis of statistical principles as functions of pulse delay, repetition, and recovery intervals for several types of pulse sequences. Two strategies for determining relaxation times are considered: two point (ratio of intensities for two experiments) and multipoint (least-squares fit of intensities to pulse-sequence functions for n experiments). For given total measurement times, values of pulse interval times are found which give minimum relaxation time noise figures. A comparison of ratio methods shows that the best is a combination saturation-recovery, inversion-recovery (SR/IR) technique. For short measurement times (less than about 10T1) this optimized SR/IR ratio determination is also superior to the best multipoint method, a series of inversion-recovery experiments with equally incremented inversion-recovery times. An examination of the effect of signal averaging on the relaxation time noise shows that up to a measurement time characteristic of the particular method used (e.g., for times up to about 5T1 for the SR/IR ratio determination, 100T1 for the multipoint inversion-recovery method), increased measurement time is more effectively allotted to longer pulse intervals than to signal averaging. Numerical examples are tabulated which can help one to set optimum values for pulse intervals, given a rough estimate of the relaxation time to be determined.

Magnetic Resonance Spectroscopy↗
PubMed1989

1H magnetic resonance of human tumours. Analysis of the transverse relaxation of the methylene protons using continuous distributions of relaxation times.

In tumours, the decay of 1H transverse magnetization (relaxation profile) of the methylene resonances is usually not a single exponential. The conventional sum-of-exponentials approximation often leads to several solutions which fit the experimental data; choosing one solution over another is highly subjective. We have therefore analyzed transverse relaxation data for the methylene resonance of lipids in human tumours, assuming a continuous distribution of relaxation times. We have studied 89 colon tumours (27 with metastasis), 12 'normal' colon tissues, 40 breast tumours (24 with metastasis) and 13 malignant lymph nodes. All were primary tumours and the patients had received no previous treatment. Two continuous distribution approximations were tested. The two-parameter lognormal distribution provides a simple representation of the relaxation profile. The constrained regularization method (Contin) complements and extends the lognormal approach. The average T2 values, mean value of T2, whether derived from the lognormal or the Contin approximations, are consistent and comparable. Tumour and 'normal' colon tissue taken from the same patient show important differences in relaxation behaviour. A considerable broadening of the lognormal distribution, with mean value of T2 shifted to shorter values, is observed for the colon tumours. This is verified by the constrained regularization method. The 'normal' colon tissues are usually characterized by a single, relatively narrow distribution, while tumours show one or more broad peaks. A substantial broadening of the distribution of relaxation times is observed in colon tumours, whether metastasized or not. A similar broadening is noted for breast tumours and malignant lymph nodes, although the range is slightly less than for colon tumours.(ABSTRACT TRUNCATED AT 250 WORDS)

Breast Neoplasms↗
PubMed2000

Effects of off-resonance irradiation, cross-relaxation, and chemical exchange on steady-state magnetization and effective spin-lattice relaxation times

In the presence of an off-resonance radiofrequency field, recovery of longitudinal magnetization to a steady state is not purely monoexponential. Under reasonable conditions with zero initial magnetization, recovery is nearly exponential and an effective relaxation rate constant R(1eff) = 1/T(1eff) can be obtained. Exact and approximate formulas for R(1eff) and steady-state magnetization are derived from the Bloch equations for spins undergoing cross-relaxation and chemical exchange between two sites in the presence of an off-resonance radiofrequency field. The relaxation formulas require that the magnetization of one spin is constant, but not necessarily zero, while the other spin relaxes. Extension to three sites with one radiofrequency field is explained. The special cases of off-resonance effects alone and with cross-relaxation or chemical exchange, cross-relaxation alone, and chemical exchange alone are compared. The inaccuracy in saturation transfer measurements of exchange rate constants by published formulas is discussed for the creatine kinase reaction. Copyright 2000 Academic Press.

Journal Article↗
PubMed2001

Relaxation behavior of laser-polarized (129)Xe gas: size dependency and wall effect of the T(1) relaxation time in glass and gelatin bulbs.

Size dependency of the relaxation time T(1) was measured for laser-polarized (129)Xe gas encapsulated in different sized cavities made by glass bulbs or gelatin capsules. The use of laser-polarized gas enhances the sensitivity a great deal, making it possible to measure the longer (129)Xe relaxation time in quite a short time. The size dependency is analyzed on the basis of the kinetic theory of gases and a relationship is derived in which the relaxation rate is connected with the square inverse of the diameter of the cavity. Such an analysis provides a novel parameter which denotes the wall effect on the relaxation rate when a gas molecule collides with the surface once in a second. The relaxation time of (129)Xe gas is also dependent on the material which forms the cavity. This dependency is large and the relaxation study using polarized (129)Xe gas is expected to offer important information about the state of the matter of the cavity wall.

Journal Article↗
PubMed2003

Extending the range of amide proton relaxation dispersion experiments in proteins using a constant-time relaxation-compensated CPMG approach.

Relaxation compensated constant-time Carr-Purcell-Meiboom-Gill relaxation dispersion experiments for amide protons are presented that detect mus-ms time-scale dynamics of protein backbone amide sites. Because of their ten-fold larger magnetogyric ratio, much shorter 180 degrees pulses can be applied to (1)H than to (15)N spins; therefore, off-resonance effects are reduced and a wider range of effective rf fields can often be used in the case of (1)H experiments. Applications to [(1)H-(15)N]-ubiquitin and [(1)H-(15)N]-perdeuterated HIV-1 protease are discussed. In the case of ubiquitin, we present a pulse sequence that reduces artifacts that arise from homonuclear (3)J(H(N)-H(alpha)) coupling. In the case of the protease, we show that relaxation dispersion of both (1)H and (15)N spins provides a more comprehensive picture of slow backbone dynamics than does the relaxation dispersion of either spin alone. We also compare the relative merits of (1)H versus (15)N transverse relaxation measurements and note the benefits of using a perdeuterated protein to measure the relaxation dispersion of both spin types.

Amides↗
PubMed2004

Effects of water on the primary and secondary relaxation of xylitol and sorbitol: implication on the origin of the Johari-Goldstein relaxation.

Dielectric spectroscopy was employed to study the effects of water on the primary alpha -relaxation and the secondary beta -relaxation of xylitol. The measurements were made on anhydrous xylitol and mixtures of xylitol with water with three different water concentrations over a temperature range from 173 K to 293 K. The alpha -relaxation speeds up with increasing concentration of water in xylitol, whereas the rate of the beta -relaxation is essentially unchanged. Some systematic differences in the behavior of alpha -relaxation for anhydrous xylitol and the mixtures were observed. Our findings confirm all the observations of Nozaki et al. [J. Non-Cryst. Solids 307, 349 (2002)]] in sorbitol/water mixtures. Effects of water on both the alpha - and beta -relaxation dynamics in xylitol and sorbitol are explained by using the coupling model.

Journal Article↗
PubMed1983

Myocardial relaxation. VI. Effects of beta-adrenergic tone and asynchrony on LV relaxation rate.

We studied the effect of left ventricular (LV) asynchrony and alterations in beta-adrenergic tone on the systolic load (pressure) dependency of LV isovolumic relaxation rate in anesthetized dogs. The time constant (T) of isovolumic exponential pressure decline was used as an index of relaxation rate. Variably afterloaded LV contractions resulted in a progressive increase in LV end-systolic pressure from 124 +/- 6 in the control beat to 176 +/- 11 mmHg in the third beat and a progressive lengthening of T from 19 +/- 2 to 30 +/- 4 ms. The direct relation between LV end-systolic pressure and T was nearly linear (r = 0.98), and the slope (k) of this relation was taken to reflect the systolic load dependency of T. Administration of isoproterenol (n = 6) produced a decrease in k from 0.11 +/- 0.02 to 0.08 +/- 0.02 (P less than 0.05); with propranolol (n = 6), k increased from 0.08 +/- 0.02 to 0.27 +/- 0.04 (P less than 0.01). Right ventricular epicardial pacing (n = 6) produced an asynchronous LV contraction and an increase in k from 0.09 +/- 0.02 (atrial pacing) to 0.25 +/- 0.04 (P less than 0.01). These studies confirm the dependency of LV relaxation rate on systolic loads and indicate that this form of load-dependent relaxation can be modified by alterations in beta-adrenergic tone and LV asynchrony. The observed alterations suggest the importance of temporal dispersion of the contraction-relaxation sequence as a mechanism responsible for disturbed relaxation.

Animals↗
PubMed1981

Myocardial relaxation. V. Postextrasystolic contraction-relaxation in the intact dog heart.

Postextrasystolic (PES) relaxation of the left ventricle was studied in 24 anesthetized dogs using the time constant (tau) of the left ventricular isovolumic pressure decline as an index of global relaxation velocity. Using programmed atrial stimulation and a control RR interval of 500 msec, the "coupling interval/compensatory pause" was varied from 400/600 msec to 250/750 msec, and left ventricular pressure-segment length data from control beats were compared with data from PES beats. Contractile state and fractional shortening increased in the PES beat, but the relaxation time constant remained unchanged (control, 35 +/- 3 msec; PES at 250/750 msec, 36 +/- 3 msec) (p = NS). Pretreatment with propranolol did not qualitatively influence these results. Isoproterenol and calcium were given in doses sufficient to increase the time derivative of isovolumic pressure (maximal positive dP/dt) by an amount equal to that obtained with PES potentiation (approximately 50%); isoproterenol produced a substantial decrease in the relaxation time constant (38 +/- 4 to 30 +/- 6 msec, p less than 0.01), whereas calcium administration produced only a small decrease in the time constant (30 +/- 5 to 27 +/- 5 msec, p less than 0.05). Thus, in the intact dog heart, some positive inotropic interventions augment contraction and speed relaxation, but PES potentiation of contraction is not associated with a change in relaxation velocity.

Animals↗
PubMed1997

Inhibitors of arterial relaxation among components of human oxidized low-density lipoproteins. Cholesterol derivatives oxidized in position 7 are potent inhibitors of endothelium-dependent relaxation.

BACKGROUND: Oxidized low-density lipoproteins (LDLs) are known to impair arterial relaxation. The aim of the present study was to identify the components of oxidized LDL that may account for inhibition of endothelium-dependent relaxation. METHODS AND RESULTS: LDLs from 12 healthy subjects were either maintained at 4 degrees C (native LDL) or incubated at 37 degrees C in the presence of copper sulfate (oxidized LDL). Unlike pretreatment with native LDL, pretreatment with oxidized LDL reduced significantly the acetylcholine-mediated relaxation of rabbit aortic segments compared with control segments incubated in Krebs' buffer (maximal relaxation [Emax], 72.0 +/- 6.7% versus 94.1 +/- 0.8%, respectively, P < .01; negative logarithm of the concentration required to produce a half-maximal relaxing effect [pD2], 6.6 +/- 0.1 versus 7.2 +/- 0.1, respectively, P < .001). The absolute difference between Emax values obtained with oxidized and native LDL (delta Emax) correlated significantly with the formation of 7 ketocholesterol, 7 alpha-hydroxycholesterol, and 7 beta-hydroxy-cholesterol. In contrast, delta Emax did not correlate with the amount of lipoperoxides or lysophosphatidylcholine formed, and the difference of pD2 values measured with oxidized and native LDL (delta pD2) did not correlate significantly with any of the oxidation-derived LDL compounds. When added individually, 7-ketocholesterol and 7 beta-hydroxycholesterol reduced Emax values but not pD2 values in a time- and concentration-dependent manner. CONCLUSIONS: Cholesterol derivatives in oxidized LDL can reduce maximal arterial relaxation through a specific effect on vascular endothelial cells.

Acetylcholine↗
PubMed1992

Potentiation of endothelium-dependent relaxations to bradykinin by angiotensin I converting enzyme inhibitors in canine coronary artery involves both endothelium-derived relaxing and hyperpolarizing factors.

Studies were designed to investigate the mechanisms underlying the augmentation by angiotensin I converting enzyme (ACE) inhibitors of the endothelium-dependent relaxations evoked by bradykinin. Isometric tension, tissue levels of cGMP, and transmembrane potential were measured in isolated canine coronary arteries as indications of the respective contribution of nitric oxide and endothelium-derived hyperpolarizing factor. In rings of coronary artery with endothelium, relaxations to bradykinin were potentiated by the ACE inhibitors cilazaprilat and perindoprilat. NG-Nitro-L-arginine (NLA), a nitric oxide synthase inhibitor, impaired relaxations to bradykinin. But the presence of ACE inhibitors partially restored this activity. Bradykinin stimulated the production of cGMP, and this was enhanced significantly by ACE inhibitors, indicating an augmented release of nitric oxide. NLA abolished the increase induced by bradykinin irrespective of the presence of ACE inhibitors. Electrophysiological studies revealed that bradykinin elicited an endothelium-dependent hyperpolarization of vascular smooth muscle that was insensitive to NLA and potentiated by ACE inhibitors. The bradykinin-induced hyperpolarization and NLA-resistant relaxations were transient and impaired by potassium depolarization. Thus, production of endothelium-derived hyperpolarizing factor may account for the NLA-resistant relaxations of canine coronary arteries. The relaxations induced by bradykinin were unaffected by the B1 kinin receptor antagonist des-Arg9,[Leu8]-bradykinin either in the absence or in the presence of NLA but were antagonized by the B2 kinin receptor antagonist D-Arg[Hyp3,D-Phe7]-bradykinin. Molecular exclusion chromatography of 125I-labeled [Tyr8]-bradykinin and its degradation products demonstrated that the breakdown of the kinin by isolated coronary arteries was prevented in the presence of perindoprilat.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed2004

Determinants of MR relaxation rates in jaw cysts: implications for diagnostic values of the relaxation times.

OBJECTIVES: The MRI signal intensities and the relaxation times (T1 and T2) have already been used for comparisons among various types of cysts. The signal intensities (or T1 and T2) were suggested to be related to cyst content. However, such a relationship between the relaxation rates (1/T1 and 1/T2) and the aspirated content of jaw cysts was not given. Therefore, an investigation on the determinants of the relaxation rates in the jaw cysts may be helpful in elucidating the biological basis for the differences in relaxation rates among the categories of jaw cysts. METHODS: The aspirated contents of 23 cysts (16 radicular and 7 haemorrhagic) were scanned using an MR imager operating at 1 T magnetic field strength. The viscosities and the dry-weight-to-water-weight ratios (Ms/Mw) were determined. Also, the mean values of cyst categories were compared using statistical analysis. RESULTS: The 1/T1 had a moderate correlation with viscosity (0.66) and Ms/Mw (0.56), while the 1/T2 had a good correlation with viscosity (0.87) and Ms/Mw (0.82). The mean values of viscosity, Ms/Mw and relaxation rates in radicular cysts were significantly lower (P < 0.05) than those of haemorrhagic cysts. CONCLUSIONS: The present data suggest that similarities and differences between relaxation rates of radicular and haemorrhagic cysts can be explained by the solid content and viscosity of cysts.

Body Water↗
PubMed1997

Neuromuscular transmission and its pharmacological blockade. Part 3: Continuous infusion of relaxants and reversal and monitoring of relaxation.

Continuous infusion is an attractive method of administration when muscle relaxation is needed for a longer period. The pharmacokinetic behaviour of a drug is an important determining factor for the suitability of relaxants for continuous infusion. At present mainly intermediately long acting relaxants are used for this purpose. At the end of surgery residual curarization may exist and thus anaesthesiologists prefer to be able to reverse the relaxants. The anticholinesterases neostigmine, pyridostigmine, and edrophonium are used clinically for this reason. Their effect is prolonged in patients with renal failure, and also affected during acid-base disturbances. Some other drugs have been used experimentally for the reversal of neuromuscular blockade, but are inadequate. Special problems can arise when reversal of a mivacurium-induced or antibiotic-induced blockade is wanted, or mivacurium was administered. Monitoring neuromuscular transmission is an important feature to determine the effect of relaxant administration or to detect residual curarization. It is based on stimulation of peripheral nerves with either single twitch, train of four, tetanic or double burst stimulation. The evoked response can be quantitated with mechanomyography, electromyography, or accelerography. The response of the various muscles to nerve stimulation varies due to the different characteristics of the muscles. Clinically, the use of the adductor pollicis muscle is advised.

Electromyography↗
PubMed1977

Relaxation of heart muscle by catecholamines and by dibutyryl cyclic adenosine 3',5'-monophosphate. Similarity of beta-adrenoceptors mediating contractile and relaxant effects of catecholamines in kitten pipillary muscle.

1. In isometrically contracting kitten papillary muscles, dibutyryl cyclic AMP (DBcAMP) enhanced peak tension, increased rates of contraction and relaxation, decreased tension of a phasic but not of a small tonic component of KCl-contractures, and caused aftercontractions. These effects resemble closely those of catecholamines. 2. The effects of DBcAMP on kitten papillary muscle were not influenced by (-)-bupranolol, a beta-adrenoceptor antagonist. 3. DBcAMP decreased KCl-contractures in strips of frog ventricle. 4. Phasic KCl-contractures in kitten papillary muscles were decreased by (-)- and (+)-isoprenaline. For similar effects, 100-fold higher concentrations of (+)-isoprenaline than of (-)-isoprenaline were required. 5. Increases in maximum rates of contraction and relaxation, increases in peak tension of isometric contractions and reduction of phasic KCl-contractures by catecholamines were antagonized competitively to a similar extent by (-)-bupranolol. Mean apparent equilibrium constants for the beta-adrenoceptor-(-)-bupranolol complex of 0.46-0.70 nM were estimated. These constants were quite similar irrespective of whether (-)-isoprenaline, (+)-isoprenaline or (-)-noradrenaline were used as agonists. 6. Increases in contractile strength, maximum rates of contraction and of relaxation of isometric contractions and decreases in KCl-contractures by (-)-isoprenaline were surmountably blocked by (+)-bupranolol. Mean apparent equilibrium constants for the receptor-(+)-bupranolol complex were 40-50 nM. 7. The equilibrium constants of (-)- and (+)-bupranolol for the receptors mediating positive inotropic and relaxant effects of catecholamines were not significantly different from constants for bupranolol-receptor complexes in cell-free membrane particles of kitten heart ventricle. It is suggested that the same beta-adrenoceptor triggers positive inotropic, relaxant and adenylyl cyclase-activating effects of catecholamines in kitten papillary muscle. 8. The partial agonist (-)-dichloroisoprenaline (DCI) (1 muM) reduced by 79% the phasic KCl-contractures of the kitten papillary muscles. DCI stimulates adenylyl cyclase activity of ventricle membranes to less than 1/4 of maximum stimulation by (-)-isoprenaline. If cyclic AMP produced by DCI is involved in the decrease of phasic KCl-contracture, small increase in cyclic AMP should be sufficient to induce this effect.

Adrenergic beta-Antagonists↗
PubMed1991

Low level hyperlipidemia impairs endothelium-dependent relaxation of porcine coronary arteries by two mechanisms. Functional change in endothelium and impairment of endothelium-dependent relaxation by two mediators.

We evaluated the effect of a low level of hyperlipidemia and the effects of in vitro exposure to atherogenic lipoproteins (LDL, VLDL) on the vascular responsiveness of isolated porcine coronary arteries. Firstly we studied the change in vascular responsiveness induced by feeding a cholesterol-rich diet to pigs for 4 and 9 weeks (C4 and C9 pigs). The serum cholesterol level in pigs fed a cholesterol-rich diet reached 218.5 +/- 32.9 mg/dl compared with 85.5 +/- 8.4 mg/dl in the controls. Segments of the left descending coronary artery were examined. The contraction induced by KCl or prostaglandin F2 alpha was not altered significantly by hypercholesterolemia nor was the relaxation induced by the Ca2+ ionophore, A23187, or by nitroglycerin. Endothelium-dependent relaxation (EDR) evoked by high, but not low, concentrations of bradykinin was reduced in the C4 pigs as compared with those in normal animals. EDRs evoked by bradykinin, substance P, and serotonin were significantly reduced in C9 pigs. Histologically, as observed by light and electron microscopy, fatty changes or intimal thickenings were not seen in the coronary arteries of the C4 pigs. Minimal changes (intimal thickening and fragmentation of internal elastic lamina) were observed only in parts of arteries of the C9 pigs. Secondly, the direct effects of LDL and VLDL on vascular responsiveness were studied. Although preincubation with LDL inhibited the EDR caused by exposure to bradykinin and A23187 in the coronary arteries of normal and cholesterol-fed pigs, preincubation with LDL inhibited the arterial relaxation induced by exposure to substance P or serotonin in both the C4 and the C9 pigs, but not in the control animals. The degree of inhibition was especially marked in the C9 pigs. The inhibitory effect of VLDL on EDR was weaker than that of LDL. Indomethacin (5 microM) did not alter this inhibitory effect of lipoproteins. Neither LDL nor VLDL had any effect on the vascular relaxation induced by nitroglycerin. These results are consistent with the idea that endothelium-dependent arterial relaxation is attenuated even at the very early stage of cholesterol-induced atherosclerosis. Atherogenic lipoproteins may further impair the decreased EDR in the arteries of hyperlipidemic pigs by two factors: one released on stimulation with bradykinin and the calcium ionophore A23187, the other released on stimulation with substance P and serotonin.

Animals↗
PubMed1997

Role of nitric oxide and nitric oxide-independent relaxing factor in contraction and relaxation of rabbit blood vessels.

It has been shown that spontaneous release of nitric oxide (NO) from the vascular endothelium attenuates contractile responses of vascular smooth muscles to norepinephrine, and that acetylcholine-induced relaxation is mediated by the evoked release of NO and endothelium-derived hyperpolarizing factor. Since the involvement of these substances (or factors) in mechanical responses is heterogeneous among blood vessels, we have investigated the role of these substances in agonist-induced contraction and relaxation in 6 rabbit blood vessels. Vascular reactivity for the contractile response to norepinephrine was potentiated after removal of endothelium and by 100 microM N(G)-nitro-L-arginine (L-NA) but not by 80 nM-0.4 microM clotrimazole. This potentiation was most marked in the mesenteric artery among the blood vessels tested, suggesting that the basal release of NO reduced the contractile response of the vascular smooth muscle to norepinephrine in this artery. Acetylcholine-induced relaxation was abolished by removal of the endothelium and was attenuated by L-NA (1-100 microM) in all blood vessels. The attenuation by 100 microM L-NA was most obvious in aorta and vein and least in mesenteric resistance artery in which the acetylcholine-induced, L-NA-resistant relaxation was inhibited by 80 nM-0.4 microM clotrimazole. These results suggested that there is a regional difference in the degree of involvement of NO in acetylcholine-induced relaxation. In mesenteric resistance artery, the NO-independent, clotrimazole-sensitive factor, possibly hyperpolarizing factor may also contribute to the response to acetylcholine at high concentrations.

Acetylcholine↗
PubMed1983

Endothelium-dependent relaxation of rabbit aorta. I. Relaxation stimulated by arachidonic acid.

Vascular responses to the addition of arachidonic acid (AA) were characterized in rings of rabbit thoracic aorta. In preparations which were precontracted to a stable plateau by 10(-7) M phenylephrine, AA (10-100 microM) elicited transient relaxation if the endothelium was intact. The same concentrations of AA only contracted tissues in which the endothelium was purposely disrupted. Indomethacin pretreatment (14 microM, 30 min) potentiated the relaxation response in intact rings. Under these conditions, relaxation in response to 100 microM AA was 32(+/- 3)% of the tension stimulated by 10(-7) M phenylephrine. Preincubation with 5,8,11,14-eicosatetraynoic acid (50 microM) or nordihydroguaiaretic acid (25 microM) completely prevented AA-induced relaxation. Contractile responses to AA were examined in rings lacking pre-existing active tension. AA (3-100 microM) elicited rapidly developing and somewhat transient contractions in rings with endothelium. Slow developing contractions which were significantly smaller in magnitude were observed in rings lacking endothelium. Indomethacin or 5,8,11,14-eicosatetraynoic acid pretreatment inhibited AA-stimulated contractions both in intact and de-endothelialized tissues. Nordihydroguaiaretic acid pretreatment had no effect on contractile responses in rings lacking endothelium and slightly potentiated responses in intact rings. We conclude that endothelium-dependent relaxation of rabbit aorta by AA is mediated by a noncyclooxygenase metabolite(s). Contractile responses are mediated by cyclooxygenase metabolites, which in intact rings are derived largely from the vascular endothelium.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed2004

1H metabolite relaxation times at 3.0 tesla: Measurements of T1 and T2 values in normal brain and determination of regional differences in transverse relaxation.

PURPOSE: To measure 1H relaxation times of cerebral metabolites at 3 T and to investigate regional variations within the brain. MATERIALS AND METHODS: Investigations were performed on a 3.0-T clinical whole-body magnetic resonance (MR) system. T2 relaxation times of N-acetyl aspartate (NAA), total creatine (tCr), and choline compounds (Cho) were measured in six brain regions of 42 healthy subjects. T1 relaxation times of these metabolites and of myo-inositol (Ins) were determined in occipital white matter (WM), the frontal lobe, and the motor cortex of 10 subjects. RESULTS: T2 values of all metabolites were markedly reduced with respect to 1.5 T in all investigated regions. T2 of NAA was significantly (P < 0.001) shorter in the motor cortex (247 +/- 13 msec) than in occipital WM (301 +/- 18 msec). T2 of the tCr methyl resonance showed a corresponding yet less pronounced decrease (162 +/- 16 msec vs. 178 +/- 9 msec, P = 0.021). Even lower T2 values for all metabolites were measured in the basal ganglia. Metabolite T1 relaxation times at 3.0 T were not significantly different from the values at 1.5 T. CONCLUSION: Transverse relaxation times of the investigated cerebral metabolites exhibit an inverse proportionality to magnetic field strength, and especially T2 of NAA shows distinct regional variations at 3 T. These can be attributed to differences in relative WM/gray matter (GM) contents and to local paramagnetism.

Adult↗
PubMed1997

Temperature dependence and phase transition of proton relaxation of hydrated collagen in intact beef tendon specimens via cross-relaxation spectroscopy.

The role of water of hydration in proton relaxation in tissues as exemplified by hydrated collagen in beef tendon was studied as a function of temperature from -40 degrees to 37 degrees C by using cross-relaxation spectroscopy. Experimental data were fitted to a simple binary spin-bath model. The outcome of this procedure allows the construction of a semi-quantitative depiction of proton relaxation in a heterogeneous system and its change as one of the water fractions freezes at about -10 to -20 degrees C, a transition observed by NMR and confirmed independently by differential scanning calorimetry. Such physical depiction provides a crude but insightful interpretation of the role "bound" water plays in proton relaxation. This may be important in shedding light on the mechanism of tissue relaxation and its role in MRI diagnosis, particularly for those diseases such as liver cirrhosis where the water-macromolecular interaction plays a prominent role.

Animals↗