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A model of the behavior of spins moving through spatially varying gradient and B1 fields is presented. The model simulates the adiabatic behavior of flowing arterial water during a two-coil arterial inversion experiment. Predictions of the degree of inversion generated by the model are compared with flow phantom results for a wide range of gradient magnitudes, nominal B1 magnitudes, and flow velocities. The high level of agreement between the model and the flow phantom results indicates that the model can be used to help select efficient pulse sequence parameters when setting up an in vivo arterial inversion experiment. In addition, the model provides valuable insights into the adiabatic behavior of arterial spins. These insights could be useful in selecting an efficient surface coil geometry which achieves maximum inversion with a minimum B1 magnitude.

Quantitative NMR measurements of perfusion using magnetic labeling of arterial water have been demonstrated previously in several different highly perfused organs. The success of these previous experiments suggested that arterial labeling may be of use in measuring perfusion in skeletal muscle, where resting perfusion is very low and where increased perfusion after exercise is transient. In the experiments described in this paper, adiabatic inversion of arterial water has been used to make single-voxel measurements of perfusion in the lower hind limb of rats. At rest, the NMR results were quantified to yield a perfusion rate of about 13.8 ml/100g/min. After perturbation due to ischemic exercise, large relative changes in the NMR signal were observed. The peak change of about 2.5% of the NMR signal occurred shortly after perturbation and was followed by a return to resting levels over a period of about 4 min.

Objective: The purpose of this study was to investigate differential effects of hyperventilation on brain lactate in patients with panic disorder and comparison subjects as a possible mechanism for explaining previous observations of an excess rise in brain lactate among panic disorder subjects during lactate infusion., Method: Seven treatment-responsive patients with panic disorder and seven healthy comparison subjects were studied with proton magnetic resonance spectroscopy to measure brain lactate during controlled, voluntary hyperventilation over a period of 20 minutes. Hyperventilation was regulated with the use of capnometry to maintain end-tidal PCO2 at approximately 20 mm Hg during the period of hyperventilation. Blood lactate was measured prior to and at the end of hyperventilation., Results: At baseline the two groups had similar brain lactate levels. Panic disorder subjects exhibited significantly greater rises in brain lactate than comparison subjects in response to the same level of hyperventilation. Blood lactate levels before and after 20 minutes of hyperventilation were not significantly different between groups., Conclusions: Controlled hyperventilation increases brain lactate and does so disproportionately in subjects with panic disorder. This increase in brain lactate may result from decreased cerebral blood flow due to hypocapnia, and individuals with panic disorder may have greater sensitivity to this regulatory mechanism.

Objective: To characterize changes associated with lactate-induced panic, proton magnetic resonance spectroscopy (MRS) was used to measure brain lactate during intravenous infusion of 0.5-M sodium lactate in panic disorder patients and comparison subjects., Method: Eight panic disorder subjects, five medicated and three unmedicated, and eight healthy comparison subjects were studied at baseline, during lactate infusion (5 meq/kg over 20 minutes), and after infusion. Localized proton MRS was used to acquire averaged spectra every 5 minutes from a 27-ml sampling volume in the insular cortex and adjacent regions. Brain lactate levels, quantitatively estimated in relationship to N-acetyl aspartate, were compared to blood lactate levels., Results: The procedure was generally well tolerated; one panic subject requested early termination before lactate infusion. Significant rises in brain lactate levels occurred for all subjects during infusion. The panic patients who responded to lactate (N = 3) had significantly higher brain lactate levels before, during, and after infusion than did the comparison subjects (N = 8) and medicated patients who were lactate nonresponders (N = 4). After infusion the panic patients with lactate-induced panic exhibited a striking dissociation between decreasing blood lactate and further increases in brain lactate levels., Conclusions: These preliminary observations indicate that brain lactate increases during a standard lactate infusion. Lactate-induced panic is associated with greater increases than in comparison subjects and with prolonged elevations in brain lactate that are decoupled from falling blood lactate levels after completion of lactate infusion. Further investigation is necessary to clarify the mechanism(s) responsible for these findings and establish whether a causal relationship to the occurrence of lactate-induced panic exists.

Proton magnetic resonance spectroscopy (1H MRS) localized to the left temporal-parietal region in 8 healthy volunteers detected a 2.1-fold +/- 0.7-fold increase (all values +/-SD) in brain lactate during intravenous infusion of 0.5 molar (M) sodium lactate (5 meq/kg over 20 minutes). Significant increases in brain lactate occurred within 5-10 minutes after starting lactate infusion, progressively rose during the infusion, then decreased towards baseline levels during 30 minutes post-infusion. Venous lactate concentration increased from 0.8 +/- 0.2 mM to 10.9 +/- 4.1 mM or 13.6-fold during the infusion. Flow phantom findings in vitro suggest attenuation of 1H MRS blood lactate signal from arteries and veins as a result of flow velocity effects. Correlations between paired blood and brain lactate measurements at each sampling time indicate a non-linear relationship between compartments during lactate infusion.