Showing papers by "Michael Meyer published in 1995"
TL;DR: When measured in living patients, association cortical benzodiazepine binding sites are relatively preserved, suggesting structurally intact cortical neuropil underlying the glucose hypometabolism identified in Alzheimer's disease.
Abstract: Objective: To evaluate the integrity of neurons and neuropil in metabolically affected association cortices of patients with Alzheimer's disease by measuring central benzodiazepine binding sites with the use of positron emission tomography. Design: In patients with Alzheimer's disease, we determined the cerebral distribution of flumazenil tagged with carbon 11 ([ 11 C]flumazenil), a ligand that binds to the gamma-aminobutyric acid A (GABA A ) receptor complex, and the distribution of fludeoxyglucose tagged with fluorine 18 fludeoxyglucose F 18), a measure of local cerebral glucose metabolism. Tracer kinetic analysis was applied to quantify data in regions of interest. These data were compared with those of normal control subjects. Subjects: Patients with probable Alzheimer's disease ([ 11 C]flumazenil, n=13; fludeoxyglucose F 18, n=11) and normal elderly control subjects ([ 11 C]flumazenil, n=6; fludeoxyglucose F 18, n=10). Results: Significant decreases of the [ 11 C]flumazenil transport rate were found in hypometabolic parietal and temporal association cortices, but [ 11 C]flumazenil binding was not significantly decreased. Conclusions: When measured in living patients, association cortical benzodiazepine binding sites are relatively preserved, suggesting structurally intact cortical neuropil underlying the glucose hypometabolism identified in Alzheimer's disease.
73 citations
54 citations
TL;DR: Results are interpreted as suggesting that an increased C02 flow to the lungs does not constitute an important factor for the initial hyperventilatory response to exercise, and are compatible with a neural origin of ph I, and would support the “neurohumoral” theory of ventilatory control during exercise.
Abstract: To gain an insight into the origin of the phase I ventilatory response to exercise (ph I) in humans, pulmonary ventilation (VE) and end-tidal partial pressures of oxygen and carbon dioxide (PETO2 and PETCO2, respectively) were measured breath-by-breath in six male subjects during constant-intensity exercise on the cycle ergometer at 50, 100 and 150 W, with eupnoeic normocapnia (N) or hyperpnoeic hypocapnia (H) established prior to the exercise test. Cardiac output (Qc) was also determined beat-by-beat by impedance cardiography on eight subjects during moderate exercise (50 W), and the CO2 flow to the lungs (Qc.Cv-CO2 where Cv-CO2 is concentration of CO2 in mixed veneous blood) was estimated with a time resolution of one breathing cycle. In N, the initial abrupt increase of VE during ph I (delta VE approximately 18 1.min-1 above rest) was followed by a transient fall. When PETCO2 started to increase (and PETO2 decreased) VE increased again (phase II ventilatory response, ph II). In H, during ph I delta VE was similar to that of N. By contrast, during ph II delta VE kept gradually decreasing and started to increase only when PETCO2 had returned to approximately 40 mmHg (5.3 kPa). Thus, as a result of the prevailing initial conditions (N or H) a temporal shift of the time-course of VE during ph II became apparent. No correlation was found between CO2 flow to the lungs and VE during ph I. These results are interpreted as suggesting that an increased CO2 flow to the lungs does not constitute an important factor for the initial hyperventilatory response to exercise. They are rather compatible with a neural origin of ph I, and would support the "neurohumoral" theory of ventilatory control during exercise.
6 citations