Velocity measurement by coherent x-ray heterodyning.

We present a small-angle coherent x-ray scattering technique used for measuring flow velocities in slow moving materials. The technique is an extension of X-ray Photon Correlation Spectroscopy (XPCS): It involves mixing the scattering from moving tracer particles with a static reference that heterodynes the signal. This acts to elongate temporal effects caused by flow in homodyne measurements, allowing for a more robust measurement of flow properties. Using coherent x-ray heterodyning, velocities ranging from 0.1 to 10 µm/s were measured for a viscous fluid pushed through a rectangular channel. We describe experimental protocols and theory for making these Poiseuille flow profile measurements and also develop the relevant theory for using heterodyne XPCS to measure velocities in uniform and Couette flows.

Effect of carbamazepine on the in vitro uptake and release of norepinephrine in adrenergic nerves of rabbit aorta and in whole brain synaptosomes.

The effects of carbamazepine, in vitro, on adrenergic neuronal and whole brain synaptosomal uptake and release of tritiated norepinephrine (3H-NE) were assessed. At 10(-4) M, carbamazepine inhibited 3H-NE uptake by 22% in rabbit thoracic aorta and in brain synaptosomes. At the same concentration, carbamazepine inhibited stimulation-induced release of 3H-NE by 42.6% and inhibited isometric contraction in rabbit ear artery helical strips by 31.6%. At 10(-5) M, carbamazepine exhibited a 17.6% inhibition of 3H-NE uptake in brain synaptosomes in the absence of effects on transmitter release. Cocaine, 10(-4) M, and imipramine, 10(-4) M, inhibited uptake by 88% and 85%, respectively, in aorta, and cocaine, 10(-4) M, inhibited synaptosomal uptake by 67.7%. Since antiepileptic blood levels of carbamazepine range between 1.3 and 3.0 X 10(-5) M, it was concluded that the observed effects of carbamazepine are insufficient to account for the anticonvulsant action of the drug. However, the blockade of 3H-NE uptake by brain synaptosomes at 10(-5) M serves to explain the recently described analeptic activity of this agent.

Biphasic effects of imipramine in experimental models of epilepsy.

In a variety of laboratory models of experimental epilepsy, imipramine exerts a biphasic action on the CNS as manifested by antiepileptic properties at low doses and convulsant effects at higher doses. In mice, imipramine (17.5-25 mg/kg, i.p.) blocks maximal electroshock seizures while exerting little or no effect on pentylenetetrazol-induced seizures. In cats, imipramine (2.5-15 mg/kg, i.v.) reduces penicillin and estrogen-induced epileptiform discharge, shortens afterdischarge duration and elevates afterdischarge threshold. Higher doses in mice induce neurotoxicity, including clonic seizures. In cats, doses above 20 mg/kg intensify chemically and electrically induced seizures and induce spontaneous epileptiform episodes. Such a biphasic action of imipramine may limit the drug's clinical utility as an antiepileptic agent and may provide an interesting tool for studies of catecholamines and brain excitability.

Comparison of two lidocaine preparations by in vivo assay methods.

An in vivo study was conducted to determine if there were differences in local anesthetic potency between two commercial brands of lidocaine. The two preparations were evaluated in terms of onset of action, peak effects and duration of action using a double-blink technique. Both products were tested at concentrations of 0.25%, 0.50% and 1%. Each were evaluated for conduction (in rats), topical (in rabbits) and in filtration (in guinea pigs) anesthesia. No clinically significant differences between the two commercial preparations were found.

The effects of antiepileptic drugs on estrogen-induced electrographic spike-wave discharge.

In locally anesthetized, paralyzed cats with bilateral conjugated estrogen (CE)-induced foci in sensory motor cortex, electrographic activity was characterized by 2 to 3 Hz spike and slow wave discharge. Commonly used anti-petit mal drugs (esthosuximide, trimethadione, acetazolamide and diazepam) all reduced CE-induced spike wave activity while diphenylhydantoin converted such activity into 9 to 12 Hz polyspike bursts separated by periods of interictal silence. Correlation appears to exist, therefore, between the ability of the drug to reduce CE-induced spike wave activity and its clinical utility in petit mal epilepsy. In addition to the above compounds, five drugs of less proven utility were evaluated. Of these, two benzodiazepine derivatives (clonazepam and clorazepate) were found to exert a potent and prolonged depressant action on CE-induced activity. The relation of CE to clinical petit mal epilepsy and the potential usefulness of CE as a laboratory model for the evaluation of anti-petit mal drugs are discussed.