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Biomedical subjects

H Weiner

Publications and source records attributed to H Weiner.

At least 289 records · Page 16Linked to original sources
PubMed1966

The effect of (+)-tubocurarine chloride and of acute hypotension on electrocortical activity of the cat.

1. The effects of I.V. injection of tubocurarine (3 mg/kg) and of acute hypotension upon electrocortical activity of cats under sodium pentobarbitone were analysed. Technical artifacts associated with changes in brain volume were minimized.2. Initially, the superficial cortical response was reduced by tubocurarine either insignificantly or by 34% or less. Cats bled before injection of tubocurarine showed initially a similar reduction but, occasionally, a severe delayed reduction was found. Any fall in the superficial cortical response started during the secondary rise in B.P., many seconds after the B.P. had reached its lowest initial level. By contrast, spontaneous electrocortical activity was reduced approximately when the peak initial fall of B.P. occurred and it started to recover during the secondary rise in B.P. Reduction of the superficial cortical response could still be elicited after spindling had been suppressed by deep barbiturate anaesthesia. The initial thalamocortical afferent component in somatosensory area I, which was evoked by dorsal column stimulation, was less reduced by injection of tubocurarine than were the post-synaptic positive-negative components.3. The depressant effects of injected tubocurarine upon the superficial cortical response and spindle activity were approximated by rapid arterial bleeding.4. The superficial cortical response was reduced following virtual arrest of the cerebral circulation by acute exsanguination or by acute oil embolization. Such reduction most likely does not depend on systemic transport of inhibitory substances to the brain.5. After injection of tubocurarine the rate of outflow from the superior sagittal sinus was variably reduced during the initial fall in B.P., and often showed a variable, secondary increase. A net deficit in cerebral blood flow was usually present during the period of 80 sec after injection.6. The variability in the effects of injected tubocurarine upon electrocortical activity is attributed to the variability of the net deficit in cerebral blood flow.

Animals↗
PubMed1966

Operant behavior and the galvanic skin potential under DRL schedule.

Motor and galvanic skin potential (GSP) activity were investigated during the conditioning, extinction, and reconditioning of motor responses under a differential reinforcement of low rate (DRL) schedule of reinforcement. Interresponse time (IRT) distributions for motor responses during conditioning and reconditioning gradually stabilized at a peak just beyond the minimal IRT required for reinforcement. Few unreinforced motor responses and "bursts" of motor responses were observed during conditioning and reconditioning. Relative to conditioning and reconditioning, extinction effected larger IRTs and smaller GSP amplitudes. GSP amplitudes were greater for unreinforced than for reinforced motor responses during conditioning and reconditioning. However, GSP amplitudes associated with the unreinforced extinction responses were smaller than either the reinforced or unreinforced responses during conditioning and reconditioning.

Adult↗
PubMedDate not supplied

Failure of T3 to potentiate tricyclic antidepressant response.

Despite a lack of documented efficacy in controlled trials, triiodothyronine (T3) is frequently administered as an adjunctive therapy for tricyclic resistant depressions. In this study, we tested the efficacy of T3 as an adjunctive treatment using a double-blind, placebo-controlled crossover design. Sixteen depressed patients who were unresponsive to 4 weeks of imipramine therapy (mean dose = 206 +/- 54 mg daily, mean combined blood level = 220 +/- 132 ng/dl) received T3 25 micrograms and placebo for 2 weeks each. There was no evidence of a T3 effect using both Hamilton depression scores and global improvement. No subgroup of responders using baseline TRH stimulation tests could be identified. T3 treatment lowered plasma free T4 (P = 0.001) and TSH (P greater than 0.02) while raising plasma T3 levels (P less than 0.01), indicating the physiological effect of the drug.

Adult↗
PubMedDate not supplied

Effects of intravenous and oral dexamethasone on selected lymphocyte subpopulations in normal subjects.

Our studies describe the effects of 1 mg oral (PO) and intravenous (IV) administration of dexamethasone (DEX) on certain subpopulations of circulating lymphocytes in normal subjects. We compared the outcomes of PO and IV DEX administration because of individual differences in gastro-intestinal absorption of DEX and the issue of noncompliance in patients undergoing the dexamethasone suppression test (DST). Both routes of DEX administration were equally effective in suppressing plasma cortisol levels below 5 micrograms/dl, the customary criterion level. Both routes of DEX administration also significantly decreased the percent and absolute number of CD4+ cells, the CD4+/CD8+ ratio, and the percent and absolute number of virgin, but not of memory, CD4+ cells.

Administration, Oral↗
PubMedDate not supplied

Disulfiram alters dopamine metabolism at sites in rat's forebrain as detected by push-pull perfusions.

The effect of tetraethylthiuramdisulfide (disulfiram) on the catabolism of dopamine within discrete regions of the brain was investigated in the unrestrained rat. After a guide cannula had been implanted stereotaxically, a given subcortical site was radiolabeled with 14C-dopamine (DA) by microinjecting 2.0 mu Ci in 2.0 microliters. Successive push-pull perfusates collected from each tissue were assayed by paper electrophoresis for the separation of DA metabolites. When disulfiram, a potent aldehyde dehydrogenase (ALDH) inhibitor, was given intragastrically in a clinically efficacious dose of 200 mg, the formation of the acids DOPAC and HVA was inhibited within perfusates of the caudate nucleus and nucleus accumbens. However, following disulfiram treatment, the proportion of alcohol metabolites did not differ from the control level in the untreated rat. The level of ALDH decreased by approximately 50% in these subcortical nuclei following the inhibition of the enzyme by disulfiram. Conversely, in samples of perfusate obtained from 14C-labeled sites within inferofrontal cortex, periform cortex, diagonal band of Broca, lateral-posterior caudate nucleus, tuberculum olfactorium, lateral olfactory tract or the olfactory nuclear complex, the proportion of DA metabolites remained stable. Generally, a low rate of deamination of the exogenously injected DA occurred within perfusion sites in the ventrobasal forebrain, whereas an intermediate rate of deamination was noted in samples collected at more dorsal loci. Thus, clearcut regional differences in DA catabolism occur in the brain of the living animal, which may depend upon the characteristics of the dopaminergic-rich area of the rat's brain.

Alcohols↗
PubMedDate not supplied

Application of metabolic profiling to study the effects of ethanol on metabolism in rats.

Rat urine was analyzed by both gas chromatography and a combination of gas chromatography/mass spectroscopy in an attempt to apply the technique of metabolic profiling to determine if ethanol consumption produced an alteration in acid excretion products. Rats were fed a liquid diet for seven days then fed ethanol in the same diet. The 24 hr urine for the last day of control and the first day of ethanol differed greatly with respect to four compounds. These were an increase in threonic, glucuronic and an undetermined acid and a decrease in pyroglutamic acid. The biological basis for the alterations was not investigated. Glucuronic acid forms conjugates with many compounds. Possibly an acute dose of ethanol may alter the removal of some compounds from the liver.

Acids↗
PubMedDate not supplied

Use of cyanamide to determine localization of acetaldehyde metabolism in rat liver.

Various techniques have been employed previously to show that acetaldehyde is primarily oxidized in the mitochondrial matrix of rat liver. In this study, a new approach was tested. Mitochondrial low-Km aldehyde dehydrogenase (ALDH) was partially inactivated and the effect on acetaldehyde oxidation measured. Cyanamide was chosen as the ALDH inhibitor. An enzymatic activation of cyanamide, probably by catalase, was necessary for the drug to inhibit ALDH activity. The level of remaining ALDH activity after cyanamide treatment was correlated with the ability of either rat liver mitochondria or liver slices to oxidize acetaldehyde. Any inhibition of ALDH resulted in a decreased rate of acetaldehyde oxidation, indicating that there is no excess of ALDH in the cell above what is needed to oxidize acetaldehyde. Approximately 15% of the acetaldehyde disappearance at 200 microM was catalyzed by high-Km ALDH, and nearly 30% of the acetaldehyde was lost through binding to cytosolic proteins.

Acetaldehyde↗