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Biomedical subjects

S Spector

Publications and source records attributed to S Spector.

At least 127 records · Page 7Linked to original sources
PubMed1977

Reduction of blood pressure and vascular collagen in hypertensive rats by beta-aminopropionitrile.

beta-Aminopropionitrile, a specific inhibitor of lysyl oxidase prevented the rise in blood pressure induced by deoxycorticosterone-salt in rats. In addition, after the onset of hypertension, administration of beta-aminopropionitrile lowered the blood pressure. Concomitant with the lowering of blood pressure, there was a reduction in the more highly crosslinked form of vascular collagen. These findings would indicate that increases in vascular connective tissue are not only sequelae of hypertension, but may also contribute to the maintenance of elevated blood pressure.

Amino Acid Oxidoreductases↗
PubMed1977

Binding of the endogenous nonpeptide morphine-like compound to opiate receptors.

The endogenous central nervous tissue substance called MLC (morphine-like compound) is shown to bind to the opiate receptors of the mouse neuroblastoma X glioma hybrid cell line NG108-15. The interaction of MLC with these opiate receptors is noncooperative, as is the interaction of morphine, naloxone, and Leu-enkephalin with these receptors. A specific antibody to morphine will bind MLC but will not bind beta-endorphin, Leu-enkephalin, or Met-enkephalin. It would appear, therefore, that MLC can be considered to be a different type of endogenous ligand for the opiate receptor.

Animals↗
PubMed1977

Cerebrospinal fluid levels of d-tubocurarine in man.

Using radioimmunoassay, d-tubocurarine (dTc) was found in the cerebrospinal fluid (CSF) of man after intravenous injection. When dTc was administered in a single dose (0.3 mg/kg) to nine patients, small quantities, 3.5 +/- .26 ng/ml (mean +/- SE), appeared in the lumbar CSF within 5 minutes. The concentration of dTc (0.3 mg/kg) were given at 90 minute intervals. Concentration of dTc in the CSF remained constant for the next 25 minutes, but then began to increase with time to to 9.3 +/- 4.4 ng/ml 30 minutes after injection, 14.5 +/- 4.4 ng/ml at one hour, and 24.9 +/- 6.5 ng/ml at six hours. In another group of six patients, three doses of dTc (0.3 mg/kg) were given at 90-minute intervals. Concentration of dTc in the CSF increased after each injection. The quantities of dTc found in the CSF are unlikely to produce any pharmacologic or adverse effect (e.g., convulsion) in man.

Humans↗
PubMed1977

Brain and vascular monoamine oxidase activity in the deoxycorticosterone-salt hypertensive rat.

1 The role of monoamine oxidase (MAO) in the maintenance of deoxycorticosterone-sodium chloride (DOCA-salt) hypertension was investigated by assaying the MAO activity both in central as well as peripheral blood vessels and in brain tissue. 2 The results suggest that the activity of MAO in the DOCA-salt hypertensive rat is similar to the activity present in the normotensive rat.

Animals↗
PubMed1977

Radioimmunoassay of atropine in plasma.

Antibodies, against atropine, were produced in rabbits immunized with atropine conjugated to bovine serum albumin. The antisera possessed a high binding affinity and were quite specific. The sensitivity of the method allowed detection of 6.25 ng of atropine per ml of plasma in a 10-microliter specimen. The method does not require an extraction procedure and can be performed using very small volumes of plasma. Plasma concentration-time profiles were determined by this method in dogs after rapid i.v. administration of atropine. Atropine declined from plasma in a biexponential fashion, exhibiting a terminal half-life of approximately 2.1 hours.

Animals↗
PubMed1976

Correlation between plasma and cerebrospinal levels of imipramine.

This study measured the levels of imipramine hydrochloride and desipramine hydrochloride (desmethylimipramine) in the plasma and cerebrospinal fluid (CSF) in 11 depressed patients. The oral doses correlated significantly with the plasma levels irrespective of different diagnostic categories. The CSF levels varied significantly. In the endogenous depressive group the CSF levels were significantly higher in responders as compared to nonresponders. The CSF levels of the nonresponders in the endogenous depressive group, and of both responders and nonresponders in the schizo-affective groups, were similar.

Depression↗
PubMed1976

N-desmethyldiazepam: a new metabolite of chlordiazepoxide in man.

Following administration of chlordiazepoxide HCl to man, N-desmethyldiazepam, a known metabolite of diazepam (Valium), was identified in plasma. The metabolite was identified on the basis of its thin-layer chromatographic (TLC) mobility, electron-capture gas-chromatographic (EC-GC) retention time, and mass spectrum relative to authentic N-desmethyldiazepam. Plasma levels of N-desmethyldiazepam in subjects receiving both single and chronic doses of chlordiazepoxide were determined by an EC-GC method with a limit of sensitivity of 10 ng/ml using 2-ml samples and by a radioimmunoassay procedure which had a limit of sensitivity of 20 ng/ml using a 0.1-ml sample. Both assay methods gave good agreement for the levels of N-desmethyldiazepam. In subjects receiving a single 30-mg oral or intravenous dose of chlordiazepoxide, measurable levels of N-desmethyldiazepam in plasma (10 to 60 ng/ml) were obtained 24 to 72 hr after administration. In 5 subjects receiving 10 mg of chlordiazepoxide three times a day, steady-state levels of N-desmethyldiazepam in plasma were reached after about 1 wk of administration. The mean maximum and minimum steady-state levels of N-desmethyldiazepam were 260 and 220 ng/ml of plasma, respectively. Similar steady-state levels were observed on treatment with 30 mg of chlordiazepoxide over 24 hr.

Animals↗
PubMed1976

Radioimmunoassay for the simultaneous determination of morphine and codeine.

Antiserum against morphine was produced in rabbits immunized with morphine hapten conjugated to bovine serum albumin. The carrier protein was conjugated to the nitrogen atom of the opiate alkaloid in order to make the phenolic hydroxy group on C3 and the alcoholic group on C6 as determinant groups. The antibody does not recognize codeine or the major metabolite of morphine, 3-O-monoglucuronide. This antibody was used in conjunction with an antibody prepared against 3-O-carboxymethylmorphine to develop a radioimmunoassay which can measure codeine in the presence of morphine. The assay was used to follow both the plasma and brain levels of codeine and its biotransformation to morphine. Codeine when administered at a dose of 5 mg/kg i.v. showed a biphasic plasma decay curve the first phase of which had a +1/2 of 26 min. Peak concentrations of morphine were detected in the plasma following that dose of codeine at 0.5 h. 30 min after the injection of 20 mg/kg i.p. codeine, the brain levels of morphine were only 2% that of codeine. Thereafter, the brain levels of morphine slowly declined.

Animals↗
PubMed1976

Disposition of propranolol isomers in mice.

l-Propranolol was found to protect mice from hyperbaric oxygen-induced seizures. The disposition of effective doses of propranolol isomers in mice was followed using stereospecific antibodies with a radioimmunoassay procedure. Serum and tissue concentrations were determined and correlated with the protective effect. Following racemic administration, there were no differences in serum disposition of d- and l-propranolol, although there was initially a preferential uptake of the 1-isomer both into cardiac and brain tissue. The d-isomer exerted synergistic action on the 1-isomer protective effect.

Animals↗
PubMed1976

Antibodies as a means of isolating and characterizing biologically active substances: presence of a non-peptide, morphine-like compound in the central nervous system.

Antibodies generated against small molecular weight substances such as drugs are being used to isolate and characterize biologically active agonists. A morphine-like compound can be extracted from brain of various species which has determinant groups that are recognized by specific morphine antibodies. It has a regional distribution which can be quantitated as immuno-equivalents. Immunological, chemical and chromatographic tests show great similatiries of the compound to morphine. This morphine-like compound has biological activity as it inhibits the electrically induced contractions both of the guinea pig ileum and mouse vas deferens but the inhibition is not reversed by naloxone or naltrexone.

Animals↗
PubMed1976

Pharmacokinetics of naloxone in rats and in man: basis for its potency and short duration of action.

Using a specific and sensitive radioimmunoassay, naloxone concentrations in the brains and sera of rats were measured at intervals for four hours following iv injection (5 mg/kg). Decrement curves of naloxone were compared with those after iv injection of morphine (5 mg/kg). Serum concentration of naloxone at 5 minutes was 1.45 +/- 0.1 mug/ml (mean +/- SE) and that of morphine was 1.0 +/- 0.08 mug/ml. Their serum half-lives from one to four hours were approximately the same, 30-40 minutes. With naloxone, the brain-serum concentration ratios ranged from 2.7 to 4.6. Concentration of naloxone in the brain declined parallel to that in the serum. However, with morphine the initial brain concentration was approximately one tenth that in the serum (0.096 +/- 0.04 mug/ml). The brain morphine concentration was sustained for one hour, while serum morphine concentrations declined from 1.0 to 0.19 mug/ml during this period. Two minutes after iv injection of naloxone HCl (0.4 mg) in nine healthy volunteers, the serum drug concentration was 0.01 +/- .001 mug/ml. At 5 minutes, 97 per cent of the administered dose was no longer found in the serum, the serum concentration being 0.004 +/- .0003 mug/ml. From 20 minutes to two hours after injection, the calculated mean serum half-life of naloxone was 64 minutes. These results suggest that the rapid penetrance of naloxone into the brain and the high brain-serum concentration ratio contribute to its rapid onset of action and potency as a narcotic antagonist. The rapid decline of naloxone concentration in the brain found in the animal model, in contrast to that of morphine, could be the basis for its relatively short duration of action.

Adult↗