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Biomedical subjects

Z S Herman

Publications and source records attributed to Z S Herman.

209 records · Page 12Linked to original sources
PubMedDate not supplied

The analgesic activity of some tuftsin- and tuftsin inhibitor-like fragments of the viral coat proteins.

Antinociceptive activity of seven pentapeptide fragments of human adenovirus type 2 (Ad2) virion proteins: Thr-Val-Pro-Pro-Arg (1), Thr-Arg-Pro-Pro-Arg (2), Thr-Gly-Pro-Pro-Thr (3), Pro-Arg-Pro-Pro-Thr (4), Phe-Val-Pro-Pro-Arg (5), Ala-Arg-Pro-Pro-Ala (6), Tyr-Gly-Pro-Pro-Lys (7)--analogs of known tuftsin inhibitor Thr-Lys-Pro-Pro-Arg, was measured by hot-plate procedure. Also two tuftsin-like fragments of epitopes of HIV-1 and HIV-2: Thr-Lys-Ala-Lys (8), Thr-Lys-Glu-Lys (9), and tuftsin analog Thr-Lys-Asp-Lys (10) were tested. In the control experiments the effects of tuftsin and pentapeptide tuftsin inhibitor were also studied. The peptides 2, 4 and 5 were found to produce very strong analgesia after the icv injection. It was observed that pretreatment with peptide 8 remarkably diminished the antinociceptive effect induced by tuftsin.

Adenoviruses, Human↗
PubMedDate not supplied

5-hydroxydopamine, unspecific centrally acting false neurotransmitter.

5-hydroxydopamine, unspecific centrally acting false neurotransmitter. Acta Physiol. Pol., 1977, 28 (1): 13-22. 3,4,5-trihydroxyphenetylamine-5-hydroxydopamine (5-OHDA) injected intracerebro-ventricularly decreases the level of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in different parts of the rat brain. It does not affect acetylcholine level. 5-OHDA causes dose-dependent hypothermia, transient hypertension and depression of locomotor and exploratory activity in rats. This behavioral phenomena are reversed by central chemical sympathectomy elicited by 6-hydroxydopamine. It is concluded that 5-OHDA is an unspecific centrally acting false transmitter.

Animals↗
PubMedDate not supplied

Effects of thiorphan, bestatin and captopril on the Lewis lung carcinoma metastases in mice.

Previously we have found that administration of thiorphan alone or in combination with bestatin exerts antitumor effect in mice, including reduction of B16 melanoma tumor growth and prolongation of survival time. These data prompted us to extend our studies to estimate the effect of treatment with thiorphan, captopril and bestatin on lung metastases in mice. Administration of thiorphan alone at a dose of 25 micrograms/mouse or in combination with bestatin (50 micrograms) or captopril (5 mg/mouse) decreased the number of spontaneous metastases in lungs of Lewis lung carcinoma bearing mice. Neither the injections of bestatin, captopril nor bestatin in combination with captopril influenced the number of lung tumor colonies. Treatment with thiorphan at a dose 25 micrograms augmented cytotoxic activity of natural killer (NK) cells and macrophages. These observations explain partly the mechanism of action of thiorphan.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Antagonistic effect of MR2266 and MR2267 on morphine or nalbuphine analgesia at the spinal levels in rats.

The aim of this paper was to study the effect of two benzomorphan derivatives MR2266 and MR2267 with predominant antagonism to kappa-opioid receptors administered intrathecally on the analgesic action of morphine and nalbuphine. Both compounds attenuated the analgesia elicited by examined opioid agonists. Our results support the hypothesis that the spinal opioid receptors take part in analgesic effect of morphine and nalbuphine. It was for the first time described that MR2267, considered as inactive enantiomer of MR2266, is an active opioid antagonist when administered intrathecally.

Analgesics, Opioid↗
PubMedDate not supplied

Captopril augments antitumor activity of cyclophosphamide in mice.

Patients suffering from cancer (responsive to chemotherapy) are usually treated with a combination of anticancer drugs. In our previous studies, we found that captopril exerted antitumor action on Lewis lung carcinoma (LLC) in mice. This prompted us to evaluate the antitumor effect of captopril combined with cyclophosphamide. BD1F1 mice with LLC received two injections of captopril (5 mg/mouse) at a 1 h interval. Two hours later they were injected with cyclophosphamide (6 mg/mouse). Captopril pretreatment augmented the antitumor action of cyclophosphamide expressed as the survival time and the number of cured mice. Captopril given for five days before cyclophosphamide treatment did not change the antitumor activity of cyclophosphamide.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Carbon monoxide: a novel neural messenger or putative neurotransmitter?

The novel data indicating the role of carbon monoxide as an eventual putative neurotransmitter are discussed. The perspectives of further studies are delineated. Actually following scarce points suggest that carbon monoxide (CO) my be eventually neurotransmitter: an uneven distribution in the nervous system of heme oxygenase, which produces CO; the generation of long term potentiation in hippocampus; possible mediation of release of hypothalamic factors; eventual signalling role of CO in immune system.

Animals↗
PubMedDate not supplied

Agmatine--a novel endogenous ligand of imidazoline receptors.

Agmatine (AGM) is decarboxylated arginine found in bovine brain which binds to imidazoline receptors. It differs substantially from earlier discovered clonidine displacing substance (CDS) and ir-CDS. AGM is synthetized in brain from arginine decarboxylase, and metabolized by diamine oxidase. It is widely and unequally distributed in peripheral tissues and in the brain. AGM interacts with both I-1 and I-2 imidazoline receptors as well as with alpha 2-adrenoreceptors. AGM can regulate cardiovascular functions and can modulate some processes in the central nervous system.

Agmatine↗
PubMedDate not supplied

Influence of isoflurane on enkephalin levels and on some indicatory enzymes in the central nervous system of rabbits.

The objective of this study was to analyse the effects of isoflurane anesthesia (lasting for 15 or 60 min) and isoflurane anesthesia termination (after 1 or 24 h) on met-enkephalin (MENK) and leu-enkephalin (LENK) levels in discrete brain areas and spinal cord segments in rabbits. Moreover histochemical analysis of activities of succinate dehydrogenase, magnesium-dependent adenosine triphosphatase (Mg++ATP-ase) and acid phosphatase in the striatum and hypothalamus were carried out to evaluate the effects of isoflurane anesthesia on energetic, transport and catabolic processes. Throughout anesthesia (15 and 60 min) and after its termination (1 h) the LENK contents were increased in hypothalamus, hippocampus, mesencephalon and lumbar segment of spinal cord. Moreover, during isoflurane anesthesia and after its termination (1 h) MENK and LENK levels decreased in cervical segment and MENK content dropped in thoracic segment of spinal cord. Histochemical data indicated, that isoflurane enhanced energetic processes as well as exchange processes in neurocytes, glial cells, capillary walls and ependymal cells of the third ventricle. Measurements of acid phosphatase activity provided evidence of no signs of toxicity of isoflurane in the examined areas. The changes in enkephalin levels observed during the isoflurane anesthesia and after its termination depended on the type of examined neuropeptides, as well as on parts of the brain and spinal cord studied. The changes observed after isoflurane administration in enkephalinergic system are discussed with regard to our earlier experiments with halothane and enflurane.

Acid Phosphatase↗
PubMedDate not supplied

Antihypertensive effect of amlodipine compared with nifedipine retard in patients with mild and moderate essential hypertension.

OBJECTIVE: The present study was undertaken to evaluate the efficacy and safety of amlodipine for hypertension treatment in comparison with nifedipine retard. METHODS: We examined 31 patients with arterial blood pressure approximately 155-165 mmHg/100-105 mm Hg at the beginning of the trial. It was a randomized double-blind, parallel-group trial including two groups of patients. Patients of the first group were given active amlodipine and nifedipine retard placebo during 6 weeks, while the second group was given active nifedipine retard and amlodipine placebo. Statistical analysis was made using the paired Student's t-test, chi-square test and ANOVA test. RESULTS: At end point we observed significant decrease in arterial blood pressure after treatment of both drugs. The treatment with nifedipine retard increased the mean heart rate of patients. Amlodipine therapy in comparison to nifedipine retard did not change the heart rate in treated patients. Safety parameters: SGOT, SGTP, creatinine and others were in laboratory norms ranges. CONCLUSION: Amlodipine proved to be an effective, more safe and better-tolerated therapeutical alternative for hypertension management than nifedipine retard.

Adolescent↗
PubMedDate not supplied

The influence of antidepressive drugs on the level of acetylcholine and on the acetylcholinesterase activity in the brain of rats.

Rats were treated ip with MAO inhibitos (MAO-I): nialamid (NL), pivalylbenzylhydrazine, tranylcypromine, pheniprazine (Ph) or pargyline, and the leve of total, free and bound acetylcholine (Ach) as well as the acetylcholinesterase (Ach-E) activity were estimated in four parts of rats brain 2 or 16 hr after the treatment. These parameters were estimated also after the treatment with tricyclic antidepressants: desmethylimipramine (DMI), amitriptyline, or protriptiline, and in the conditions of the reversal of reserpine-like syndrom. MAO-I, 2 hr after their application and the reversal of reserpine like-syndrom have not changed the level of measured fractions of Ach in parts of the brain. DMI increased the level of all Ach fractions in the striatum. NL caused the decrease of bound Ach level in all parts of the brain with no changes of free Ach level, 16 hr after the treatment. Ph, 16 hr after the treatment, decrease both fractions of ACh only in the cortex. All studied drugs affected evidently ACh-E activity in various parts of brain. It is concluded that:1) Cholinergic mechanisms in the rat brain are involved in the central action of DMI and of some MAO-I., 3) Cholinergic function of the brain may be modulated by the adrenergic activity, 2) Individual parts of the brain have different susceptibility to the influence of different MAO-I on the ACh-E activity.

Acetylcholine↗