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Biomedical subjects

S Gitter

Publications and source records attributed to S Gitter.

At least 19 recordsLinked to original sources
PubMed1991

Behavioral and biochemical studies in rats following prenatal treatment with beta-adrenoceptor antagonists.

Increased motor activity and poor performance in the active avoidance test were observed in the offspring of rats treated with dl-propranolol or sotalol during pregnancy, but not with atenolol and d-propranolol. All substances were administered in drinking water from days 8-22 of gestation. A significant increase in the density of muscarinic acetylcholine receptors in the hippocampus was found for dl-propranolol and sotalol, at 35 and 20 days of age, respectively. Twenty-day-old pups born to dl-propranolol-treated rats exhibited a non-significant decrease in the number of beta-adrenoceptors in the frontal cortex. Assuming that all the beta-adrenoceptor antagonists tested had access to the developing fetal brain, the effect of dl-propranolol and sotalol on behavior could stem from central beta 2-adrenoceptor blockade. In view of the lack of behavioral changes after atenolol, a beta 1-selective adrenoceptor antagonist, it is suggested that the clinical use of beta 1-selective adrenoceptor antagonists during pregnancy might be safer for the fetus than beta 2-adrenoceptor antagonists.

Administration, Oral↗
PubMed1991

Different behavioral deficits are induced by anoxia/hypoxia in neonatal and senescent rats: blockade by MK-801.

Rats exposed on their first postnatal day to 100% nitrogen for 25 min developed hyperactivity and lower performance in passive avoidance task during development. Administration of MK-801 (0.5 mg/kg i.p.) 1 h before anoxia or (0.25 and 0.5 mg/kg) 1 h after completely reversed this behavioral impairment. Senescent rats (24-26 months) exposed to hypoxia (92% N2 + 8% O2) for 5 h failed in their performance in C.A.R., 30 days later. Pretreatment with MK-801 (1 mg/kg i.p.) completely reversed this impairment. These data suggest that activation of endogenous NMDA receptors produces different behavioral consequences in neonatal and senescent rats and that MK-801 administration close to exposure of animals to anoxia or hypoxia can prevent such damage, thus preventing behavioral impairments in postnatal as well as in senescent rats.

Aging↗
PubMed1990

Central catecholaminergic dysfunction and behavioural disorders following hypoxia in adult rats.

Wistar male rats, 3-4 months old, were made to breathe for 6 h a sub-lethal hypoxic atmosphere consisting of 8% oxygen and 92% nitrogen. Following this treatment, these rats were subjected to a series of behavioral and biochemical tests starting 30 days and ending at about 180 days after the hypoxic insult. an age-matched control group was subjected to the same series of tests. The following findings were made at the time interval indicated, relative to controls: (1) At 30-35 days, diurnal (3 h) and nocturnal (12 h) locomotor activities decreased by about 25%. (2) At 40-45 days, amphetamine in the dose range of 0.25-1 mg/kg proved less effective in eliciting an increase in motor activity and stereotypic behavior. (3) At about 50 days, apomorphine in the dose range 0.25-0.5 mg/kg caused an increase in stereotypic behavior. (4) At 60-65 days, alpha-methyl-p-tyrosine at the dose of 50 mg/kg caused a more pronounced hypoactive syndrome and a slower rate of recovery of motor activity. (5) At 75-90 days, performance in the active avoidance test was inferior to that of controls. (6) At 180 days, and one hour after a dose of 200 mg/kg alpha-methyl-p-tyrosine, the turnover rates of hippocampal norepinephrine and caudate-putamen dopamine were much below control. One may tentatively conclude that one of the effects of hypoxia in adult rats is a lesion producing long-term behavioral disorders which are partly ascribed to dopaminergic and, possibly noradrenergic, dysfunction.

Age Factors↗
PubMed1989

Tacrine or arecoline mediates reversal of anoxia- or AF64A-induced behavioural disorders in the developing rat.

A 25 min anoxia, or an intracerebroventricular bilateral 2 nmol dose of ethylcholine aziridinium (AF-64A), administered postnatally to male rat pups, elicited on further development of these behavioural disorders, which are partly related to central cholinergic hypofunction. These included a hyperkinetic syndrome and inferior performance in the passive avoidance test. The anoxia-lesioned group but not the AF-64-A-lesioned one, showed an inferior performance in the active avoidance test. Administration of tacrine, an inhibitor of cholinesterase, or arecoline, a cholinergic agonist, in the drinking water to the nursing mothers, at an estimated daily dose of 15 and 10 mg/kg, then directly to the juvenile rats after weaning and until the age of 40 days, partly reversed the effects of anoxia or AF-64A, normalizing the level of locomotor activity and improving performance in passive avoidance, but not in active avoidance. These beneficial effects persisted long after discontinuation of administration of either drug, suggesting that stimulation of spared cholinoceptors in brain at development had prompted the recovery of cholinergic function.

Animals↗
PubMed1989

Myocardial response to alpha-agonist (phenylephrine) in relation to age.

We studied the inotropic effect of the alpha-agonist phenylephrine on human and rat myocardium in relation to age. Strips of human atrial myocardium, discarded during cardiac surgery, were obtained from pediatric (2 to 18 months) and adult (40 to 60 yr) patients, and their electrically driven contractions were studied. The inotropic response of pediatric myocardium to phenylephrine was five times larger than that of the adult myocardium (p less than .05). The beta-agonist, isoproterenol, was also administered to the same myocardial specimens, and the average pediatric myocardial response was three times larger than that of the adult myocardium (p less than .05). Strips of right ventricular myocardium were obtained from four age groups of rats: 14 days, 3 months, 6 months, and 18 months, and exposed to phenylephrine. We demonstrated two age-related phenomena: a) a biphasic response with an early short negative inotropic effect preceding a sustained positive inotropic effect was registered in most of the rats aged 3 months and older, but in none of the youngest age group. b) A high mean positive inotropic response (211% of basal response) was generated in the youngest age group, whereas the oldest age group of rats showed only a slight response (8% of basal response, p less than .05). We conclude that loss of myocardial responsiveness to alpha and beta-agonist with increasing age is a prominent feature. The pattern of the ventricular responsiveness to phenylephrine also changes during aging as it turns from monophasic to biphasic.

Adult↗
PubMed1989

Benzene-derived free radical--a possible mediator of its carcinogenicity. I. Ultrastructural and functional studies on the effect of benzene on human white blood cells and its possible prevention.

The assumption that benzene exerts its leukemogenic action on cell components after being converted to a transient and relatively stable free radical is supported by the in vitro effect of benzene on the ultrastructure of human peripheral blood polymorphonuclear (PMN) cells, lymphocytes and monocytes. The effect was examined with a transmission and scanning electron microscope and was found to affect both the internal and external architecture of PMN cells and monocytes in a dose-dependent manner. No effect was observed on lymphocytes. Benzene did not affect the phagocytic activity of PMN cells or monocytes. Preincubation with 2-aminoethylthiosulfuric acid, a free radical scavenger, prevented the observed effects of benzene.

Benzene↗
PubMed1988

Behavioral differences in the developing rat following postnatal anoxia or postnatally injected AF-64A, a cholinergic neurotoxin.

Rat pups were submitted postnatally to one of two procedures: a 25-min exposure to 100% nitrogen or an i.c.v. bilateral injection of AF-64A, 2 nmol contained in 1-microliter saline. Throughout further development of either group, their performance in passive and active avoidance tests and in amphetamine-induced stereotype behavior was followed and compared. Both groups exhibited hyperactivity which persisted until 42 days of age in the anoxia group and beyond 120 days in the AF-64A group. Both groups were equally inferior to controls in the passive avoidance test, but only the anoxia group was inferior to controls in the active avoidance test. Amphetamine-induced stereotype behavior was much less pronounced in the anoxia group relative to AF-64A-treated rats or to controls. The results suggest that the lesion induced by the neurotoxin is more specific and less widespread than the one caused by anoxia.

Animals↗
PubMed1988

A novel cardiotoxic polypeptide from the venom of Atractaspis engaddensis (burrowing asp): cardiac effects in mice and isolated rat and human heart preparations.

A new cardiotoxic polypeptide isolated from the venom of the snake Atractaspis engaddensis has an LD50 of 15 micrograms/kg body weight in white mice. Intravenous administration in mice of lethal doses of the toxin causes, within seconds, marked changes in the ECG, consisting primarily of a transient slope elevation of the S-T segment, a temporary diminution of the S-wave and an increase in the amplitudes of the R- and T-waves. Concomitantly, and apparently unrelated to these changes, a severe A-V block develops and leads to complete cardiac arrest within a few min. Studies with rat and human isolated heart preparations showed that the toxin exerts a powerful coronary vasoconstriction (rats), and positive inotropic effects (rats and humans).

Animals↗
PubMed1988

Enhanced electroretinogram in cats induced by exposure to mercury acetate.

The present study was undertaken in order to verify whether, and how, retinal functions are affected by subacute poisoning with organic mercury. Mercury acetate in various concentrations (0.025-0.25 mg/kg per day) was injected subcutaneously every second day to adult cats (N = 20) throughout a 2.5-4.0-week period. The electroretinogram (ERG) was recorded and the Hg2+ concentrations in the blood were determined. In nearly 90% of the intoxicated cats an enhanced electroretinogram (scotopic b-wave amplitude) was found as compared to its level in the normal control cats (N = 10). The latency of the ERG was found to be appropriately shorter, up to a maximal difference of nearly 20% in comparison to the controls. Hg2+ was present in the blood of the exposed cats during a 2.5-month period following the exposure. It is concluded that exposure to mercury acetate induces a permanent increase in the excitability level of the cat's retina.

Animals↗
PubMed1987

Nonopiate effect of naloxone on cardiac muscle contractility.

To test the hypothesis that naloxone exerts a direct positive inotropic effect on the cardiac muscle, we employed two in vitro models. In one set of experiments we demonstrated that injection of 1 mg naloxone into an isolated perfused rat heart produced a significant increase in the amplitude of contraction. In another set of experiments we exposed an isolated and spontaneously contracting rat right atrium in a tissue bath to naloxone, and demonstrated that the amplitude of contraction increased significantly within a few minutes of naloxone administration. We showed that this effect of naloxone was not related to opiate receptors, since a similar effect was obtained with d-naloxone (the stereoisomer that is inactive as an opiate antagonist) and it was not affected by pretreatment with morphine. We also demonstrated that addition of alpha- and beta-adrenergic antagonists phentolamine and propranolol, in doses that effectively block alpha- and beta-adrenergic agonists, did not have any effect on naloxone's inotropic action. We validated our results in two electrically driven strips of human atrial myocardium in the tissue bath. A positive inotropic response to naloxone, measured as an increase of 80 and 50% in the amplitude of contraction, was noted. We postulate that naloxone's previously described cardiovascular pressor effect in states of shock may not only be related to reversal of the effects of endorphins but also to its direct inotropic action.

Animals↗
PubMed1986

Split immunosuppression of contact cell-mediated and of IgE hypersensitivity responses to dinitrofluorobenzene in mice.

Contact sensitivity (CS), anti-DNP (dinitrophenyl) IgG and IgE type antibodies were induced by skin applications of the contact sensitizer dinitrofluorobenzene. CS response was suppressed by treatment with the monovalent hapten dinitrobenzene sulfonate (DNBS) but was not affected by treatment with the DNP-conjugates (DNP22-Ficoll, DNP17-polyethylene glycol and DNP2-polyvinylpyrrolidone). On the other hand, IgE type response was depressed by treatment with the various DNP conjugates but was not affected by DNBS. The IgG type response was not appreciably affected by any of the treatments.

Animals↗
PubMed1978

Serum dopamine beta-hydroxylase activity in acute cardiac disease.

The activity of dopamine beta-hydroxylase in the serum was measured in patients with acute cardiac disorders who were admitted to a coronary care unit. The activity of the enzyme on admission was similar in patients with acute myocardial infarction and in those with other conditions; on discharge, the activity was reduced significantly. Patients with myocardial infarction had the greatest fall in the activity of dopamine beta-hydroxylase. Patients with multiple signs of sympathetic hyperactivity had significantly higher values for the activity of dopamine beta-hydroxylase on admission. Pain was found to significantly increase the activity of the enzyme. These data confirm findings that the activity of dopamine beta-hydroxylase in the serum reflects the intensity of sympathetic activity. The factors contributing to the elevated sympathetic activity in some patients with acute myocardial infarction seem to be nonspecific, but because of the ominous nature of increased sympathetic tone in this condition, it could be advantageous to identify these patients.

Acute Disease↗
PubMed1977

Prevention by drugs of tachyphylaxis at nicotinic receptors in the cat superior cervical ganglion in situ.

A new compound, AF3 (4-ethyl-6-oxa-1-azatricyclo)4.2.2.02,7)dodecan-5-one), and its 4-phenyl analogue, AF6, embodying the structural elements of acetylcholine in a highly rigid framework, were shown to evoke nicotine-like responses in the nictitating membrane (NM) and blood pressure when applied to the superior cervical ganglion in anaesthetized cats. In this respect, their equiactive molar ratio was (nicotine : 1),20-30. However, at doses that were too low to evoke any response, AF3 appeared to potentiate the responses to nicotine or tetra-methylammonium (TMA) by preventing or abolishing tachyphylaxis to the two latter drugs, the effect being dose-dependent with AF3. DMPP which produces much less tachyphylaxis, or preganglionic nerve stimulation, was little or not potentiated in presence of AF3. It is proposed that potentiation to nicotine or TMA occurs following occupancy by AF3 of a regulatory subsite, thereby preventing further access to it by nicotine or TMA. In this respect, AF3 plays the role of a "neutral" molecule.

Animals↗