Biomedical subjects
Publications and source records attributed to Y Cohen.
d-Amphetamine was injected into isolated and aggregated rats at a dose of 4 mg/kg. Treatment of individually caged rats led to no difference in striatal dopamine elimination compared to controls. Aggregation of animals, however, resulted in an increased striatal elimination of dopamine.
Male albino rats given as intraperitoneal injection of kainic acid (11 mg/kg) showed a behavioural syndrome of wet-dog shakes, vertical paddling and tonic convulsions followed by aphagia and aggressivity. The phase of wet-dog shakes, vertical paddling and convulsions was reduced by pretreatment with benserazide and alpha-methylparatyrosine at low doses, while FLA-63 and high doses at AMPT (greater than 200 mg/kg) were toxic together with kainic acid. The phase of aphagia was not influenced reliably by any of the pretreatments, while the phase of aggressivity was potentiated strongly by parachlorophenylalanine and slightly by reserpine and AMPT. The findings suggest that dopaminergic and serotoninergic functions play a role in effects of kainic acid on behaviour in rats.
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The early and late effect of three anticholinesterase agents (physostigmine, paraoxon and soman) on core temperature and brain acetylcholinesterase (AcChE) inhibition are compared. The study was performed in adult male rats using sublethal doses of all drugs. AcChE activity was determined by hypothalamus, striatum, hippocampus, medulla oblongata-pons and rest of the brain. The co-existence of intoxication symptoms, hypothermia and AcChE inhibitions was clearly shown by the early effects. However, no relationship was found between the degree of hypothermia and that of inhibition whatever brain area. In contrast, late AcChE inhibition was not accompanied by symptoms and lowering of core temperature. Several hypotheses have been suggested to explain this phenomenon: de novo synthesis of enzyme, decreased sensitivity of neurotransmitter or return to normal of brain acetylcholine level through a negative feed back at the presynaptic level. The present data suggest that this latter assumption is the most likely.
Cardiovascular effects after intravenous administration of dihydralazine (0.5 mg/kg), diazoxide (10 mg/kg) and minoxidil (1 mg/kg) were studied in normotensive (NT) and renal hypertensive rats (HT) pretreated or not for seven consecutive day with propranolol (5 mg/kg per os). The hypotension induced by the three vasodilators in NT and HT rats was caused by decreased peripheral resistance and, in the case of minoxidil in HT rats by decreased cardiac output as well. Propranolol pretreatment of HT rats decreases the hypotensive effect induced by the three vasodilators. In the cases of dihydralazine and diazoxide, this effect is due to a lesser decrease of peripheral resistance; with minoxidil, it results from the absence of decreased cardiac output. Pretreatment of hypertensive rats with propranolol (5 mg/kg per os) for one week had no effect on blood pressure, but decreased heart rate and cardiac output and increased peripheral vascular resistance. Despite these cardiovascular modifications, the reactiveness to intravenous isoprenaline (1 to 4 microgram/kg) was the same in control and propranolol pretreated animals.
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Experiments in vitro have shown 1-(4-hydroxyphenyl)-2-methylamino-propanol-(1) (oxilofrine, 4-HMP) to release noradrenaline from cardiac ventricular sections. This effect sets in at a concentration of 10(-5) mol/l and reaches the 30% level at 5X10(-5) mol/l. The inhibition of noradrenaline storage is still more pronounced. At 5 X 10(-5) mol/l the inhibition is 60%. The significance of both mechanisms of action of the sympathomimetic agent is discussed in comparison with compounds of related structure.
Practolol (15 mg/kg i.c.) and atenolol (3 mg/kg i.v.) induced in rats hypotensive effects different from one group to another. However these hypotensive effects were always more important in hypertensive than in normotensive animals. IN Okamoto rats, hypotensive effect of atenolol increased with the age of the animals. In normotensive rats, atenolol had no effect whatever the animal age. Evans blue injected by intracarotid route in normotensive and hypertensive rats showed an increased permeability in Okamoto rats blood-brain barrier. After lesion of blood-brain barrier by intracarotid injected cetrimonium, hypotensive effect of the two beta-blocking drugs appeared in both normotensive and hypertensive rats, with a greater degree than in control rats.
The elimination rate constant, half-life and turnover time of dopamine (DA) and norepinephrine (NE) were determined, after inhibiting their biosynthesis by alpha-methyl-para-tyrosine (alpha MT), in the hypothalamus, striatum and the remainder of the brain of rats exposed to different degrees of hypobaric hypoxia, corresponding to altitudes of 1,800, 3,800, 5,200 and 7,000 meters. The effects varied as a function of the degree of hypoxia and the brain region studied. The turnover time of NE in the hypothalamus remained unchanged, regardless of the altitude, while in the rest of the brain the rate constant of neurotransmitter elimination decreased inversely as a linear function of the degree of hypoxia. On the contrary, the changes of the DA turnover time in the striatum and the rest of the brain, were biphasic, being accelerated by moderate altitudes (1,800 m) and retarded by the two highest simulated altitudes studied as a function of hypoxia. The differential effects of hypoxia on NE and DA turnovers are attributed to different sensitivities of the respective enzyme systems.
Twenty-one patients with malignant melanoma stage III and IV were treated by intradermal injections of MER--methanol extraction residue of Baccillus Calmette-Guérin (BCG). Twelve of the patients, all with active disease, received chemotherapy in addition. Tests of skin reactivity to recall antigens and in vitro lymphocyte transformation by phytohemagglutinin (PHA), purified protein derivative (PPD), Canadidine, and Varidase were performed in 19 of the patients before and after the MER therapy. The skin reactivity improved in 8 patients, 5 patients maintained their cutaneous competence, 3 remained incompetent, and in 3 other patients a decrease in reactivity occurred. Improvement or maintenance of cutaneous response was more common in stage III than in stage IV patients. The in vitro lymphocyte stimulation tests have shown that reactivity increased or remained at a high level in 9 of 11 patients in stage III. It dropped or remained low in 2 patients in respect to all antigens used in spite of repeated MER injections. In most patients with stage IV disease no improvement could be detected. MER seems to be a potent immunostimulator in patients in stage III. The side effects were tolerable in all patients and consisted of local reactions and influenza-like symptoms. In 4 patients treated with MER by intralesional injections, transient flattening of nodules occurred but no complete regression was observed.
The behavioral effects following IP injection of kainic acid in rats could be cancelled with hypobaric hypoxia (8% O2 corresponding to 7000 m altitude) or with IP injections of 7-amino-hex-5-enoic acid at a dose of 0.9 g/kg-1. This protection may result from increased accumulations of GABA in brain tissues.
The DNA polymerase, thymidine kinase and deoxyribonuclease activities were studied in cells infected with wild type (wt), ultraviolet (UV)-irradiated and defective herpes simplex virus type 1. All three enzymatic activities were expressed in cells infected with wt virus. In cells infected with UV-irradiated virus, the thymidine kinase and deoxyribonuclease activities were inhibited and the DNA polymerase activity was markedly suppressed. In cells producing defective virus, there was thymidine kinase activity, but the viral deoxyribonuclease activity was considerably reduced. The DNA polymerase activity was fully expressed in cells producing defective virus at passage level 5, but at passage level 6, the activity of the viral DNA polymerase declined.
1. The central hypotensive activity of (+)- and (-)-propranolol (100 microgram), pindolol (100 microgram) and isoprenaline (1 and 4 microgram) injected intracerebroventricularly (i.c.v.) was studied in rats anaesthetized with urethane and chloralose. Blood pressure, cardiac output and heart rate were measured; systolic stroke volume and peripheral vascular resistance were calculated. 2. (+)- and (-)-Propranolol and pindolol induced a fall of blood pressure but (+)-propranolol was less active. The heart rate was reduced more by (-)-propranolol than by (+)-propranolol or (-)-pindolol. The decrease of systolic stroke volume was greater for (-)-propranolol and pindolol than for (+)-propranolol. Peripheral vascular resistance was reduced to the same level but with different time courses, (-)-propranolol having a longer effect than (+)-propranolol and pindolol. 3. Isoprenaline induced a hypotensive effect, while cardiac output and heart rate increased; the systolic stroke volume remained stable but peripheral vascular resistance was significantly decreased. 4. These results suggest that different central regulatory centres are involved in the control of cardiac function and peripheral vascular tone.