Acta physiologica latino americana最新文献

In anesthetized dogs the intravenous injection of prostaglandins (PGs) A2 and E2 (5-200 micrograms/kg) produced a dose-dependent fall (P less than 0.001) of the blood pressure with blockade of the baroreceptor reflex. The hypotension can increase the heart rate and decrease myocardial contractile force, which is neither prevented by atropine, phentolamine, diphenhydramine, verapamil nor by inhibitors of prostaglandin synthesis. Intravenous, intraaortic or intraventricular (left) injections evoked an equipotent fall of the arterial pressure. Less decrement is elicited by the intramuscular injection. The gastric route is ineffective. The intracisternal injection of high doses (20-130 micrograms/kg) of prostaglandins A2 or E2 decreases the blood pressure slightly after 5-10 minutes, probably because of prostaglandins transport across the blood-brain barrier. The blood pressure increases by stimulation of the sympathetic nerves of the spleen and of the liver, or by exogenous noradrenaline are equally significative before and after the injections of prostaglandins A2 or E2. Indomethacin and aspirin failed to affect the pressor increase produced by stimulation of the sympathetic nerves, or that of the exogenous noradrenaline in the normal dogs or in animals injected previously with PGs. It is concluded that the hypotensive action of the PGs is due to peripheric vasodilatation apparently without inactivation by the lung.

A novel treatment for the inhibition of an enzyme-catalyzed reaction due to a ligand that combines with the substrate to form a non-productive inhibitor-substrate complex is presented. When compared to the conventional kinetic treatment of substrate depletion systems, the treatment presented here has two major advantages, namely (a) it is of general validity since no approximations are required for derivation of the pertinent equations; and (b) establishes a linear relationship between the reciprocal concentration of substrate-inhibitor complex and the ratio of free enzyme to enzyme-substrate complex concentrations, thus giving linear plots which allow the direct computation of the Km/Ki ratio. With purified enzyme preparations, this treatment allows the calculation of the absolute concentrations of all the species present in the reaction medium, although a purified preparation is not a pre-requisite for its applicability. The presented treatment has its most useful application in re-testing the Km value of an enzyme-catalyzed reaction when other experimental approaches cannot be employed.

Different and frequently opposed theories and models of the hippocampal function have been developed. A first type of theories proposed that when some expectatives are not accomplished the hippocampus would inhibit: a) attention, b) activation or c) non-reward responses. A second type of theories supported that the hippocampal function would be the selection of the information to be stored: a) into the trace, b) into the long-term memory. A third type of theories proposed that in the hippocampus it would be stored: a) contextual maps, b) spatial maps, c) temporal maps, d) attentional-associative networks, e) contingencies detectors, f) semantics systems, g) recognition memory, h) work memory. The common element among all theories would be the detection of the differences between a neural model and a new input, as Sokolov proposed in 1960.

The effects of an excessive ingestion of iodide by the rat during pregnancy and lactation on the transcription of RNA were studied in the brain of the pups at 10, 15 and 20 days of age. Cerebral weight, DNA content and synthesis of heterogeneous RNA were not affected during the period studied. The activity of endogenous RNA polymerase I, alpha-amanitin resistant, measured in isolated cell nuclei was significantly reduced in twenty day old rats. Similar conditions meaningfully diminished body weight at the same age.

The immunogenicity of two fractions (1 500 F and 10 000 F) from epimastigotes of Trypanosoma cruzi as well as the supernatant from culture media (SF) were studied using hens, rabbits and opossums. For comparative purposes, sera from individuals with chronic Chagas' disease were also used. A similar, positive response was obtained for the fractions in all the animal species studied using indirect hemagglutination test. Supernatants from culture media were the least immunogenic. By double immunodiffusion test, it was possible to detect a positive response to a different number as well as to different antigens in the three animal species, but there was response to a common antigen by all the different animal species. The common antigen called here major, was present in all the fractions assayed. Human sera from individuals chronically infected showed a variable response. When assayed by double immunodiffusion technique, the major antigen could be detected in just a few samples.

A six-compartment model is proposed to study hippuran kinetics in several tissues and body fluids. This comprises plasma (in which the tracer is introduced), extravascular space (anatomically not defined), kidneys (left and right), "delay" (the dead space through which the urine passes from kidneys to the bladder) and the cumulative urinary excretion. Based on accurate internal measurements of radioactivity, theoretical values which reproduced the experimental data have been fitted to a SAAM program. A good fit was observed between the curves. This study is intended to be of value for better understanding and use of tests for clinical evaluation of renal function.

The inhibition of 3H-noradrenaline (3H-NA) release by adenosine, and the possible involvement of purine receptors in the regulation of transmitter release in the portal vein were studied. The inhibitory effect of different concentrations of adenosine (10, 30, 100 and 300 microM) decreased with frequency of stimulation, but there was no marked concentration-dependence. Tetraethylammonium (TEA) enhanced the 3H-NA overflow induced by transmural stimulation. The adenosine-induced inhibition of 3H-NA overflow was antagonized by TEA. Transmural stimulation induced release of tritium from tissues prelabelled with either 3H-NA or 3H-adenine had a similar pattern of distribution. In contrast, when the rat portal vein was stimulated with (-) NA, the overflow of purine derivates was delayed and the maximum release was achieved 5 min later than the maximum induced by transmural stimulation. Phenoxybenzamine (PBA) increased 3H-NA overflow two-fold, but had no effect on the 3H-purine release induced by transmural stimulation. PBA reduced the 3H-purine release by exogenous (-) NA. These results indicate that in rat portal vein, the purine compounds have pre- and postjunctional origins and that the purine that modulates adrenergic neurotransmission might be of neuronal origin, possibly independent of adrenergic innervation.

The increase in protein adsorption by charcoal as ionic strength increases (salting-out adsorption), was used to separate the bound and free fractions of glucagon, insulin, hGH, hLH and hPRL in the radioimmunoassay. The hormones were labelled with 125I and to express the immunocomplex, gamma-globulin was labelled with 125I. The charcoal used to produce the separation was suspended in magnesium sulfate 3 M (charcoal-SO4Mg). The optimum amount of charcoal and the final concentration of magnesium sulfate determined for each hormone were: glucagon (charcoal 5 mg/tube, 0.125 M); insulin (charcoal 5 mg/tube, 0.131 M); hGH (charcoal 40 mg/tube, 0. 447 M); hLH (charcoal 40 mg/tube, 0.447 M) and hPRL (charcoal 60 mg/tube, 0.321 M). The serum concentration was 1/20 for all hormones, excepting glucagon, where 1/10 was used. The stability of the immunocomplex was studied and it was shown that, under suitable conditions, increased ionic strength does not cause the dissociation of the bound fraction.

Mouse liver cells were isolated with Ca2+ and K+ chelating agents. Cell concentrations in all experiments ranged from 2.5 X 10(5) to 1.44 X 10(6) cells/tube. The kinetics of insulin-receptor binding was studied at 2 C and 20 C. Binding of 1.67 X 10(-11) M 125I-insulin reached equilibrium at 2 C at 180 min; Ka at 50% binding was 0.736 X 10(7) M-1 sec-1. At 20 C equilibrium occurred at 30 min; Ka at 50% binding was 7.519 X 10(7) M-1 sec-1. Non-specific binding was measured by adding 16.6 microM native insulin. Kinetics studies of association point to a pure bimolecular reaction since the constant remains unaltered at different times. In studies of bound complex dissociation, insulin release from the receptor involves first order kinetics, 50% of the bound insulin becoming released during the experimental period. Dissociation was studied at 20 C only, either by dilution or addition of 16.6 microM native insulin. Both methods yielded the same result, showing the dissociation kinetics to be a first order reaction with a half-life of 101 min and Kd: 2.5 X 10(-4) sec-1. Competitive inhibition of native insulin (1.67 X 10(-10), 3.33 X 10(-10), 1.67 X 10(-9), 3.33 X 10(-9), 1.67 X 10(-8), 3.33 X 10(-8), 1.67 X 10(-7), 3.33 X 10(-7) M) against 1.67 X 10(-11) M 125I-insulin was studied in equilibrium. Heterogeneity among active binding sites was found: one population of high affinity and low capacity (2 C: K = 4.64 X 10(7) L/M, Ro = 213 X 10(-11) M; 20 C: K = 2.90 X 10(8) L/M Ro = 28.5 X 10(-11) M) and one of low affinity and high capacity (2 C: K = 6.81 X 10(7) L/M Ro: 836 X 10(-11) M; 20 C: K = 2.63 X 10(6) L/M, Ro: 1080 X 10(-11) M). The results show the use of chelating agents in the separation of liver cells to be of value in physicochemical studies of insulin-receptor interaction.