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Biomedical subjects

S Porta

Publications and source records attributed to S Porta.

At least 19 recordsLinked to original sources
PubMed1992

Opposite effects of mild and severe stress on in vitro activation of rat peripheral blood lymphocytes.

The effects of short-term handling and different durations of immobilization on serum levels of catecholamines, ACTH, prolactin, and corticosterone and in vitro functions of lymphocytes were examined in rats. The results show that changes in the immune response of peripheral blood lymphocytes (PBL) depend on the intensity of the stressor: Short (1 min) handling of cannulated rats induced an enhanced stimulation of PBL to respond to T and B cell mitogens, whereas immobilization of the same animals led to suppression, dependent on the time this stressor was applied. The decrease in the mitogen reactivity of PBL after 120 min of immobilization was reversible within 24 h, and could be largely prevented by adrenalectomy, confirming that factors released by this gland are mainly responsible for immunosuppression. In contrast to PBL, spleen cells showed an enhanced mitogen response to immobilization and adrenalectomy, indicating that the immune response is differently regulated in the various compartments of the immune system. Possible correlations of the various effects with changes in stress hormone levels are discussed.

Adrenal Glands↗
PubMed1992

A tail-artery cannulation method for the study of blood parameters in freely moving rats.

The aim of this study was to improve the chronic tail-artery cannulation technique for repeated substance administration and blood sampling under stress-free conditions in freely moving rats. For that purpose, a special metal capsula and spring-tube system were developed, which not only protects the inserted cannula but also provides a less injurious insertion procedure and improves the animals' welfare as illustrated by normal cleaning and feeding behavior. Intraarterial application of test substances and repeated blood sampling can be done under minimal stress conditions as shown by unaltered plasma levels of highly stress-sensitive prolactin and the catecholamines (CA), epinephrine (E), norepinephrine (NE), and dopamine (DA), after infusion of 300 microL saline.

Animals↗
PubMed1991

Prolonged administration in vivo of alpha and beta adrenergic agonists decreases insulin binding to rat myocardial membranes in vitro by different mechanisms.

Male Sprague Dawley rats were continuously treated in vivo for 6, 12 and 20 hours with a combination of an alpha- (beta-) adrenoreceptor agonist and a beta- (alpha-) adrenoreceptor antagonist in subcutaneously implanted depot tablets. Crude membranes prepared from myocardial cells exhibited a decreased maximum binding of [125I]-insulin after 20 hours irrespective of the treatment applied. Scatchard and non-linear regression analysis of the displacement curves assuming two non-cooperative binding sites revealed a downregulation of the high affinity receptors for about 85% and a concomitant 2.5-fold increased receptor affinity under beta-adrenergic influence. In contrast, alpha-adrenergic treatment did not affect the receptor number but decreased the high affinity by 70%. The low affinity binding sites were virtually unaffected by the different treatments. The phospholipid and cholesterol contents of the membranes were not significantly altered. The phospholipid/cholesterol ratios after 12 and 20 hours of alpha-adrenergic treatment, however, were decreased. We suggest that the decreased binding activity of insulin receptors on rat myocardial membranes after continuous in vivo treatment with alpha- and beta- adrenergic agonists is mediated by different mechanisms.

Adrenergic alpha-Agonists↗
PubMed1991

Isoprenaline cannot act on pancreatic beta cells without hyperglycemia or alpha-block.

During long-term increase in isoprenaline (pronounced beta-effect) and isoprenaline plus regitine (pure beta-effect) pancreatic insulin-secretion still depended mostly on blood glucose levels. This means that increased beta-effect during normo- or hypoglycemia could not cause a higher insulin-secretion. Only during additional alpha-receptor blockade insulin-secretion was slightly but insufficiently increased. Catecholamines seem to be more regulator than originator of the insulin secretory process.

Animals↗
PubMed1990

Interindividual comparability of blood glucose alterations after meals of complex carbohydrates.

Young male and female probands underwent an DGTT (oral glucose tolerance test) using a glucose load of 1 g/kg b.wt. The alterations in blood glucose levels were checked and plotted by a Biostator. A week later groups of those probands were fed an isocaloric meal of complex CH, namely either potatoes, noodles or white bread. The resulting BG curves were also checked by a Biostator. It turned out that: 1. the shapes of the BG curves after glucose load were not interindividually comparable. 2. there was neither a similarity of the shapes of the BG curves within the groups after any of the different CH levels. 3. But if one compares the shape of the BG curves after glucose load and after a meal of any of the complex CH of one and the same person, there is a striking similarity in those curve shapes. The differences between them lie just in the mostly lower BG values of the curves after CH meals compared with those after glucose load. 4. Therefore the resulting graph of both of those curves is in all observed cases a straight line with a probability better than 0.001, called OGTT-calibrating resulting graph.

Adult↗
PubMed1990

Characterization of 3H-N-methylscopolamine binding to intact rat thymocytes.

The binding parameters of muscarinic antagonists in intact rat thymocytes were determined from competitive binding experiments with 3H-N-methylscopolamine (3H-NMS). The muscarinic antagonists inhibited binding of 3H-NMS in a dose-dependent manner. Non-linear regression analysis of the displacement curves indicated the presence of two affinity states for the muscarinic compounds. The beta-blocking agents R-propranolol, S-propranolol and alprenolol inhibited the binding of 3H-NMS to one, low affinity binding site on rat thymic lymphocytes. The ganglionic blocking substance hexamethonium did not affect the binding of 3H-NMS. The results indicate the presence of two binding sites for the radioligand on rat thymocytes, of which only one is specific for muscarinic receptor antagonists.

Animals↗
PubMed1990

Critical comments on the classic concept of hypoglycemia induced epinephrine secretion.

Our experiments showed that a continuous chronic administration of norepinephrine (NE) to rats for 20 h by means of subcutaneously implantable retard tablets, led to a highly significant epinephrine(E) depletion of the adrenal medulla during normoglycemia. The rise of free plasma NE was accompanied by increased free plasma E values at 12 hours. At this time the liver contents of glycogen and free intracellular glucose showed their most pronounced decrease. At 12 and 20 hours both liver glycogen and medullar E values were very low. To check a possible causal relationship between those two events another experiment was performed in which the breakdown of liver glycogen should be inhibited. NE treated rats were force fed with 50% glucose solution 9 h after tablet implantation. This resulted in only mild glycogen depletion, which was no more able to trigger E liberation from the medulla. Therefore we conclude that pronounced liver glycogen depletion possesses a triggering ability for medullar E output by which hypoglycemia could be prevented.

Animals↗
PubMed1989

Dynamics of metabolic responses to prolonged elevation of circulating adrenaline in resting and exercising rats.

The purpose of this study was to follow the time course of metabolic responses to hyperadrenalinemia sustained up to 3 days. Hyperadrenalinemia was produced in rats by s.c. implantation of tablets releasing adrenaline (A) at a constant rate (1.6 micrograms x min-1). After 6, 12, 24 and 72 h of hyperadrenalinemia and 3 days after the tablet removal rats were sacrificed and liver, 3 types of muscles and blood samples were taken. Each time 14 rats were used: 7 of them were sedentary and 7 performed treadmill endurance exercise before decapitation. Sham operated animals served as controls. In preliminary experiments working ability was examined in 10 hyperadrenalinemic and 10 control rats. Duration of exercise until exhaustion was reduced in hyperadrenalinemic rats on the average by 40%. In sedentary rats, hyperglycemia, marked depletion of liver glycogen (by approx. 80%) and muscle glycogen (by 60-80%) as well as an elevation (2-4 times) of muscle lactate (LA) were found only during the first day after A-tablet implantation. At the end of the experiment these values approached the control ones. Muscle contents of ATP and creatine phosphate (CrP) were decreased by approx. 20% and 30-60%, respectively. Plasma FFA were markedly enhanced, varying in the time-course of the experiment from 0.8 to 1.4 mmol x l-1. Post-exercise values for blood glucose, liver and muscle glycogen were always lower in hyperadrenalinemic rats than in controls sacrificed after time-matched exercise (30 min). Circulating FFA decreased during exercise at all time points following A-tablet implantation, but they were still above the post-exercise levels in sham-operated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Norepinephrine triggers medullar epinephrine depletion during normoglycemia.

Our experiments did show that chronic 12 hours administration of norepinephrine (NE) to rats by means of subcutaneously implantable retard tablets, led to a highly significant epinephrine (E) depletion of the adrenal medulla during normoglycemia. The expected rise of free plasma NE at 6 and 12 hours was accompanied by increased free plasma E values at 12 hours. At this very time point the liver contents of glycogen and free intracellular glucose showed their most pronounced decrease. Since at 12 hours both liver glycogen and medullar E values were at their lowest, a second experiment was performed to examine a possible causal relationship. In order to curb the breakdown of liver glycogen, rats were force fed with 50% glucose solution 9 hours after NE tablet implantation. Glucose feeding not only caused a much less pronounced liver glycogen fall at 12 hours, but, at the same time also prevented E depletion of the adrenal medulla. These observations suggested that rapid fall of liver glycogen and/or liver intracellular free glucose might be the trigger for medullar E depletion, even before hypoglycemia.

Adrenal Medulla↗
PubMed1988

Arachidonic acid metabolism in HEL/30 murine epidermal cell line.

The established mouse epidermis-derived cell line HEL/30 was incubated in the presence of 3H arachidonic acid (AA) for 1 h. After medium removal, cells were reincubated with fresh medium in the presence or absence of the calcium ionophore A23187 and tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA). The AA metabolites formed were extracted from cell-free medium and analyzed using TLC and HPLC. The distribution of the recovered radioactivity showed PGE2, 15-hydroxy-eicosatetraenoic acid (15-HETE), and leukotriene B4 (LTB4), as major products of AA metabolism. The presence of calcium ionophore A23187 increased the release of radioactivity, without affecting the profile of metabolites present in the medium. TPA elicited a preferential increase of cycloxygenase metabolism, this effect being reversed by indomethacin. 5,8,11,14-eicosatetraynoic acid (ETYA) almost completely inhibited LT and HETE formation in A23187 and TPA-treated cells. The results show that HEL/30 cells are able to metabolize AA via both cyclo- and lipoxygenase pathways and that these activities can be modified by chemical means. This cell line might be a suitable tool for studying the involvement of arachidonic acid cascade in cell response to exogenous stimuli.

Animals↗
PubMed1988

Characteristics of ingress and life span of neutrophils at a site of acute inflammation, determined with the Sephadex model in rats.

Neutrophils labelled in vivo with 3H-thymidine accumulate in subcutaneously injected Sephadex, which causes an acute inflammation. Cells die and disintegrate within the Sephadex implants, leaving behind labelled nuclear fragments representing the number of dead cells. The total of immigrated cells and their life span can be calculated from the number of intact cells along with disintegrated cells found in a Sephadex implant. Intensive neutrophil ingress starts after 5 h, and after 6.5 h reaches a maximum of 52 x 10(6) cells per hour. After 11 h, a total of 137 x 10(6) cells has entered a Sephadex implant. The life span varies during the course of the experiment. The shortest life span of 20 min was measured during the period of intensive neutrophil ingress 5.5 h after onset of inflammation. Cellular death and disintegration is evidently due to self-destruction of the cells by peroxidation.

Animals↗
PubMed1988

Preventive action of phentolamine on adrenaline induced blood glucose elevation in humans.

A comparison of the action of adrenaline infusion and a combined adrenaline + alpha blocker (phentolamine, Regitine) infusion on blood glucose (BG), plasma immunoreactive insulin (IRI), BG/IRI ratio, C-peptide, and plasma cortisol levels was made in healthy young human subjects. The purpose of the experiment was to check, whether alpha block could abolish adrenaline-induced enhancement of blood glucose levels. The results show that during enhanced adrenaline levels, the use of regitine could indeed normalize blood glucose levels, not so much by increasing the IRI secretion, but by diminishing adrenaline-induced liver glycogenolysis via alpha receptors. This could be a model to prevent stress (adrenaline) induced metabolic deviations in diabetics, especially before and during predictable stress situations, e.g. examinations or surgery.

Adrenergic alpha-Antagonists↗
PubMed1987

Effects of prolonged elevation of plasma adrenaline concentration in vivo on insulin-sensitivity in soleus muscle of the rat.

1. Prolonged elevation of the plasma adrenaline concentration was produced in rats by implantation of adrenaline-releasing retard-tablets. With this technique, a hyperadrenalinaemic state is maintained for at least 5 days. 2. At 6 h after implantation of the retard-tablet it was found that plasma glucose and fatty acid concentrations increased and insulin concentration decreased compared with values obtained from placebo-tablet-implanted rats. Administration of a subcutaneous glucose load demonstrated an impaired glucose tolerance in vivo, and incubation of soleus muscle strips from 6 h-hyperadrenalinaemic rats in vitro demonstrated a decreased sensitivity of the rates of glycolysis and glucose transport to insulin. 3. The sensitivities of the rates of glycolysis, glucose transport and glycogen synthesis to insulin were determined for the incubated soleus muscle preparation isolated from animals after 48 h, 72 h and 120 h duration of hyperadrenalinaemia. At 48 h after retard-tablet implantation, the sensitivity of the processes of glucose transport and glycolysis was decreased; at 72 h, the insulin-sensitivities of the rates of glycolysis and glucose transport in skeletal muscle were similar to those determined for control animals; at 120 h, however, the sensitivities of the processes of glucose transport and glycolysis were both statistically significantly increased. In contrast, no changes in the sensitivity of the process of glycogen synthesis were observed at any of the time intervals studied. 4. The possible biochemical basis for the observed changes in skeletal-muscle insulin-sensitivity with prolonged hyperadrenalinaemia is discussed.

3-O-Methylglucose↗
PubMed1987

Long-term adrenergic beta-action decreases and alpha-action enhances corticosterone levels in rats.

A 20 h hyperadrenalinemia in rats was produced by subcutaneously implanted A-retard tablets with an output rate of 1.8 micrograms/min/250 g. This caused a moderate (6 h, 20 h) to expressed (12 h) rise in Corticosterone. Concomitant beta-blockade leads to equal (12 h, 20 h) or even more expressed (6 h) enhancement of plasma corticosterone, while A + alpha-blockade lowers those levels significantly against A or A + Prop treated animals. At 6 and 20 h they are even significantly lower than control values. We therefore conclude that enhanced alpha-adrenergic influence increases and beta-adrenergic influence decreases plasma Corticosterone levels in rats.

Adrenocorticotropic Hormone↗
PubMed1987

Decrease of rat-liver-T4-5'-deiodinase activity during chronical isoprenaline beta-action in vivo.

Pure adrenergic beta-action, brought about by long-term adrenaline + regitine application in rats, was able to increase liver T4-5'-deiodinase activity for 8 h (Nauman et al. 1984a). Long-term isoprenaline application without alpha-blocking yielded contrary results. One of the compensatory mechanism to be probably blamed could have been the very high endogenous adrenaline-levels (Porta et al. 1985). Simultaneous treatment with isoprenaline and alpha-methyltyrosinemethylester did not settle the problem since even then deiodinase activity was still drastically decreased. Two more components have been found which could very well be the reason for that "paradox beta-action" in vivo, namely very low glucose and insulin levels, both of which are known to influence deiodinase activity. In vivo--contrary to in vitro--it is seemingly not possible that catecholaminergic beta-action could increase the peripheral production of T3 unless general alpha-blocking took place.

Animals↗
PubMed1986

First trimester fetal karyotyping: one thousand diagnoses.

Cytogenetic investigations for diagnostic purposes were performed on 1000 first trimester samples of chorionic villi (CVS) in two laboratories using similar techniques. Fetal karyotyping was the primary indication for CVS in 912 and maternal age was the major indication in 758 of them. The risk category "previous child/fetus with chromosome abnormality" included 74 diagnoses, while the category "chromosome abnormality in one of the parents" included 38 diagnoses. Sex determination was the primary indication for CVS in 53 pregnancies. The overall incidence of chromosomal abnormalities was 70, of which 47 were balanced and 23 unbalanced. The results are detailed for each of the risk categories and the incidence of abnormal karyotypes is given for each year of maternal age. In the maternal age of 35-37 years the incidence of unbalanced karyotypes was 2.9% and in the years 38 onwards it was 6.6%. The incidence of unbalanced karyotypes was about 4% when the sampling was made in the weeks 9 to 12 but six abnormal karyotypes were found among 39 CVS performed at the eight week of gestation. The 11 trisomies of the type not found at birth were clustered between the 8th and the 10th week of pregnancy. The technical problems encountered in this experience and the preliminary estimates of fetal loss are discussed.

Abortion, Spontaneous↗
PubMed1986

Albumin as one-way transport vehicle into sites of inflammation.

Intravenously injected Evans blue combines with albumin. The resulting complex appears in the inflammatory exudate that collects in Sephadex G 200 subcutaneously injected into rats. A comparison between the concentrations of albumin and Evans blue in the blood and in the inflammatory exudate shows that the life-span of albumin in the Sephadex is drastically reduced. After decomposition of albumin, the combined Evans blue is liberated, accumulates in the Sephadex and, after 24 h, attains concentrations higher than in the blood. The experiment is a plausible model for transport and deposition of albumin-bound drugs into and at sites of inflammation.

Albumins↗