Systemic adrenergic actions on liver T-4 5' deiodinase differ considerably from those seen in vitro.
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Animals↗
Biomedical subjects
S Porta
Publications and source records attributed to S Porta.
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↗
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↗
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↗
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↗
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↗
Laboratory handling and its influence on hormonal and metabolic parameters during acute inflammation in rats. A critique of long-term treatment by repeated injections.
Twice a day, rats were exposed to handling stress by sham i.p. injections during a period of five days. This procedure progressively drove up the basic blood levels of free adrenaline, noradrenaline and dopamine, while insulin decreased to below normal. Blood glucose returned successively from hyperglycemia during the beginning of the experiment to normal later on. If rats subjected to acute inflammation were handled, the parameters blood catecholamines, glucose and the lymphocyte ingress into the site of inflammation all showed the same patterns of changes, suggesting a certain synchronization of the metabolic events. This synchronization failed to occur in animals with inflammation, but without handling. In any case, the disturbed metabolism of handled animals did not normalize during the test period of five days. Therefore, application of test substances by repeated injections is a useless method for the correct investigation of chronic exogenous influences.
Acute Disease↗
Long-term application of some catecholamines elevates levels of other catecholamines in rats.
Male Sprague-Dawley rats were treated during 20 h with subcutaneously implanted tablets (controlled release systems) containing either adrenaline (A), noradrenaline (NA), isoprenaline (ISO) or just placebos. Levels of the exogenously administered catecholamines (CA) in plasma and liver homogenate were significantly higher than in controls throughout the test time. During NA application endogeneous A and dopamine (DA) plasma values rose considerably, while ISO application enhanced endogenous NA and A levels. Adrenaline application increased NA and DA plasma levels. Several possibilities for this phenomenon are discussed, and it is concluded that previous papers dealing with observations of long term action of CA's should be reevaluated unless the influence of the artificially given CA on the elevation of endogenous CA's has been already taken into consideration.
Animals↗
Enhancement of adrenaline plasma-levels shortens adrenaline half-life.
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Animals↗
The long-term influence of isoproterenol (ISO) retard tablets on the course of an acute inflammation.
Rats were exposed for 21 d to Isoproterenol (ISO) applied by subcutaneously implanted retard tablets. ISO causes a rise in the number of lymphocytes at the site of inflammation (injected sephadex) until the tenth day. The reaction of the connective tissue is moderately enhanced. The weight of the salivary glands is constantly elevated,and the weight of the hearts increases in a linear pattern until the end of the experiment. Neither in test nor in control animals is there any correlation between the number of white cells in the blood and their appearance at the site of inflammation.
Acute Disease↗
Adrenaline application by controlled release system shows that it does play a physiological role in glycogenolysis.
In a frequently cited paper Sokal , Sarcione and Henderson (1964) doubted the physiological glycogenolytic role of adrenaline (A). By using isolated perfused rat livers, they found adrenaline to be effective at doses higher than 140 ng/ml while a mere tenfold increase in glucagon leads to expressed glycogenolysis. Our in vivo experiments carried out with controlled release systems for adrenaline show that marked glycogenolysis takes place at an adrenaline serum level of not more than 20 ng/ml while endogenous glucagon levels do not differ from controls. We think, that the reason for those controversial results lies in the fact that Sokal , Sarcione and Henderson (1964) diminished the glycogenolytic action of adrenaline by blocking its alpha-component for the reason of an easier perfusion, and they further diminished its glycogenolytic action by omitting corticosterone, which is well known for its permissive role in adrenaline induced glycogenolysis in vivo.
Animals↗
The influence of permanent adrenalin application on the triacylglycerol concentration and fatty acid synthesis in various tissues of the rat.
Adrenalin tablets (15 mg) or placebos were implanted into the neck of male Sprague-Dawley rats weighing between 150 to 250 g. 18 hours after implantation a significant lipolysis as well as enhanced concentrations of triacylglycerol in liver, kidney cortex and skeletal muscle can be observed in adrenalin treated rats. Measurements of fatty acid synthesis (3H method) in these tissues indicate that in kidney cortex and liver there is no contribution of local synthesis to elevated triacylglycerol content. In skeletal muscle local synthesis seems to be efficient to some degree. The main cause for lipid deposition in adrenalin supplied rats is, therefore, uptake of free fatty acids from the blood and following esterification with glycerol.
Animals↗
Peculiar long-term effects of catecholamines and their blockers in rats on insulin, glucose and pancreas.
To be able to study the long-term effects of moderately enhanced catecholamine levels in rats, we developed subcutaneously implantable retard systems, granting a linear output of various agents throughout the test time. Adrenaline application leads to hyperglycemia without elevation of serum immune-reactive-insulin (IRI) during 20 h of uninterrupted adrenaline (A) action. This we call an A-induced diabetes like reaction. It could be completely abolished by simultaneous application of low phentolamine (Regitin) doses. Simultaneous application of propranolol (P) gradually diminished blood glucose levels from about 200 mg/dl after 6 h to 120 mg/dl after 20 h. Since here insulin levels are uniformly low, decline of blood glucose could not be due to enhanced insulin-action. The moderate hyperglycemia after 6 h isoprenaline (ISO)-treatment alone goes with a hyperinsulinemia at the same time. Obviously this hyperinsulinemia cannot cope with the increased blood glucose probably due to enhanced liver-glycogenolysis by intact alpha-action. Later on insulin--despite of beta-action on pancreas--declines strictly proportional with diminishing blood-glucose-levels. A comparison between the action of catecholamines and their blockers showed that alpha-blockers tend to diminish blood glucose levels by two independent ways, namely by the inhibitory action on pancreas and the inhibitory action on liver glycogenolysis.
Animals↗
The effect of adrenaline pretreatment on the in vitro generation of 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine (reverse T3) in rat liver preparation.
The effects of adrenaline (A) on liver T3 and rT3 neogenesis from T4 were studied in Wistar rats. The animals were implanted subcutaneously either with A or placebo (P) especially coated tablets which linearly released the hormone. The serum A values 6 hrs after implantation of 7.5, 15.0 and 45.0 mg tablets were 6.5 +/- 1.31, 6.8 +/- 1.8 and 16.4 +/- 1.9 ng/ml, respectively vs 4.4 +/- 2.5 ng/ml seen in P pretreated group. The output rates of A were 0.11 (7.5 mg), 0.18 (15 mg) and 0.52 microgram/ml (45 mg). The pretreatment with A led to hyperglycemia and the "low T3 syndrome". Neogenesis of T3 from T4 in medium containing liver microsomes of P pretreated rats was 5.49 +/- 0.25 pmol of T3/mg protein/min and decreased in A pretreated rats to 3.82 +/- 0.17, 3.12 +/- 0.27 and 3.06 +/- 0.11 pmol of T3/mg of protein/min. Neogenesis of rT3 from T4 in microsomes from P group was 1.52 +/- 0.09 pmol rT3/mg protein/min and increased after A to 2.71 +/- 0.11, 2.60 +/- 0.21 and 2.21 +/- 0.34 pmol of rT3/mg protein/min thus showing no dose dependency. Enrichment of microsomes medium with cytosol either from P or A pretreated rats had no effect on T3 generation thus excluding effect of A on cytosolic cofactor. Although cytosol further increased rT3 neogenesis this was seen regardless of whether cytosol was obtained from A or P implanted rats. It is concluded that A decreases the activity of T4-5'-deiodinase in liver, and possibly increases the activity of T4-5-deiodinase.
Animals↗
Effects of adrenaline pretreatment on in vitro binding of 125I-triiodothyronine to nuclear receptor, intracellular distribution of endogenous triiodothyronine and activities of alfa-glycerophosphate dehydrogenase and malic enzyme in rat liver.
Especially coated adrenaline tablets (A) or placebo tablets (P) which release linearly the hormone were implanted in male Wistar rats. Six hours later animals were sacrificed and kinetic parameters of T3-125I binding to nuclear receptor, intracellular distribution of endogenous T3 and activities of alfa-GPD and ME were investigated. The association constant values (Ka) of nuclear receptor were increased after pretreatment with 7.5, 15 and 45 mg A tablets and were 1.07, 1.35 and 1.48 X 10(9) M-1 vs 0.85 X 10(8) M-1 value seen after P. The maximal binding capacity (MBC) values decreased after pretreatment with the same doses of A and were 0.044, 0.036 and 0.025 pmol T3/100 micrograms DNA vs. 0.065 pmol T3/100 micrograms DNA in P pretreated. Adrenaline pretreatment significantly increased the amount of endogenous T3 present in liver nuclei while the amount of T3 present in cytosol decreased. Activity of mitochondrial alfa-GPD was increased after 15 and 45 mg of A. Significant rise of activity of cytosol ME was seen only after pretreatment with 45 mg of A.
Animals↗
[A case of partial 9p monosomy].
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Child, Preschool↗
Comparison of adrenaline-induced hyper- and hypoglycaemia by histological and biochemical investigation.
Chronic treatment of rats by subcutaneously implanted A-depot capsules lead through a ca. 12 h hyperglycaemia to hypoglycaemia at 18 h p.o. SDH and G-6-Phase activities in the liver were compared during hyper- and hypoglycaemia using both histochemical and biochemical methods. The results show high triglyceride-contents, lack of glycogen and high G-6-Pase activities in the livers of animals during both hyper- and hypoglycaemia. Striking differences were found concerning SDH-activities: While biochemical measurements show enhanced activities during hyperglycaemia, hypoglycaemic values remain in the "normal" range. Nevertheless histochemical investigations show an amazing re-distribution of SDH-activities from the periportal areas towards the lobule centre. Therefore we think, that biochemical and histochemical methods should be combined to unveil such pseudonormalities. Further, this re-distribution shows the ability of the liver to cope with damage by shifting important processes away from fat-infiltrated areas.
Animals↗
Neutrophil aggregation during migration in vivo.
Stacks of six membrane filters (8-mu pore size) were placed over the mouths of plastic tubes. The tubes were filled with casein (test) or NaCl (control) solution and implanted subcutaneously in white rats; each animal received one tube with casein and one control tube. After 12, 18, 24, and 36 h, the tubes were removed and the filters stained and examined microscopically. Immigrant neutrophils were found either individually or in spherical aggregations within the filter meshwork. Crucial factors in the formation of aggregates included the frequency of individual cells, the chemotactic milieu (casein or NaCl), the duration of exposure, and the location within the filter stacks. The size of the aggregates depended on the duration of exposure. The phenomenon of "neutrophil aggregation" is thought to participate in the formation of the granulocyte wall around a focus of inflammation.
Animals↗