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Biomedical subjects

I Rinner

Publications and source records attributed to I Rinner.

17 recordsLinked to original sources
PubMed1992

Continuous in vivo treatment with catecholamines suppresses in vitro reactivity of rat peripheral blood T-lymphocytes via alpha-mediated mechanisms.

A 20 h continuous treatment of rats with catecholamines, using subcutaneously implantable retard tablets, had either no (adrenaline, isoproterenol, midodrine) or a slight (noradrenaline) suppressive effect on the in vitro responsiveness of peripheral blood T-lymphocytes. A marked suppression of the mitogen response ensued when adrenaline, noradrenaline or midodrine, but not isoproterenol, was applied together with the beta-receptor blocker propranolol, whereas the combination with the alpha-receptor blocker phentolamine had no effect. The mitogen response of splenic lymphocytes was not affected by any of these treatments. This alpha-mediated adrenergic suppression of peripheral blood T-cells was not correlated with general metabolic alterations, shifts in white blood cell counts or CD4+/CD8+ subsets, or with elevated glucocorticoid levels. The data suggest that to consistently influence the reactivity of rat peripheral blood lymphocytes by chronic adrenergic stimuli in vivo requires both high catecholamine levels and a bias towards alpha-adrenergic receptivity.

Animals↗
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↗
PubMed1992

Bidirectional interaction between immune and neuroendocrine systems. An experimental approach.

The purpose of this article is to review recent experimental data from our laboratory on immune-neuroendocrine communications, whereby the following findings will be discussed: (i) Experiments using an experimental stress model in rats revealed different doses of a defined stressor to exert opposite effects on the in vitro reactivity of peripheral blood lymphocytes (PBL). Stress effects are also dependent on the tissue origin of lymphocytes, and they seem to be exclusively mediated by adrenal hormones. (ii) The balance between the sympathetic and parasympathetic nervous system may be critical in extrinsic immunoregulation: Experimentally induced hypercatecholaminemia in rats seem to protect lymphocytes from immunosuppressing effects of other, endogenous stress hormones, but causes suppression of PBL activation, if beta-receptors are blocked at the same time. Chronic cholinergic stimuli exert enhancing effects on the cells of the thymus. (iii) A defect in the immune-neuroendocrine crosstalk may contribute to the occurrence of forbidden immune reactions, as has been shown in spontaneous and experimentally induced autoimmune diseases in animals models. Recent data indicate that the parasympathetic nervous system is involved in the transmission of immune messages to the central nervous system.

Animals↗
PubMed1991

The parasympathetic nervous system takes part in the immuno-neuroendocrine dialogue.

In a series of experiments the communication between the parasympathetic nervous system and the immune system was examined in rats. The data are summarized as follows: (1) In vivo administration of physostigmine increased the number of plaque-forming cells whereas in vitro addition of cholinergic agonists decreased the specific antibody response. (2) Prolonged in vivo treatment with atropine or physostigmine influenced concanavalin A stimulation of lymphocytes of different compartments in different ways. (3) Immunization with sheep red blood cells changed the number and the affinity of muscarinic cholinergic receptors in the hippocampus. (4) Cholinergic stimulation in vivo inhibited the transient increase of plasma corticosterone following immunization. Our results provide evidence that the parasympathetic nervous system is included in the dialogue between the neuro-endocrine and the immune systems.

Animals↗
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

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↗
PubMed1988

Binding of muscarine receptor antagonists to pig coronary smooth muscle.

In order to characterize the muscarinic binding site on coronary smooth muscle, we investigated the binding properties of (3H)quinuclidinyl benzilate (QNB) in membrane preparations of pig coronary arteries and atria. Scatchard analysis and Hill plot showed that (3H)QNB binds to a single population of sites in both tissues. The binding profiles of the muscarine receptor antagonists atropine, 11-[2-[dimethylamino)methyl)-1-piperidinyl)acetyl)-5,11-dihydro-6H-pyrid o(2,3- b) (1,4)benzodiazepine-6-one (AF-DX 116), pirenzepine, and 4-diphenylacetoxy-N-methylpiperidine methiobromide (4-DAMP) in both tissues were compared with binding data from other tissues, representative for different muscarinic binding site subtypes. It is concluded that the pig coronary smooth muscle muscarinic binding site is different from M1 and M2 binding sites investigated so far.

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

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

Distribution of choline acetyltransferase activity in rat spinal cord--influence of primary afferents?

Choline acetyltransferase (CAT) activity was measured in various regions of rat spinal cord. In the ventral cord, enzyme activity was 2 to 3 times higher than in dorsal cord. In dorsal spinal cord, there was a gradient in enzyme activity, increasing CAT activity being observed in more caudal segments. In autonomic regions intermediate levels were measured. Bilateral transection of the sciatic nerve reduced CAT activity in the ventral horn of lumbar spinal cord, whereas CAT activity in the dorsal horn remained unchanged. Capsaicin pretreatment had no effect on CAT activity in any spinal cord region. Although a similar distribution of cholinergic neurones and primary afferent endings in rat dorsal spinal cord was described, no conclusive statement as to a possible functional interaction can be given.

Afferent Pathways↗
PubMed1985

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↗