α-Adrenoceptor Changes after Oestrogen Treatment in Platelets and other Tissues in Female Rabbits

1985 ◽  
Vol 69 (2) ◽  
pp. 235-238 ◽  
Author(s):  
N. Mishra ◽  
C. A. Hamilton ◽  
C. R. Jones ◽  
C. Leslie ◽  
J. L. Reid
Keyword(s):  
Radioligand Binding ◽  
Blood Platelets ◽  
Rabbit Platelet ◽  
Oestrogen Treatment ◽  
Α2 Adrenoceptor ◽  
Adrenoceptor Agonists ◽  
Receptor Number ◽  
And Function

1. α2-Adrenoceptors on blood platelets have been widely used as a model for α-adrenoceptors in less accessible tissues. 2. The effect of oestrogen (200 μg/day intramuscularly) on α2-adrenoceptor number and function was studied in immature female rabbits. α2-Adrenoceptor number was measured in whole platelets, and membrane preparations of forebrain, hindbrain, spleen and kidney by radioligand binding. α2-Adrenoceptor function was examined by measuring platelet aggregation in vitro and circulatory responses to selective α2-adrenoceptor agonists in vivo. 3. Oestrogen treatment resulted in a significant decrease in platelet α2-adrenoceptor number and function. However, no changes were observed either in receptor number in other tissues or in responses to α2-agonists in vivo. 4. The results suggest that oestrogen modulation of rabbit platelet α2-adrenoreceptor number and function may be different from that of brain, kidney and spleen. Caution should be exercised in extrapolating results from platelets to α-adrenoceptors at other sites.

α-Adrenoceptor regulation in vivo and in vitro in the rabbit

1985 ◽  
Vol 68 (s10) ◽  
pp. 125s-128s ◽  
Author(s):  
C. A. Hamilton ◽  
C. R. Jones ◽  
J. L. Reid
Keyword(s):  
Radioligand Binding ◽  
Receptor Activation ◽  
Oestrogen Treatment ◽  
Α2 Adrenoceptor ◽  
Adrenoceptor Agonists ◽  
Organ Response ◽  
Adrenoceptor Regulation ◽  
Adrenaline Infusion

1. The relationship between α-adrenoceptor number and response has been studied in rabbits under a range of physiological and pathological conditions. 2. The effects of irreversible α-adrenoceptor blockade, maturation, ageing, oestrogen treatment, adrenaline infusion, perinephritis hypertension and sinoaortic denervation on α-adrenoceptor number and response were examined. 3. α-Adrenoceptor number was measured by radioligand binding. [3H]Prazosin and [3H]clonidine were used as ligands to measure α1- and α2-adrenoceptor number in spleen and [3H]yohimbine to measure α2-adrenoceptor number on platelets. Responses in vivo were studied by examining the pressor responses to a range of α-adrenoceptor agonists. The functional response of platelets was examined in vitro by using the aggregatory response to adrenaline. 4. Reductions in α2-adrenoceptor ligand binding were consistently accompanied by equivalent reductions in α2-adrenoceptor-mediated responses. In contrast large reductions in [3H]prazosin binding were observed with little or no change in α1-adrenoceptor-mediated responses. 5. These results would be consistent with a large receptor reserve for α1-adrenoceptors but few if any spare α2-adrenoceptors in the vasculature or on platelets. 6. Increased responses to both α1- and α2-adrenoceptor agonists were observed in animals with sinoaortic denervation and to α1-adrenoceptor agonists in rabbits with perinephritis hypertension. These increases in response were not accompanied by increases in radioligand binding and may be related to alterations in the coupling of receptor activation to end-organ response.

Acute and chronic regulation of α2-adrenoceptor number and function in man

1985 ◽  
Vol 68 (s10) ◽  
pp. 129s-132s ◽  
Author(s):  
C. R. Jones ◽  
C. A. Hamilton ◽  
K. F. Whyte ◽  
H. L. Elliott ◽  
J. L. Reid
Keyword(s):  
Radioligand Binding ◽  
Plasma Catecholamines ◽  
Platelet Response ◽  
Dynamic Regulation ◽  
Α2 Adrenoceptor ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Receptor Inactivation ◽  
And Function

1. Agonist regulation of platelet α2-adrenoceptors was examined in human volunteers after acute elevations of adrenoceptor agonist and during chronic elevation of plasma catecholamines in two patients with phaeochromocytoma. 2. Platelet α2-adrenoceptor number was measured by radioligand binding ([3H]yohimbine) and α2-adrenoceptor function measured by turbidimetric platelet aggregation. 3. Short term infusion of adrenoceptor agonists with α2 activity caused reductions in the platelet response to adrenaline in vitro; conversely an increase in activity was observed postoperatively in two patients after removal of phaeochromocytoma. 4. The changes in platelet response were not accompanied by changes in α2-adrenoceptor number. 5. It is proposed that a process of receptor inactivation occurs during desensitization and this is responsible for the dynamic regulation of platelet responses.

Desensitization of platelet α2-adrenoceptors after short term infusions of adrenoceptor agonist in man

1986 ◽  
Vol 70 (2) ◽  
pp. 147-153 ◽  
Author(s):  
C. R. Jones ◽  
M. Giembcyz ◽  
C. A. Hamilton ◽  
I. W. Rodger ◽  
K. Whyte ◽  
...  
Keyword(s):  
Binding Sites ◽  
Human Platelet ◽  
Short Term ◽  
Α2 Adrenoceptor ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Adrenaline Infusion ◽  
And Function

1. The effect of intravenous infusion of catecholamines and related drugs on human platelet α2-adrenoceptor number and function was investgated. 2. Short (60–120 min) infusions of catecholamines with α2 agonist activity in vivo produced attenuation of the platelet responses to adrenaline in vitro. This desensitization was specific for the adrenaline induced aggregatory response. 3. The maximum number of [3H]yohimbine binding sites on platelets was not altered by adrenaline infusion. 4. The ability of adrenaline to reduce platelet cyclic AMP levels was significantly reduced after the infusions. 5. Acute infusions of α2-adrenoceptor agonists may alter the coupling of the platelet α2-adrenoceptor to adenylate cyclase.

Storage of Human Blood Platelets

1974 ◽  
Vol 32 (02/03) ◽  
pp. 405-416 ◽  
Author(s):  
M. R Hardeman ◽  
Carina J L. Heynens
Keyword(s):  
Storage Temperature ◽  
Platelet Rich Plasma ◽  
Blood Platelets ◽  
Storage Period ◽  
Serotonin Uptake ◽  
Hypotonic Shock ◽  
Glycolytic Intermediates

SummaryStorage experiments were performed at 4°, 25° and 37° C with platelet-rich plasma under sterile conditions. In some experiments also the effect of storing platelets at 4° C in whole blood was investigated.Before, during and after three days of storage, the platelets were tested at 37° C for their serotonin uptake and response to hypotonic shock. In addition some glycolytic intermediates were determined.A fair correlation was noticed between the serotonin uptake and hypotonic shock experiments. Both parameters were best maintained at 25° C. Also platelet counting, performed after the storage period, indicated 25° C as the best storage temperature. Determination of glycolytic intermediates did not justify any conclusion regarding the optimal storage temperature. Of the various anticoagulants studied, ACD and heparin gave the best results as to the serotonin uptake and hypotonic shock response, either with fresh or stored platelets. The use of EDTA resulted in the lowest activity, especially after storage.The results of these storage experiments in vitro, correspond well with those in vivo reported in the literature.

Influence of Platelet Membrane Sialic Acid and Platelet-Associated IgG on Ageing and Sequestration of Blood Platelets in Baboons

1993 ◽  
Vol 70 (04) ◽  
pp. 676-680 ◽  
Author(s):  
H F Kotzé ◽  
V van Wyk ◽  
P N Badenhorst ◽  
A du P Heyns ◽  
J P Roodt ◽  
...  
Keyword(s):  
Sialic Acid ◽  
Life Span ◽  
Blood Platelets ◽  
Senescent Cell ◽  
Platelet Membrane ◽  
Antigen Complex ◽  
The Mean ◽  
Aggregation Of Platelets

SummaryPlatelets were isolated from blood of baboons and treated with neuraminidase to remove platelet membrane sialic acid, a process which artificially ages the platelets. The platelets were then labelled with 111In and their mean life span, in vivo distribution and sites of Sequestration were measured. The effect of removal of sialic acid on the attachment of immunoglobulin to platelets were investigated and related to the Sequestration of the platelets by the spleen, liver, and bone marrow. Removal of sialic acid by neuraminidase did not affect the aggregation of platelets by agonists in vitro, nor their sites of Sequestration. The removal of 0.51 (median, range 0.01 to 2.10) nmol sialic acid/108 platelets shortened their life span by 75 h (median, range 0 to 132) h (n = 19, p <0.001), and there was an exponential correlation between the shortening of the mean platelet life span and the amount of sialic acid removed. The increase in platelet-associated IgG was 0.112 (median, range 0.007 to 0.309) fg/platelet (n = 25, p <0.001) after 0.79 (median, range 0.00 to 6.70) nmol sialic acid/108 platelets was removed (p <0.001). There was an exponential correlation between the shortening of mean platelet life span after the removal of sialic acid and the increase in platelet-associated IgG. The results suggest that platelet membrane sialic acid influences ageing of circulating platelets, and that the loss of sialic acid may have exposed a senescent cell antigen that binds IgG on the platelet membrane. The antibody-antigen complex may then provide a signal to the macrophages that the platelet is old, and can be phagocytosed and destroyed.

Inhibition of Human and Animal Platelet Adhesiveness to Glass Bead Columns by Adenosine, Dipyridamole, Chlorpromazine and Acetylsalicylic Acid

1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu
Keyword(s):  
Guinea Pig ◽  
Acetylsalicylic Acid ◽  
Guinea Pigs ◽  
Glass Bead ◽  
Animal Species ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Platelet Adhesiveness

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.

Action of Lysolecithin on Blood Platelets

1963 ◽  
Vol 09 (03) ◽  
pp. 512-524 ◽  
Author(s):  
Chava Kirschmann ◽  
Sara Aloof ◽  
Andre de Vries
Keyword(s):  
Blood Platelets ◽  
Protective Action ◽  
Platelet Surface ◽  
Washed Platelet ◽  
Sufficient Concentration ◽  
Saline Medium

SummaryLysolecithin is adsorbed to washed blood platelets and, at sufficient concentration, lyses them, inhibits their clot-retracting activity and promotes their thromboplastin-generating activity. Lysolecithin adsorption to the platelet was studied by using P32-labelled lysolecithin obtained from the liver of rats injected with labelled orthophosphate. The amount of lysolecithin adsorbed to the surface of the washed platelet in saline medium is dependent on the concentration of lysolecithin in solution and reaches saturation — 5 × 10-8 jig per platelet — at a concentration of 9—10 µg per ml. Platelet lysis in saline medium begins at a lysolecithin concentration higher than 18 jig per ml. Plasma and albumin prevent adsorption of lysolecithin to the platelet and protect the platelet from damage by lysolecithin. Albumin is able to remove previously adsorbed lysolecithin from the platelet surface. The protective action of plasma explains the lack of platelet damage in blood, the plasma lecithin of which has been converted to lysolecithin by the action of Vipera palestinae venom phosphatidase, in vitro and in vivo.

scholarly journals Grafts Derived from an α-Synuclein Triplication Patient Mediate Functional Recovery but Develop Disease-Associated Pathology in the 6-OHDA Model of Parkinson’s Disease

2020 ◽  
pp. 1-14
Author(s):  
Shelby Shrigley ◽  
Fredrik Nilsson ◽  
Bengt Mattsson ◽  
Alessandro Fiorenzano ◽  
Janitha Mudannayake ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Lines ◽  
Functional Recovery ◽  
Embryonic Stem ◽  
Hesc Line ◽  
Alternative Source ◽  
And Function

Background: Human induced pluripotent stem cells (hiPSCs) have been proposed as an alternative source for cell replacement therapy for Parkinson’s disease (PD) and they provide the option of using the patient’s own cells. A few studies have investigated transplantation of patient-derived dopaminergic (DA) neurons in preclinical models; however, little is known about the long-term integrity and function of grafts derived from patients with PD. Objective: To assess the viability and function of DA neuron grafts derived from a patient hiPSC line with an α-synuclein gene triplication (AST18), using a clinical grade human embryonic stem cell (hESC) line (RC17) as a reference control. Methods: Cells were differentiated into ventral mesencephalic (VM)-patterned DA progenitors using an established GMP protocol. The progenitors were then either terminally differentiated to mature DA neurons in vitro or transplanted into 6-hydroxydopamine (6-OHDA) lesioned rats and their survival, maturation, function, and propensity to develop α-synuclein related pathology, were assessed in vivo. Results: Both cell lines generated functional neurons with DA properties in vitro. AST18-derived VM progenitor cells survived transplantation and matured into neuron-rich grafts similar to the RC17 cells. After 24 weeks, both cell lines produced DA-rich grafts that mediated full functional recovery; however, pathological changes were only observed in grafts derived from the α-synuclein triplication patient line. Conclusion: This data shows proof-of-principle for survival and functional recovery with familial PD patient-derived cells in the 6-OHDA model of PD. However, signs of slowly developing pathology warrants further investigation before use of autologous grafts in patients.

scholarly journals Extracellular vesicles as mediators and markers of acute organ injury: current concepts

2021 ◽  
Author(s):  
Birte Weber ◽  
Niklas Franz ◽  
Ingo Marzi ◽  
Dirk Henrich ◽  
Liudmila Leppik
Keyword(s):  
Extracellular Vesicles ◽  
Inflammatory Diseases ◽  
Organ Injury ◽  
Isolation And Characterization ◽  
Communication Processes ◽  
Incidence And Mortality ◽  
New Biomarkers ◽  
And Function

AbstractDue to the continued high incidence and mortality rate worldwide, there is a need to develop new strategies for the quick, precise, and valuable recognition of presenting injury pattern in traumatized and poly-traumatized patients. Extracellular vesicles (EVs) have been shown to facilitate intercellular communication processes between cells in close proximity as well as distant cells in healthy and disease organisms. miRNAs and proteins transferred by EVs play biological roles in maintaining normal organ structure and function under physiological conditions. In pathological conditions, EVs change the miRNAs and protein cargo composition, mediating or suppressing the injury consequences. Therefore, incorporating EVs with their unique protein and miRNAs signature into the list of promising new biomarkers is a logical next step. In this review, we discuss the general characteristics and technical aspects of EVs isolation and characterization. We discuss results of recent in vitro, in vivo, and patients study describing the role of EVs in different inflammatory diseases and traumatic organ injuries. miRNAs and protein signature of EVs found in patients with acute organ injury are also debated.

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