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PubMedDate not supplied

The neurobiology of aging and the neurobiology of depression: is there a relationship?

The relationship between the biology of aging and the biology of affective disorders remains obscure, largely for two reasons. First, and most important, is the equivocal nature of the data that indicates that increasing age predisposes an individual to episodes of major depression. Second, is the lack of tools to assess neurotransmitter turnover and availability in humans. Indirect measures such as neuroendocrine function tests, platelet, plasma and CSF studies contain too many confounding factors, to allow for adequate testing of neurochemical hypotheses. Development of novel approaches based on dynamic brain imaging methods may ameliorate these shortcomings.

Aged↗
PubMed1996

Cardiopulmonary bypass leads to a preferential loss of activated platelets. A flow cytometric assay of platelet surface antigens.

OBJECTIVE: In a prospective study surface antigens associated with platelet activation, aggregation, and adhesion and the platelet volume were measured to investigate the mechanism of the platelet function defect of cardiopulmonary bypass (CPB). METHODS: Blood samples were obtained during cardiac surgery before and after heparinization, as well as during and following extracorporeal circulation. The expression of the platelet surface glycoproteins (GP) IIb-IIIa, Ib, 53, and the granule membrane protein (GMP) 140 were measured using flow cytometry in platelet-rich plasma (PRP) before and after in vitro stimulation with adenosine diphosphate. A full blood count including mean platelet volume (MPV) was taken. RESULTS: Heparinization resulted in a significant increase of GP 53 and GMP 140 and a significant decrease of GP Ib expression. During and following CPB, GP IIb-IIIa and Ib were significantly decreased. Similarly, the expression of the activation markers was reduced significantly. The mean platelet volume decreased significantly from 8.6 +/- 0.7 fl at baseline to 7.9 +/- 0.8 fl at the end of the study period. CONCLUSION: Our data suggest that heparinization induces platelet activation. We assume that a loss of larger and more activated platelets from the circulation contributes substantially to the platelet function defect of CPB.

Adult↗
PubMed1999

Efficacy of abciximab induced platelet blockade using a rapid point of care assay.

Anciximab provides potent, but variable degrees of platelet inhibition both during the duration of intravenous administration and at 12 hours following therapy. Platelet function was assessed using the PC-RPFA system in 78 patients scheduled for percutaneous coronary revascularization who were administered the standard abciximab weight-adjusted bolus and 12-hour infusion. The PC-RPFA system is a cartridge-based, semiautomated point-of-care whole-blood assay that incorporates fibrinogen-coated polystyrene beads, buffers, and a modified thrombin receptor activating peptide (Isotrap) in lyophilized form. The instrument detects the agglutination rate between the stimulated platelets and the fibrinogen-coated beads, and provides a quantitative digital display in less than 2 minutes. No differences in the level of platelet inhibition were observed in these abciximab-treated patients by diabetic status, gender, smoking, diagnosis (unstable angina, chronic stable angina, recent myocardial infarction), or abciximab treatment status (first time vs. retreatment). Nocorrelation of the PC-RPFA rate of platelet aggregation with clinical demographic factors was observed, with the exception of baseline hematocrit (r2 = 0.4556). The relationship between the PC-RPFA rate of aggregation and hematocrit reflects light absorbance by erythrocytes and is specific to the PC-RPFA system. The absolute rate of platelet aggregation (slope) reported by the PC-RPFA is correlated with percent aggregation, thus making it potentially possible to predict the level of aggregation without reference to a baseline (pretreatment) measure of platelet function. This correlation was closest for patients having <40% baseline aggregation (r2 = 0.55). Thus, PC-RPFA provides a rapid point-of-care assessment of platelet function that could allow for adjustment of abciximab dosing to achieve targeted levels of platelet inhibition. The utility of this device to optimize therapy with platelet glycoprotein IIb/IIIa inhibitors is currently being evaluated.

Abciximab↗
PubMed2001

Platelet aggregation inhibition with glycoprotein IIb--IIIa inhibitors.

Inhibitors of the platelet receptor glycoprotein (GP) IIb--IIIa are a novel and potent class of antithrombotic drugs for the management of patients with non-ST-segment elevation acute coronary syndromes (ACS) and those undergoing percutaneous coronary intervention (PCI). Pharmacodynamic studies with three currently approved agents in this class (abciximab [ReoPro, Centocor, Inc., Malvern, Pennsylvania, and Eli Lilly & Company, Indianapolis, Indiana]; eptifibatide [INTEGRILIN, COR Therapeutics, Inc., South San Francisco, California, and Key Pharmaceuticals, Inc., Kenilworth, New Jersey]; and tirofiban HCI [Aggrastat, Merck & Co., Inc., Whitehouse Station, New Jersey]) all sought to identify dosing regimens that would establish and maintain >80 % inhibition of ex vivo platelet aggregation throughout the duration of intravenous infusion. Direct comparison of these prior studies is difficult, however, because the assays used different anticoagulants (sodium citrate [abciximab, tirofiban HCI] or D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone [PPACK] [eptifibatide]) and different concentrations of the platelet agonist adenosine diphosphate (ADP) (5 micromol [tirofiban HCI] or 20 micromol [abciximab, eptifibatide]). More recent work has attempted to overcome these limitations by using similar assay conditions for all GP IIb--IIIa inhibitors. These studies have indicated that the concentrations of all three agents required to provide the targeted effect for platelet inhibition are considerably higher in the presence of an anticoagulant that does not chelate calcium ions (e.g., heparin or PPACK) than in the presence of calcium-chelating anticoagulant (i.e., sodium citrate). Of the three currently approved GP IIb--IIIa inhibitors, eptifibatide is the only agent whose approved dosing is based on an ex vivo platelet aggregation assay that uses such an anticoagulant. Additionally, Kereiakes et al. have recently reported that the high levels of platelet inhibition (>80 %), using PPACK as an anticoagulant and ADP (20 micromol) as an agonist, are more consistently achieved with the approved dosing regimen of eptifibatide. The antiplatelet effect of abciximab showed more interpatient variability, whereas the median inhibition of ex vivo platelet aggregation with the approved dosing regimen for tirofiban HCl was <80 % at almost all time points during drug infusion.

Abciximab↗
PubMed2000

High platelet count in platelet-rich plasma reduces measured platelet inhibition by abciximab but not tirofiban nor eptifibatide glycoprotein IIb/IIIa receptor antagonists.

We evaluated the differential effect of platelet count in platelet-rich plasma (PRP) on the level of ex vivo inhibition of platelet aggregation provided by abciximab, eptifibatide, and tirofiban as part of a randomized, comparative trial of these agents on platelet function in patients with unstable angina pectoris undergoing percutaneous coronary intervention. Platelet count <350 K/microL in PRP reduced measured platelet inhibition by abciximab, but not eptifibatide nor tirofiban. This observation suggests the need for standardized, uniform platelet counts in PRP during future comparisons of the degree of platelet inhibition by these agents.

Abciximab↗
PubMed2002

Abciximab is rapidly effective in preventing and arresting established platelet aggregation.

BACKGROUND: Abciximab reduces the thrombotic complications of angioplasty. It is also used, as a 'bail out' treatment when angioplasty is complicated by thrombus but its speed of action is not known. This study sought to establish how quickly abciximab blocks the aggregation of both quiescent and activated platelets to explain this rapid efficacy. METHODS: Optical aggregometry (OA) and whole blood electrical impedance platelet aggregometry (WBEA) were performed with blood from 10 healthy volunteers. Abciximab 5 microg/ml was added in each case with saline control 5 minutes before agonist, 10 seconds before agonist and during aggregation. RESULTS: (1) Abciximab administered 5 minutes before agonist, completely inhibited aggregation with OA: (medians and ranges) 0% (all 0), control: 71% (50-95%) p < 0.001. and with WBEA: 0 omega (all 0 omega), control: 7.5 omega (4.8-12.5 omega) p = 0.016. (2) When administered 10 s before agonist with OA a small initial degree of aggregation occurred but this was rapidly reversed (time to reversal: 2 mins (1-4.5 mins) to low levels of aggregation 16.5% (0-22%), control 72.5% (55-95%) p = 0.002. With WBEA aggregation was completely inhibited: 0 omega (all 0 omega), control: 7.5 omega (4.8-12.3 omega) p = 0.016. (3) When administered during aggregation, with OA the rise in the aggregometry tracing was rapidly arrested (time to arrest: 1.5 mins (0.1-3 mins)) with no further aggregation occurring: 42% (30-57%), control: 80% (60-100%) p = 0.002. With WBEA the findings were similar: (time to arrest 1.5 mins (1-2 mins)) 6.3 omega (1.5-11.3 omega), control: 10 omega (3-12 omega) p = 0.031. CONCLUSIONS: These data suggest that when administered during a procedure in which thrombus has occurred, aggregation may be rapidly arrested. This applies to quiescent platelets but also activated platelets undergoing aggregation.

Abciximab↗
PubMed2002

Decreased platelet reactivity in blood anticoagulated with bivalirudin or enoxaparin compared with unfractionated heparin: implications for coronary intervention.

BACKGROUND: Platelet reactivity predicts complications after percutaneous coronary intervention (PCI). Accordingly, agents that suppress platelet reactivity should decrease adverse events after PCI. This study was designed to determine the effects of therapeutic concentrations of unfractionated heparin (UFH), bivalirudin, or enoxaparin alone or in combination with tirofiban on platelet reactivity. METHODS: Blood taken from 13 patients with coronary artery disease was exposed to each anticoagulant alone or in combination with tirofiban ex vivo. Platelet reactivity was characterized with flow cytometry to quantify the percentage of platelets capable of binding fibrinogen (activation of glycoprotein IIb-IIIa) and expressing P-selectin in response to adenosine diphosphate (ADP, 0, 0.2, and 1 microM). RESULTS: Platelet reactivity was greater in blood treated with UFH than in blood anticoagulated with bivalirudin with respect to both the capacity to bind fibrinogen (by 4 +/- 1.8%, p = 0.01) and P-selectin expression (by 7.7 +/- 0.7%, p, < 0.0001) in response to 1 microM ADP. Platelet reactivity was greater in blood treated with UFH than in blood exposed to enoxaparin with respect to P-selectin expression (by 7 +/- 1.1%, p, < 0.0001) in response to 1 microM ADP. Platelet reactivity was similar in blood treated with bivalirudin or enoxaparin. Addition of tirofiban suppressed the capacity to bind fibrinogen in the presence of each anticoagulant to a similar extent. CONCLUSIONS: As platelet reactivity is greater in blood anticoagulated with UFH in comparison with blood anticoagulated with enoxaparin or bivalirudin, the use of bivalirudin or enoxaparin rather than UFH during PCI should contribute to a reduced incidence of adverse cardiac events after PCI.

Adenosine Diphosphate↗
PubMed2006

Suspected clopidogrel resistance in a patient with acute stent thrombosis.

BACKGROUND: A 67-year-old man with supraventricular tachycardia associated with angina underwent coronary angiographic assessment. This investigation revealed mild coronary artery disease in his left main coronary artery and significant stenosis of the ramus medianus (left intermediate artery). A drug-eluting stent was deployed and treatment with clopidogrel and eptifibatide started. The patient subsequently developed chest pain accompanied by hypotension, hypoxemia and electrocardiographic changes that indicated acute myocardial infarction. Emergency angiography revealed occlusion of the ramus medianus despite clopidogrel therapy. INVESTIGATIONS: Coronary angiography, hypercoagulable work up and platelet function tests. DIAGNOSIS: Acute stent thrombosis and suspected clopidogrel resistance, culminating in ST-segment elevation myocardial infarction after percutaneous coronary intervention. MANAGEMENT: Warfarin, aspirin and clopidogrel drug therapy.

Aged↗
PubMed2000

Bernard-Soulier syndrome in a patient doubly heterozygous for two frameshift mutations in the glycoprotein ib alpha gene.

We report here the genetic basis of Bernard-Soulier syndrome in a compound heterozygote for two mutant glycoprotein (GP) Ib alpha alleles. One allele contained a novel four base-pair deletion (TGAG) that eliminated the last base of the codon for Ser39 (AGT) and the entire codon for Glu40 (GAG), causing a reading frame shift that yielded a stretch of 51 amino acids before a premature stop codon. The other allele also contained a frame-shift mutation, caused by deletion of the last two bases of the codon for Tyr492 (TAT). This allele produced a truncated glycoprotein Ib alpha that, although not expressed on the surface of the patient's platelets, was detectable in the plasma. The second allele has been identified previously by our group and other investigators as the cause of Bernard-Soulier syndrome in patients of northern European ancestry. This allele carried a haplotype identical to those of the previously reported cases, with the following polymorphic markers: two tandem repeats in the VNTR region, C at nucleotide -5 from the ATG start codon and a substitution of G for A in the third base for codon Arg342. These findings suggest that this particular Bernard-Soulier mutation occurred once on the background of a rare haplotype and has spread throughout the northern European population.

Bernard-Soulier Syndrome↗
PubMedDate not supplied

Five-day storage of platelet concentrates.

The short 72-hour shelf-life of platelet concentrates stored in standard PL146 (Fenwal) plastic bags often results in shortages of platelets. This 3-day limitation is based on the biochemical and physiological changes that occur during storage and that result in decreased viability and survival after transfusion. We assessed both in vitro and in vivo function of platelet concentrates stored for 3 and 5 days in two new plastic packs: PL732 (Fenwal) and CLX (Cutter). The concentrate pH was maintained above 7.0 in both bags and there was little change in platelet count or size following 5 days of storage. Aggregation response to adenosine diphosphate, epinephrine, and collagen was maintained well. The PCO2 values indicated good gas escape with lower values after 5 days of storage than at 0 time. Lactate accumulation and glucose utilization were also lower in these new bags. Autologous survivals of chromium-labeled platelets stored for 5 days were 6.0 days (PL732) and 5.1 days (CLX), which are equal to or better than those found for platelets stored for 3 days in PL146. Posttransfusion increments in thrombocytopenic patients were acceptable; 49 percent after 1 hour and 31 percent after 24 hours for concentrates stored in CLX and 44 percent after 1 hour and 28 percent after 24 hours for concentrates stored in PL732. Both of these new bags, which contain different types of plasticizers, provide an environment that results in an improved product and will permit 5-day storage of platelet concentrates; these two benefits will help to alleviate the difficulties in supply of platelet concentrates.

Blood Platelets↗
PubMedDate not supplied

Use of PGE1 for preparation of platelet concentrates.

Platelets stored as platelet concentrates (PCs) undergo biochemical, functional, and morphological changes that may inhibit their hemostatic effectiveness. Prostaglandin E1 (PGE1) (5.9 X 10(-8) M) added to platelet-rich plasma (PRP) immediately before PC preparation reduced platelet activation during PC preparation and storage as determined by inhibition of beta-thromboglobulin release and thromboxane B2 production. However, PCs prepared with PGE1 contained less glycogen after storage than PCs prepared by standard methods. All PC platelets lost their ability to aggregate in response to adenosine diphosphate (ADP) during storage, but sensitivity to dual stimulation with epinephrine and ADP was retained. These findings suggest that addition of PGE1 to PRP may permit production of platelets that are hemostatically superior to conventional PCs. In vivo studies to evaluate this possibility are indicated.

Alprostadil↗
PubMedDate not supplied

Prevention of acquired defects in platelet function during blood processing.

Two kinds of platelet concentrates were prepared in this study: one as pelleted platelets from platelet-rich plasma (PCs), and the other as a platelet suspension from the buffy coat fraction (nonpelleted PCs). The characteristics of both platelet concentrates were studied. White cell contamination in the nonpelleted PCs was below the threshold of detection by a microcell counter (less than 300 cells/microliter of concentrate); in the pelleted PCs, it was 3 +/- 1 x 10(7) cells per concentrate. The difference between the white cell contamination in pelleted PCs and nonpelleted PCs was significant (p less than 0.001). The degree of aggregation induced in pelleted PCs by ADP (9 microM) and collagen decreased to 33 and 55 percent, respectively, of that in platelet-rich plasma. The secondary wave of platelet aggregation induced by ADP and epinephrine was absent in pelleted PCs, and ATP secretion from these platelets by ADP stimulation also decreased remarkably. However, the degrees of aggregation and ATP secretion in nonpelleted PCs were similar to those in platelet-rich plasma. Furthermore, it was found that the amount of platelet factor 4 release seen in pelleted PCs was large in comparison to that in nonpelleted PCs and platelet-rich plasma. These results suggested that the deterioration of platelet function might have resulted from the platelet activation induced by pellet formation during the preparation of PCs from platelet-rich plasma.

Adenosine Triphosphate↗