A method for investigating the role of calcium in the shape change, aggregation and serotonin release of rat platelets.

Belville, J S; Bennett, William F.; Lynch, Gary

doi:10.1113/jphysiol.1979.sp013040

Cited by 19 publications

(7 citation statements)

References 21 publications

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“…Activation of platelets was induced and assessed by observing the aggregation of platelets (visible clumping followed by gradual clearing of the initially cloudy solution), and through microscopy with a hemacytometer (Fisher Scientific; Pittsburgh, PA) in which the clumps of platelets are observed along with a large decrease in their number in PRP (2,31). PRP and platelet-poor plasma (PPP) were prepared as described previously (2,11). Briefly, 10 ml of blood from a donor cat was collected into a polystyrene tube containing 3.8% sodium citrate (9:1 vol/vol) and was then centrifuged at 150 g for 10 min at 22°C (Allegra 6R centrifuge; Beckman Coulter; Fullerton, CA).…”

Section: Platelet Activation With Agonistsmentioning

confidence: 99%

Role of activated platelets in excitation of cardiac afferents during myocardial ischemia in cats

Longhurst

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Myocardial ischemia activates cardiac spinal afferents that mediate chest pain and excitatory reflex cardiovascular responses. Platelets are activated during myocardial ischemia and release 5-hydroxytryptamine, which stimulates abdominal spinal afferents. This study investigated the role of activated platelets in excitation of cardiac spinal afferents during ischemia. Platelet-rich plasma (PRP) and platelet-poor plasma (PPP) were obtained from cats and incubated with collagen (2 mg/ml) or thrombin (5 U/ml). We observed reduction of platelets in PRP indicative of platelet activation by collagen and thrombin, respectively. Activity of single-unit, ischemia-sensitive cardiac spinal afferents was recorded from the left sympathetic chain in anesthetized cats. Injection of 1.5 ml PRP + collagen (activated platelets) into the left atrium (LA) stimulated 12 of 13 cardiac afferents. PRP + saline (nonactivated platelets, LA) and PPP + collagen did not alter activity of these afferents. PRP + thrombin (1.5 ml, LA) stimulated eight of nine other cardiac afferents, whereas PPP + thrombin did not stimulate any of the nine afferents. Antiplatelet immune serum (1 ml/kg iv) significantly decreased circulating platelets as well as neutrophils (polymorphonuclear leukocytes, PMNs) in eight other cats, and in each animal, attenuated the ischemia-related increase in activity of cardiac afferents. Conversely, responses of five separate cardiac afferents to ischemia were not diminished after treatment with anti-PMN immune serum when concentration of circulating platelets was maintained by infusion of donated PRP despite the decrease in circulating PMNs. These data indicate activated platelets stimulate ischemia-sensitive cardiac spinal afferents and contribute to activation of these afferents during ischemia.

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Section: Platelet Activation With Agonistsmentioning

confidence: 99%

Role of activated platelets in excitation of cardiac afferents during myocardial ischemia in cats

Longhurst

2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…18), both substances induce platelet aggregation (19,20), trigger histamine secretion from peritoneal mast cells (21)(22)(23), and induce paw edema (24,25) and neutrophil chemotaxis in the peritoneal cavity of rats (26)(27)(28).…”

Section: Introductionmentioning

confidence: 99%

The hyperinsulinemia produced by concanavalin A in rats is opioid-dependent and hormonally regulated

Francisco-DoPrado¹,

Zambelli²,

Lima³

et al. 1998

Braz J Med Biol Res

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The present study examines the effect of concanavalin A (Con A) on the blood insulin and glucose levels of rats. Male and female rats treated with Con A (62.5-500 µg/kg) for three days showed a dose-and time-dependent hyperinsulinemia that lasted more than 48 h. Male rats were more sensitive to Con A. Thus, 6 h after treatment with Con A the circulating insulin levels in male rats had increased by 85% (control: 10.2 ± 0.9 mU/l and Con A-treated: 18.8 ± 1 mU/l) compared to only 38% (control: 7.5 ± 0.2 mU/l; Con A-treated: 10.3 ± mU/l) in females. An identical response was seen after 12 h. Con A (250 µg/kg) produced time-dependent hypoglycemia in both sexes but more pronounced in males. There was no correlation between the hypoglycemia and hyperinsulinemia described above. The Con A-induced hyperinsulinemia in rats of both sexes was abolished in gonadectomized animals (intact males: +101 ± 17% vs orchiectomized males: -5 ± 3%; intact females: +86 ± 23% vs ovariectomized females: -18 ± 7.2%). Pretreating intact male and female rats with human chorionic gonadotropin also significantly inhibited the Con A-induced hyperinsulinemia. Estradiol (10 µg/kg, im) significantly blocked the Con A-induced increase in circulating insulin in male rats (101 ± 17% for controls vs 32 ± 5.3% for estradiol-treated animals, P<0.05) while testosterone (10 mg/kg, im) had no similar effect on intact female rats. Pretreating Con A-injected rats with opioid antagonists such as naloxone (1 mg/ kg, sc) and naltrexone (5 mg/kg, sc) blocked the hyperinsulinemia produced by the lectin in males (control: +101 ± 17% vs naloxonetreated: +5 ± 14%, or naltrexone-treated: -23 ± 4.5%) and females (control: +86 ± 23% vs naloxone-treated: +21 ± 20%, or naltrexonetreated: -18 ± 11%). These results demonstrate that Con A increases the levels of circulating insulin in rats and that this response is opioiddependent and hormonally regulated.

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“…['251]-Thrombin was inactivated with diisopropylphosphofluoridate (DFP) as previously described [3]. Medium A contains 0.12 M NaC1, 4.3 mM KC1, 8.5 mM MgC12, 3 mM glucose, 10 mM HEPES, pH 6.5 [9]. Medium B was prepared by adding 10 mM creatine phosphate, 40 pg/ml creatine phosphokinase, and 0.5 mM EGTA to medium A [lo].…”

Section: Methodsmentioning

confidence: 99%

Formation of protease nexin‐thrombin complexes on the platelet surface

Gronke

Curry

Baker

1986

J of Cellular Biochemistry

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We have recently described a platelet factor that is similar to the fibroblast thrombin inhibitor protease nexin I (PNI). The present manuscript shows that this platelet form of PN (PNp) does not complex [125I]-thrombin that has been blocked at its active site, consistent with the conclusion that it is a thrombin inhibitor. When platelets are incubated with [125I]-thrombin, PNp-[125I]-thrombin complexers accumulate both in the medium and on the platelet surface. In the case of fibroblasts, PNI-[125I]-thrombin complexes that form in solution bind to the cells as a consequence of a receptor-mediated clearance process [Low et al, Proc Natl Acad Sci USA 78:2340, 1981]. We show here that the PNp-[125I]-thrombin complexes that accumulate in platelet-binding incubation medium do not bind to platelets. Thus, the platelet-associated complexes must form by [125I]-thrombin binding to PNp that is associated with the platelet surface. Pretreatment of platelets with heparin markedly increases the number of PNp-[125I]-thrombin complexes that form on platelets. The basis for this increase is unclear. This effect seems incompatible with a heparinlike factor acting as the surface binding site for PNp.

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A method for investigating the role of calcium in the shape change, aggregation and serotonin release of rat platelets.

Cited by 19 publications

References 21 publications

Role of activated platelets in excitation of cardiac afferents during myocardial ischemia in cats

Role of activated platelets in excitation of cardiac afferents during myocardial ischemia in cats

The hyperinsulinemia produced by concanavalin A in rats is opioid-dependent and hormonally regulated

Formation of protease nexin‐thrombin complexes on the platelet surface

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