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Platelet Aggregation in Feline Cardiomyopathy   总被引：2，自引：0，他引：2  
Platelet aggregation in response to adenosine diphosphate (ADP) was evaluated in 16 healthy cats and in 10 cats with cardiomyopathy. The minimum threshold concentration of ADP required to induce irreversible (2nd-phase) aggregation was determined in each cat. The minimum ADP concentration needed for 2nd-phase aggregation in platelets from healthy cats ranged from 1 microM to 100 microM ADP, with 56% (9/16) requiring 100 microM ADP. Of the remaining seven normal cats, three had platelets responding irreversibly to 10 microM ADP, and four had platelets responding to 1 microM ADP. In cats with cardiomyopathy, the threshold concentrations ranged from 0.01 microM ADP to 10 microM ADP. Two cats had platelets responding irreversibly to 0.01 microM ADP, whereas another cat had a threshold response at 0.1 microM ADP. Platelets from the remaining seven cats with cardiomyopathy exhibited 2nd-phase aggregation in response to 1 microM ADP (five cats) or 10 microM ADP (two cats). Platelet counts ranged from 210,000/mm3 to 630,000/mm3 in healthy cats and from 218,000/mm3 to 624,000/mm3 in cats with cardiomyopathy. There was no apparent correlation between the platelet count and the magnitude of the threshold aggregation response, as measured by lag phase and slope of the aggregation curves. The results indicate that some cats with cardiomyopathy have platelets that are hyperaggregable to ADP in vitro.  相似文献   

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Platelet transfusions might be indicated in horses with thrombocytopenia. The need for a transfusion cannot be determined by platelet numbers alone, as primary or co‐existing disease processes, platelet function and age of the recipient also need to be considered. In patients with no co‐morbidities, relevant bleeding is uncommonly observed with platelet counts >10 x 109/l and a therapeutic approach with initiation of treatment when signs of bleeding are observed might be justified.  相似文献   

6.
Platelet Hyperfunction in Dogs With Malignancies   总被引：1，自引：1，他引：0  
In vitro platelet aggregometry was performed on whole blood samples from 59 dogs with malignancies and 24 control dogs. Three reagents were used for the aggregation studies: collagen, arachidonic acid, and adenosine diphos-phate (ADP). The parameters measured to evaluate response to collagen included delay in the aggregation response, slope of the aggregation curve, maximum aggregation, and adenosine triphosphate (ATP) secretion. The platelets of dogs with malignancies exhibited significantly ( P < .05) shorter delays in the aggregation response, higher maximum aggregation, and higher ATP secretion when compared to control dogs. For the weaker reagents, ADP and arachidonic acid, the lowest concentration resulting in aggregation was determined. Platelets of dogs with malignancies tended to aggregate in response to lower concentrations of ADP than did those of controls ( P < .05). The response of platelets to the concentrations of arachidonic acid employed in this study was poor, with few samples achieving measurable aggregation. The findings of this study suggest that dogs with malignancies have hyperaggregable platelets.  相似文献   

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A serious symptom of cattle affected with Chediak-Higashi syndrome (CHS) is a bleeding tendency. This diathesis is characterized by insufficient platelet aggregation as a result of depressed response to collagen. One possible cause for the depression is a decrease in contribution of endogenous agonists such as ADP or thromboxane A(2), which are released following collagen stimulation. However, these endogenous agonists play only a minor role in collagen-induced aggregation of bovine platelets. More importantly, activation of phospholipase C as a result of a direct action of collagen is depressed, leading to a depression of Ca(2+) mobilization, in platelets from CHS-affected cattle. Several types of collagen receptor are proposed to work in concert to induce aggregation. Among them, glycoprotein VI (GPVI) and GPIa/IIa (integrin alpha2 beta1) have been supposed to play dominant roles in collagen-induced aggregation. However, there are arguments about the role of each receptor, especially the role of GPIa/IIa, and the crosstalk between receptors. Recently, we reported that the Ca(2+) signaling produced by rhodocytin, which had been first reported to be an agonist for the collagen receptor GPIa/IIa, produced much less Ca(2+) signaling in CHS platelets than in normal ones, whereas that produced by GPVI activators was normal. These suggest that GPIa/IIa or the rhodocytin-associated pathway is impaired in CHS platelets. CHS platelets are valuable to reassess the mechanism of collagen-dependent signal transduction system and to delineate the inter-relationship among collagen receptors.  相似文献   

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激动剂诱导细胞内钙离子浓度升高是血小板活化止血和血栓形成的必要条件,它是通过细胞内钙离子释放和质膜内钙离子进入而发生的。Ca2+库释放是一种行之有效的过程,首先磷脂酶(PL)C产生肌醇-1,4,5-三磷酸肌醇(IP3),进而通过IP3通道受体释放细胞内储存的Ca2+,从而完成Ca2+释放。在血小板活化过程中钙离子浓度明显升高有助于活化的各个步骤。钙离子作为细胞的第二信使,参与大多数的生物活动过程,尤其在细胞内钙池引发的钙离子的进入(store-operated Ca2+entry,SOCE)在血小板激活过程中发挥着重要的作用。血小板在血管内激活极易引起血栓,因此研究血小板活化机理可能会对某些疾病的治疗起到关键作用。  相似文献   

10.
Platelets in blood collected from pigs identified as normal (21) or stress susceptible (25) on the basis of their response to halothane challenge, were subjected to electron microscopic examination in order to test whether the ultrastructural features of stress susceptible pigs exhibit any deviation from those of normal. The most striking feature of the platelets from stress susceptible pigs was the extent of dilatation of the open canalicular system (OCS). The difference in platelet morphology between normal and stress susceptible pigs was consistent regardless of the anticoagulants used for blood collection indicating that the platelet alteration may be an inherent component of the porcine stress syndrome.  相似文献   

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A2-year-old Thoroughbred filly presented to the Veterinary Medical Teaching Hospital (VMTH) at the University of California, Davis, for evaluation of a bleeding disorder. The bleeding tendency was 1st noted 3 weeks before presentation on the morning after the horse was pin fired. Prolonged bleeding was noted after intramuscular injection of procaine penicillin G, and the trainer noted blood from the horse's right nostril 2 days before presentation. The filly had been seen by a referral practice, which found a prolonged prothrombin time but no other problems. The horse received an injection of vitamin K intravenously the day before presentation. The current owners purchased the horse ˜1 year before the initial bleeding episode, during which time she had not injured herself or had any intramuscular injections. The filly had received 1 dose PO of a dexamethasone (5 mg) and trichlormethiazide (200 mg) combinationa and 1 or 2 doses of phenylbutazone (unknown amount) but had not received aspirin. The exact dates of administration of these drugs were not known, but they were not within the week before presentation. She had never bled from venipuncture sites  相似文献   

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Platelet aggregation induced by ADP was studied in dogs after vaccination with a modified live-virus distemper vaccine. A significant decrease in platelet counts was observed about 1 week after the vaccination. There were no consistent changes in the aggregability of the platelets. In 4 samples the aggregability was significantly increased compared to the prevaccination values. The observed changes will not cause a defective hemostasis in otherwise normal dogs.  相似文献   

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Despite ingenious concepts, there are no unequivocal clues as to what, when, and how some undefined biochemical factor(s) or constituent(s) that localizes in the arterial wall can precipitate a thromboatheromatous lesion or arterial disease. The present study focused on the extraction, partial purification, and characterization of a collagen-active platelet stimulator from the aortas of aged burros. The aggregator moiety in the aorta extracts invariably had a higher affinity for platelets in citrated platelet-rich plasma of human beings than for platelets of homologous burros. The platelet-aggregating factor(s) in the aorta extract was retained by incubation with alpha-chymotrypsin. Platelet-aggregating activity was rapidldy abolished after incubation with collagenase, as determined by plateletaggregometry tests. Evidence based on light microscope and polysaccharide histochemical reactions indicates a probability that the intracellular amorphous matrix (PAS-positive) and filamentous components (PTAH-positive) expelled from smooth muscle cells disrupted during homogenization of the aorta may be a principle source of a precursor collagen species which is a potent inducer of platelet aggregation.  相似文献   

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Background

Cats with hypertrophic cardiomyopathy (HCM) are at risk for development of systemic thromboembolic disease. However, the relationship between platelet activation state and cardiovascular parameters associated with HCM is not well described.

Objectives

To characterize platelet activation by flow cytometric evaluation of platelet P‐selectin and semiquantitative Western blot analysis of soluble platelet‐endothelial cell adhesion molecule‐1 (sPECAM‐1).

Animals

Eight normal healthy cats (controls) owned by staff and students of the School of Veterinary Medicine and 36 cats from the UC Davis Feline HCM Research Laboratory were studied.

Methods

Platelet‐rich plasma (PRP) was used for all flow cytometry studies. Platelet surface CD41 and P‐selectin expression were evaluated before and after ADP stimulation. sPECAM‐1 expression was evaluated by Western blot analysis of platelet‐poor plasma that had been stabilized with aprotinin. Standard echocardiographic studies were performed.

Results

Resting platelets from cats with severe HCM had increased P‐selectin expression compared to controls, and expressed higher surface density of P‐selectin reflected by their increased mean fluorescence intensities (MFI). Stimulation with ADP also resulted in significantly increased P‐selectin MFI of platelets from cats with severe HCM. Increased P‐selectin expression and MFI correlated with the presence of a heart murmur and end‐systolic cavity obliteration (ESCO). sPECAM‐1 expression from cats with moderate and severe HCM was significantly increased above those of control cats.

Conclusions and Clinical Importance

P‐selectin and sPECAM expression may be useful biomarkers indicating increased platelet activation in cats with HCM.  相似文献   

16.
Platelet activation in ponies with airway inflammation   总被引：3，自引：0，他引：3  
REASON FOR PERFORMING STUDY: Platelet activation occurs in human obstructive airway diseases and in laboratory animal models. However, there is limited evidence that platelets may be involved in equine recurrent airway obstruction (RAO) and other inflammatory diseases. This study investigated whether platelet activation also occurred in RAO. HYPOTHESIS: Platelet function is altered in ponies with active RAO. This alteration can be detected ex vivo by measuring platelet adhesion. METHODS: An in vitro platelet adhesion assay measuring acid phosphatase (AcP) activity colorimetrically was adapted for use with equine platelets and responses to selected agonists were established. Platelet adhesion and aggregation was evaluated in vitro on platelets isolated from 6 ponies with RAO before, during and after a 7 h natural antigen challenge. Three ponies with no history of airway disease were also studied. RESULTS: Adhesion of equine platelets to serum coated plastic was detected at concentrations of 10-100 radicaló 10(9)/l. Adhesion increased in response to stimulation with platelet activating factor and thrombin, but not equine interleukin 8. Prior to the antigen challenge, adhesion of nonstimulated platelets was low and increased significantly (P<0.05) 24 h after initiation of the challenge in RAOs, but not in the normal animals. No changes in platelet aggregation were noted in either group. CONCLUSIONS: The described assay offers an alternative method to evaluate platelet function in healthy and diseased horses and can detect changes not observed using a classic aggregation assay. Circulating platelets are activated 24 h after antigen challenge of ponies with RAO and may play a role in pulmonary inflammation and/or the pathophysiology of RAO. POTENTIAL RELEVANCE: Investigating platelet function in RAO and airway inflammation may reveal new aspects of the pathogenesis of inflammatory lung disease in the horse.  相似文献   

17.
BACKGROUND: Greyhounds have lower platelet concentrations (PC) than dogs of other breeds have. No underlying cause has been investigated. HYPOTHESIS: We hypothesized that Greyhounds have lower mean PC because of breed variation, not immune-mediated causes. Our secondary hypothesis was that PC is dependent on the method of analysis. ANIMALS: Sixty privately owned Greyhounds in Kansas. METHODS: Blood samples were collected into evacuated glass tubes containing ethylenediamine tetraacetic acid (EDTA). Blood smears were evaluated for platelet clumps. All 60 samples had PC determined by manual, impedance, and buffy coat analyzer methods. Results of the 60 samples were compared with results of samples with (n = 25) and without (n = 35) clumps, and with control dogs. Platelets were assayed for the presence of surface-associated antigen (PSAIgG) by direct immunofluorescence. RESULTS: The mean PC was below that of the control dogs for the impedance method (P < .001). No significant difference in PC was detected between analysis methods or between samples with or without platelet clumps. Three of 60 (5%) of the Greyhounds had PC between 50,000 and 100,000/microL with impedance analysis; no samples had < 100,000/microL via buffy coat analysis. PSAIgG was not identified in any samples. CONCLUSIONS AND CLINICAL IMPORTANCE: The mean Greyhound PC for the impedance method was below the reference interval for control dogs but was not significantly different from PC determined by other methods. An immune-mediated cause for the lower PC was unlikely because no samples had PSAIgG. The decreased PC is most consistent with breed variation. As only 0-5% of samples, depending on analysis method, had PC < 100,000/microL, a Greyhound with a PC < 100,000/microL is not necessarily consistent with breed variation, thus diagnostic testing is indicated.  相似文献   

18.
Background: Pentoxifylline (PTX) possesses a number of vasomotor, immunomodulatory, and hemorheologic properties. Based upon the hypothesis that equine laminitis and navicular disease result from microthrombosis, the inhibitory effects of PTX on inflammatory cytokines, and its inhibitory effects on human platelet aggregation, PTX has been widely used to treat equine endotoxemia, navicular disease, and laminitis. Despite this, the effects of PTX on equine platelet aggregation have not been investigated previously. Hypothesis: PTX decreases platelet aggregation in equine whole blood at concentrations approximating those achieved in horses given clinically relevant doses of PTX. Animals: Seven healthy adult horses from a research herd. Methods: Whole blood impedance aggregometry using whole equine blood incubated with varying concentrations of PTX. Adenosine diphosphate (ADP) and collagen were used to initiate aggregation. Results: The onset time of collagen‐induced equine platelet aggregation was significantly shortened by PTX. The maximum slope of resistance change (dR/dt) and total resistance change of collagen‐induced platelet aggregation were unaffected by PTX. No effects of PTX on ADP‐induced onset time of aggregation, dR/dt, or total resistance change were observed. Conclusions and Clinical Importance: Our hypothesis is not supported by the results. PTX hastens the onset of collagen‐induced platelet aggregation in equine whole blood, but has no effect on the rate of collagen‐induced aggregation. PTX does not affect ADP‐dependent equine platelet aggregation. Given these findings, PTX may not be a reasonable therapeutic option to decrease platelet aggregation in horses.  相似文献   

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20.
Nonsteroidal anti-inflammatory drugs are commonly used in the treatment of inflammatory conditions, and have potential value in the treatment of thrombotic disease in the horse. This study compares the potency of three nonsteroidal anti-inflammatory drugs phenylbutazone, naproxen (equiproxen) and flunixin meglumine (banamine) with respect to their effects on equine platelets. Two functional responses of horse platelets were evaluated in vitro: their ability to aggregate and their ability to make available platelet factor 3 procoagulant activity.

Flunixin at a concentration of 10-6 M significantly depressed the maximum degree of adenosine diphosphate-induced (10-6M) aggregation while much higher concentrations of phenylbutazone and naproxen (5 X 105M) were required to produce similar effects. None of the non-steriodal anti-inflammatory drugs significantly affected the duration of the lag phase or the initial velocity of adenosine diphosphate-induced aggregation within the range of drug concentrations used (10-6-10-3M). The lag phase and initial velocity of acid-soluble collagen-induced aggregation were significantly affected by 10-6 M flunixin and 10-4 M phenylbutazone or naproxen was required to produce equivalent effects. Concentrations of 5 X 10-6 M flunixin and 5 X 10-4 M phenylbutazone or naproxen were required to significantly depress the degree of collaen-induced aggregation of horse platelets.

Although the effects of the nonsteroidal anti-inflammatory drugs were qualitatively similar, flunixin was a much more potent inhibitor of platelet aggregation than either of the other two drugs (which were equipotent). At very high drug concentrations (5 X 10-4 M and greater), all three drugs produced the same degree of inhibition of equine platelet aggregation.

Platelet factor 3 activity was made available by exposing horse platelets to 10-5 M adenosine diphosphate or 1:800 acid-soluble collagen; but not by exposure to a suspension of kaolin particles. Only a small portion of the total platelet factor 3 activity was made available on stimulation with either adenosine diphosphate or collagen. Pretreatment of horse platelets with any of the nonsteroidal anti-inflammatory drugs (10-4 M concentration) had no significant effect on adenosine diphosphate or collagen-induced platelet factor 3 availability.

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