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1.
A bleeding disorder due to abnormal platelet function occurs in Simmental cattle. Whole blood from these animals underwent good clot retraction. Platelet aggregation in response to adenosine diphosphate (ADP) and collagen in a whole blood aggregation system was markedly impaired. Normal bovine platelets in a whole blood aggregation system showed very little aggregation in response to epinephrine and arachidonic acid. Aggregation in platelet-rich plasma was negligible in response to ADP, collagen and thrombin. Dense granule release of radiolabelled serotonin from the platelets of one affected cow was similar to that of normal bovine platelets. Platelet membrane glycoprotein electrophoresis with the platelets of one affected cow revealed no quantitative abnormalities. These findings reveal similarities and differences in thrombopathic Simmental platelet function when compared to human Glanzmann's thrombasthenia and Basset Hound thrombopathia.  相似文献   

2.
Eight Simmental cattle were presented to the Western College of Veterinary Medicine over the past decade with historic or current prolonged episodes of bleeding. Spontaneous epistaxis, superficial hematomas, and prolonged bleeding following injury or minor surgery (such as tattooing) were frequent observations. Animals presented because of prolonged hemorrhage were anemic and debilitated. Compensatory erythropoiesis was compromised in these animals by depletion of iron stores due to chronic blood loss. Screening tests to assess coagulation were normal as were numbers and morphology of platelets. In vitro platelet aggregation was abnormal in all affected cattle. Three animals were euthanized due to uncontrollable hemorrhage but the precise source of hemorrhage was undetectable. These findings are consistent with bleeding due to a platelet function disorder which has been described previously in Simmental cattle.  相似文献   

3.
OBJECTIVE: To compare the interaction of endogenous ADP with collagen and thromboxane A(2) (TXA(2)) during collagen-induced platelet aggregation between platelets from healthy cattle and those with Chediak-Higashi syndrome (CHS). POPULATION SAMPLE: Platelets harvested from blood samples from healthy Japanese Black cattle and those with CHS. PROCEDURES: Aggregation of gel-filtered platelets; release of ATP-ADP; and generation of thromboxane B(2) (TXB(2)), a metabolite of TXA(2), were measured. RESULTS: The potency of collagen to induce aggregation in platelets of cattle with CHS (ie, CHS platelets) was less than a tenth of that in platelets of healthy cattle (ie, control platelets). Platelet aggregation induced by collagen at an intermediate concentration depended on the coexistence of ADP and TXA(2), suggesting that released ADP cannot cause platelet aggregation by itself. Collagen-induced ADP release was markedly decreased, whereas TXB(2) production was slightly low in CHS platelets, compared with that in control platelets. A combination of subthreshold amounts of ADP and 9,11-dideoxy-9alpha, 11alpha-methano-epoxy-prostaglandin F(2) (U46619), a TXA(2) analogue, caused platelet aggregation. Similarly, a combination of subthreshold amounts of collagen and ADP caused platelet aggregation, whereas collagen and U46619 were not synergistic. CONCLUSIONS AND CLINICAL RELEVANCE: Deficient ADP release ensuing from the delta-storage pool deficiency in platelets from cattle with CHS resulted in reduction of collagen-induced platelet aggregation, through attenuation of synergism between TXA(2) and ADP and between ADP and collagen. Furthermore, results of the study reported here indicated that TXA(2) was important for aggregation of bovine platelets.  相似文献   

4.
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   

5.
OBJECTIVE: To determine whether viral involvement with platelets obtained from cattle persistently infected (PI) with bovine viral diarrhea virus (BVDV) is associated with altered platelet function or decreased platelet counts. SAMPLE POPULATION: Platelets obtained from 8 cattle PI with BVDV and 6 age-, sex-, and breed-matched uninfected control cattle. PROCEDURE: Manual platelet counts were determined, and platelet function was assessed through optical aggregometry by use of the aggregation agonists ADP and platelet-activating factor. Identification of BVDV in serum and preparations of purified platelets was determined by use of virus isolation tests. RESULTS: No significant difference in platelet counts was detected between cattle PI with BVDV and control cattle. In response to the aggregation agonists, maximum aggregation percentage and slope of the aggregation curve were not significantly different between cattle PI with BVDV and control cattle. We isolated BVDV from serum of all PI cattle and from purified platelets of 6 of 8 PI cattle, but BVDV was not isolated from serum or platelets of control cattle. CONCLUSIONS AND CLINICAL RELEVANCE: Isolation of BVDV from platelets in the peripheral circulation of cattle immunotolerant to BVDV does not result in altered platelet function or decreases in platelet counts.  相似文献   

6.
Whole blood platelet aggregation in dogs with liver disease   总被引：1，自引：0，他引：1  
Whole blood platelet aggregation was determined in response to collagen, arachidonic acid, and adenosine diphosphate in 20 dogs with liver disease and in 20 control dogs. Platelet aggregation in response to collagen and arachidonic acid was reduced in dogs with liver disease, compared with control dogs (P less than 0.05), whereas there was no significant difference in platelet response to adenosine diphosphate between the 2 groups of dogs. Adenosine diphosphate was found not to be a reliable aggregation agent for determination of whole blood platelet aggregation in dogs. Dogs whose platelets did not aggregate in response to collagen and/or arachidonic acid manifested bleeding tendencies that could be attributed to platelet dysfunction.  相似文献   

7.
Electron microscopic observation was performed on platelets activated by collagen stimulation in Japanese Black cattle with delta-storage pool deficiency (delta-SPD) to identify their morphological and functional abnormalities compared from normal bovine platelets. Platelets of normal Japanese Black cattle changed their shapes to spherical and were in the phase of release reactions 5 min after the collagen (90.9 microg/ml) stimulation, and most of platelets were aggregated. On the other hand, in GSPD cattle, most of a granules were still dispersed in activated platelets, although the spherical shape change of the platelets was observed. These results suggested that there are abnormalities in the release reactions in platelets of delta-SPD cattle.  相似文献   

8.
The beige (bgJ/bgJ) mouse is a well-described murine model of Chediak-Higashi syndrome. Platelet function was examined in normal and beige mice to better characterize the defective aggregation response in platelets from mice with Chediak-Higashi syndrome. Platelet aggregation after collagen, thrombin, and phorbol-12-myristate 13-acetate stimulation was significantly (P less than 0.025) decreased in platelets from beige mice, relative to platelets from normal mice. Compared with beige and normal mice, those heterozygous for the bg trait had intermediate responses to collagen and thrombin, but not phorbol-12-myristate 13-acetate. The defect(s) in aggregation of platelets from beige mice was associated with a dense granule storage pool deficiency and decreased stores of serotonin and adenine nucleotides in platelets. Mice heterozygous for the bg trait had normal platelet serotonin and adenine nucleotide concentrations. Platelets from beige mice were approximately 10 times more sensitive to prostacyclin inhibition of collagen-induced aggregation than were platelets from control mice. However, a significant difference in platelet cyclic AMP concentration was not apparent between beige and normal mice after prostacyclin stimulation. Platelet endoperoxide synthesis measured by quantification of thromboxane B2, was normal in beige mice. Protein phosphorylation patterns in mouse platelets were similar to those seen in human platelets. Thrombin and collagen-induced [32P] phosphorylation of 40- and 20-kD proteins in platelets from normal and beige mice was similar. Results indicate that the biochemical defect(s) in platelet function in beige mice is partially attributable to storage pool deficiency and does not result in an absolute defect in phosphorylation of 40- and 20-kD proteins.  相似文献   

9.
Equine platelet aggregation responses to bovine collagen, adenosine diphosphate (ADP), serotonin, epinephrine, and arachidonate in a platelet aggregometer were recorded. Equine platelets exhibited irreversible aggregation when incubated with ADP at a final concentration of 10 microM and bovine collagen. A secondary aggregation wave was recorded from platelets from certain horses at final ADP concentrations of 1 to 5 microM. Serotonin and arachidonate induced a weak reversible aggregation response, but a response was not observed following epinephrine addition. Equine platelet aggregation was influenced by concentration of anticoagulant (sodium citrate). Platelet aggregation responses at 37 C were indistinguishable from those recorded at 39 C. Platelet aggregation responses also were altered if the aggregation tests were not performed within 4 hours of blood sample acquisition. An assessment of platelet aggregation from multiple blood samples from the same horse indicated that the procedures described provide a reliable method to assess equine platelet aggregation in vitro.  相似文献   

10.
A fibrillar collagen molecule was extracted from the upper thoracic aorta of an old burro (Equus asinus). Presence of the collagen in the extract was determined by amino acid analysis, scanning and transmission electron microscopy, incubation with collagenase, and assays of its platelet-aggregating capacity by "aggregometry". Based on the amino acid rations of proline/hydroxyproline and lysine/hydroxylysine, the collagenous protein most nearly resembles type I of 4 main published types of collagen. Quantitative assays of the collagen as a mediator of platelet aggregation showed human platelets more sensitive and sheep platelets slightly less sensitive than burro platelets. Incubation with collagenase abolished platelet aggregation capacity and converted the fibrillar collagen to a gel-like mass. Incubation with galactose oxidase neither lessened nor intensified the collagen-mediated platelet aggregation. Incubation with burro plasma decreased platelet aggregating activity and changed the collagen ultrastructure (demonstrated with scanning electron microscopic imaging). The significance of a naturally occurring plasma (protein) factor(s) which may have a regulatory role in reducing the chemical activity of the fibrillar collagen molecule with platelets is also discussed.  相似文献   

11.
It has been reported that antibiotics of the penicillin family impair the functional response of human, canine and lapine platelets to a broad range of agonists. In contrast, we have shown that the bovine platelet retained full functional responses to stimulation by adenosine diphosphate (ADP) or platelet activating factor (PAF) following administration of penicillin G to clinically normal cattle at 20,000 IU/kg for three days. The aggregation response to collagen was transiently reduced to approximately 50% of pretreatment values, but only while the drug was detectable in the circulation. When penicillin was added to platelet rich plasma suspensions, ADP-induced aggregation was similar to that of the control untreated platelets, while the PAF-induced aggregation response was reduced by not more than 25%. Only collagen-induced aggregation exhibited a modest dose-dependent inhibitory response in the presence of penicillin. It is postulated that the relative insensitivity of the bovine platelet to penicillin may be related to differences in postreceptor biochemical events compared to the human platelet.  相似文献   

12.
Failure of aspirin to impair bovine platelet function   总被引：1，自引：0，他引：1  
The effect of aspirin on bovine platelet function and thromboxane A2 (TXA2) production in stimulated platelets was evaluated. A single dose of aspirin (100 mg/kg of body weight) was administered orally to Holstein cows, and blood samples were obtained before and at regular intervals for 7 days after treatment. The production of TXA2 was assessed by measuring the stable metabolite thromboxane B2, using a specific radioimmunoassay. Within 4 hours of aspirin administration, the production of TXA2 was significantly (P less than 0.05) decreased, irrespective of whether collagen, adenosine diphosphate, or platelet activating factor was used to initiate platelet aggregation. Despite the inhibition of TXA2 release from the stimulated platelets, platelet function, assessed by initial rate of aggregate formation and extent of aggregation, was unaffected by aspirin administration. The extent of aggregate formation in response to collagen, adenosine diphosphate, or platelet activating factor was independent of the amount of TXA2 released from platelets before and after aspirin treatment. The results suggested that TXA2 formation is not the primary biochemical pathway involved in the aggregation of stimulated bovine platelets.  相似文献   

13.
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   

14.
The effects of whole blood storage time on platelet aggregation and on post-transfusion platelet survival time were assessed in dogs. Citrate phosphate dextrose adenine-1 (CPDA-1) was used as a blood cell preservative. Storage time dependent decay of platelet aggregability was assessed. Platelet aggregation responses to collagen and ADP were maintained for at least 8 hr at room temperature. During blood storage, immunoglobulin became nonspecifically bound to platelets, suggesting the potential for immune destruction of platelets by the mononuclear phagocyte system after transfusion. To assess this assumption, the survival times of infused platelets, which were stored for 0 to 8 hr in whole blood, were measured. Post-transfusion survival of platelets was not affected by these storage times. These results suggest that canine platelets maintain viability when stored at room temperature for up to 8 hr in CPDA-1 treated whole blood intended for transfusion.  相似文献   

15.
Background: Limited information exists regarding hemostasis in camelids despite the importance of platelet function testing in the accurate identification of platelet disorders. As further importation of llamas to North America is restricted, variability in breeding stock will continue to decrease, potentially leading to an increase in heritable bleeding disorders. Objective: The objective of this study was to measure platelet aggregation responses in clinically healthy llamas and provide baseline data to which abnormal platelet function may be compared in the future. Methods: Blood samples were collected from 39 healthy adult llamas, citrated, and centrifuged to produce platelet‐rich plasma (PRP). Within 4 hours of the blood draw, 20 μL of each agonist reagent were added to 180 μL of PRP. Final concentrations of agonists were 2 × 10?5 M ADP, 0.19 mg collagen/mL PRP, 1 × 10?4 M epinephrine, and 500 μg arachidonic acid/mL PRP. Results: Llama platelets were most responsive to ADP and collagen, with a maximum percent aggregation (mean±SD) of 71.3±18.6% and 55.8±19% and aggregation rates of 9.5±3.9 and 6.7±3.7 cm/min, respectively. Llama platelet aggregation in response to epinephrine and arachidonic acid was minimal to absent. Conclusions: This study is the first of its kind to establish baseline values for platelet aggregation in healthy adult llamas.  相似文献   

16.
Hemograms on blood obtained from 10 clinically normal West Indian Manatees (Trichechus manatus) were studied. The red cells were large and in lower number than in most terrestrial species. The manatee does not have a neutrophil as is present in most species, but it has a heterophil whose granules stain pink with the Wright-Giemsa stain. The eosinophil has uniform red-staining granules that make its differentiation from heterophils difficult. Both large and small lymphocytes, monocytes and basophils are present. The total number of white blood cells was comparable to that of common domestic species as were the platelet numbers. No reticulocytes were found.  相似文献   

17.
Hereditary platelet function disorders are clinically characterized by recurrent surface bleeding and prolonged bleeding time, despite normal platelet count and coagulation tests. The authors describe persistent thrombopathies in two young dogs with increased bleeding tendencies but with normal plasma coagulation times and von Willebrand factor (vWf) concentrations. Buccal mucosal bleeding times were prolonged in both dogs. In aggregation studies, platelets underwent only a shape change or minimal aggregation in response to adenosine diphosphate and collagen. Whole-platelet adenine nucleotide concentrations were normal. Electron microscopic evaluation of fibrinogen and vWf binding to the platelets of case no. 1 demonstrated the presence of glycoprotein IIb/IIIa and Ib receptors. Thus, the intrinsic platelet function defects may be different in these two dogs and may likely represent secretion/signal transduction disorders.  相似文献   

18.
A 3‐year‐old, female Greater Swiss Mountain dog developed a hemoperitoneum following an exploratory laparotomy and ovariohysterectomy. Platelet count, PT, APTT, and plasma von Willebrand factor antigen concentration were within RIs. A buccal mucosal bleeding time (BMBT) was prolonged. Given the probability of a hereditary thrombopathia, the dog was administered desmopressin, fresh platelet transfusions, and aminocaproic acid to control hemorrhage. Subsequently, DNA testing for the P2Y12 receptor gene mutation identified the dog as being a heterozygote (carrier). Further platelet function testing was performed following complete recovery. Results of a repeat BMBT and a point‐of‐care screening test using the Platelet Function Analyzer‐100 (collagen/adenosine‐diphosphate [ADP] test cartridge) were within RIs. Flow cytometric studies demonstrated a marked reduction in fibrinogen binding to the dog's platelets in response to ADP ‐ adenosine diphosphate activation. Likewise, turbidimetric aggregometry revealed a complete absence of platelet aggregation in response to ADP. However, there were a normal aggregation response to the platelet agonist convulxin and a mild reduction in amplitude in response to γ‐thrombin. This is the first report of a dog heterozygous for the P2Y12 receptor gene mutation exhibiting a bleeding tendency and having evidence of impaired platelet function in vitro in response to ADP activation. Given that the mutant allele for the P2Y12 thrombopathia appears to be widespread in the Greater Swiss Mountain dog breed, veterinarians need to be aware that both homozygotes and heterozygotes for this platelet receptor mutation are at risk of developing life‐threatening bleeding following trauma or surgery.  相似文献   

19.
Objective: To review the current understanding of the mechanisms responsible for primary hemostasis and to give an overview of primary hemostatic syndromes in small animal patients. Current and future therapeutic options for dysfunction of primary hemostasis are discussed. Data sources: A thorough search of the human and veterinary literature using the keywords platelets, primary hemostasis, von Willebrand factor (vWF), von Willebrand disease, aspirin, thromboxane, and aggregation, were performed. Databases searched included OVID Medline, Pubmed, and CAB abstracts. Conclusions: Primary hemostasis occurs when platelets adhere to an injured or disrupted endothelial surface. Adherence is followed by activation, or the release of platelet granule contents. The agonists released from platelet granules recruit additional platelets and induce their activation and aggregation. Adhesion, activation, and aggregation are mediated by different receptors and ligands depending on the local blood flow conditions. vWF and adenosine diphosphate are the primary mediators of adhesion, activation, and aggregation under high shear conditions. During low shear conditions collagen, fibronectin, and laminin mediate adhesion, thromboxane A2 promotes activation, while aggregation is mediated by glycoprotein Ib‐IX‐V (GP Ib–IX–V) and fibrinogen. Knowledge of the receptor interactions during different blood flow conditions is crucial to the understanding of the various inhibitors of primary hemostasis available to clinicians.  相似文献   

20.
A recently identified intrinsic platelet function defect in 2 Spitz dogs is described. Both affected dogs had a history of chronic intermittent bleeding primarily from the nasal, oral, and gastrointestinal mucosa. Platelet aggregation in response to adenosine diphosphate (ADP), collagen, and platelet activating factor (PAF) was absent; however, platelet shape change did occur. Platelets aggregated in response to gamma thrombin, although a delayed onset and a reduced velocity of aggregation were present. Platelet 14C-serotonin release was diminished in response to collagen and PAF. Glycoprotein Illa was detected on the surface of platelets by flow cytometry. Platelets were morphologically normal under light and electron microscopy. Two male Spitz dogs, related to one of the affected dogs, did not have a bleeding diathesis. Collagen-induced platelet aggregation, however, was diminished in these 2 dogs. This platelet defect most closely resembles the defect described in Basset hounds.  相似文献   

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