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1.
Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in alpha 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.  相似文献   

2.
Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.  相似文献   

3.
Haemostatic alterations in dogs naturally infected by ehrlichiosis and/or leishmaniasis were studied. Platelet count, ADP and collagen-induced platelet aggregation, prothrombin time, activated partial thromboplastin time (APTT) and plasma fibrinogen concentration were measured. An evident reduction of platelet aggregation response was shown for Leishmania-Ehrlichia co-infected dogs where platelet aggregation was lower in comparison with control and leishmaniotic dogs (ADP and collagen, P < or = 0.01) and ehrlichiotic dogs (ADP 10 and 7.5 microm, P < or = 0.05). Moreover, a significant increase in APTT as well as a reduction of the albumin/globulin rate (A/G) for leishmaniotic and co-infected dogs versus control and ehrlichiotic dogs was detected. The hypothesis of a synergism between leishmaniosis and ehrlichiosis in altering platelet function by different pathways is discussed.  相似文献   

4.
To develop an experimental animal model for immune-mediated glomerulonephritis and nephrotic syndrome, nine healthy dogs were sensitized by intravenous injection with 1 microg of endotoxin and 5 mg of native bovine serum albumin. After 1 week, 120 mg of cationized bovine serum albumin was injected intravenously 5 times a week. Among nine dogs, five dogs were confirmed as having developed glomerulonephritis and nephrotic syndrome by increase of urine protein-to-creatinine ratio (>1.0), hypoalbuminemia (<1.5 g/dl), hypercholesterolemia (>240 mg/dl), and edema. This model should be useful for studying immune-mediated glomerulonephritis and nephrotic syndrome.  相似文献   

5.
The effect of antiplatelet antibody on in vitro platelet function was investigated in 15 dogs with immune-mediated thrombocytopenia (ITP). Platelet aggregation was assessed after addition of serum from healthy dogs (n = 5) or dogs with ITP (n = 15) to platelet-rich plasma from a healthy donor dog. The aggregation responses to adenosine diphosphate, thrombin, and collagen/epinephrine were measured as the maximum aggregation observed after 2 minutes. In 13 of 15 dogs with ITP, maximal aggregation was significantly inhibited in response to ADP, thrombin, or collagen/epinephrine. The slope of the aggregation curve was decreased after addition of serum from 9 of 15 patients. A polyclonal rabbit anti—dog platelet antiserum induced inhibition of aggregation with all 3 agonists.
Serum from control dogs neither inhibited nor activated platelet aggregation. Aggregation experiments were repeated with all 3 agonists after addition of patient immunoglobulin (lg)G or IgG from a healthy dog to platelet-rich plasma. The IgG fraction from 9 of 10 dogs with ITP suppressed platelet aggregation. The IgG fraction from polyclonal rabbit anti—dog platelet antiserum inhibited platelet aggregation with all agonists. These results suggest that many canine ITP patients have circulating antibodies that, in addition to causing platelet destruction, may cause platelet dysfunction.  相似文献   

6.
The purpose of this prospective study was to investigate platelet function using in vitro tests based on both high and low shear rates and von Willebrand factor (vWf) multimeric composition in dogs with cardiac disease and turbulent high-velocity blood flow. Client-owned asymptomatic, untreated dogs were divided into 4 groups: 14 Cavalier King Charles Spaniels (Cavaliers) with mitral valve prolapse (MVP) and no or minimal mitral regurgitation (MR), 17 Cavaliers with MVP and moderate to severe MR, 14 control dogs, and 10 dogs with subaortic stenosis (SAS). Clinical examinations and echocardiography were performed in all dogs. PFA100 closure times (the ability of platelets to occlude a hole in a membrane at high shear rates), platelet activation markers (plasma thromboxane B2 concentration, platelet surface P-selectin expression), platelet aggregation (in whole blood and platelet-rich plasma with 3 different agonists), and vWf multimers were analyzed. Cavaliers with moderate to severe MR and dogs with SAS had longer closure times and a lower percentage of the largest vWf multimers than did controls. Maximal aggregation responses were unchanged in dogs with SAS but enhanced in Cavaliers with MVP (regardless of MR status) compared with control dogs. No significant difference in platelet activation markers was found among groups. The data suggest that a form of platelet dysfunction detected at high shear rates was present in dogs with MR and SAS, possibly associated with a qualitative vWf defect. Aggregation results suggest increased platelet reactivity in Cavaliers, but the platelets did not appear to circulate in a preactivated state in either disease.  相似文献   

7.
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   

8.
Using the Born method, based on light transmission in platelet rich plasma, the minimum effective concentration (threshold values) of several platelet agonists for inducing maximum platelet aggregation was determined in healthy dogs. The final concentrations of aggregation agonists were as follows: adenosine diphosphate (ADP) (0.5-50 micromol/L; n = 75 healthy dogs), collagen (0.5-20 mg/mL; n = 75), thrombin (0.1-5 IU/mL; n = 75), ristocetin (1-10 mg/mL; n = 10), and epinephrine (5-50 micromol/L; n = 10). Reference values for maximum aggregation with a lower limit of > 80% were achieved for agonist concentrations 25 micromol/L ADP (80-98%), > or = 10 microg/mL collagen (80-96%), and > or = 1 IU/mL thrombin (80-97%). None of the concentrations of epinephrine and ristocetin used in this study induced quantitative aggregation in the whole group of healthy dogs. We also studied platelet aggregation in 14 uraemic dogs using selected concentrations of aggregation agonists. Aggregation was significantly decreased in uraemic dogs using intermediate agonist concentrations, i.e., in the region of the threshold concentration. In contrast, maximum aggregation was increased in uraemic patients compared to reference values using low concentrations of all three agonists (ADP: 1 micromol/L, collagen: 1 microg/mL, and thrombin: 0.1, 0.2 IU/mL).  相似文献   

9.
Mitral valve prolapse (MVP) is a fundamental feature of myxomatous mitral valve disease in the dog. In humans, primary MVP is associated with increased platelet reactivity. In Cavalier King Charles Spaniels (CKCS), a breed predisposed to myxomatous mitral valve disease, there is a high prevalence of hypomagnesemia and platelet anomalies, such as thrombocytopenia and macrothrombocytosis. The objective of this study was to evaluate platelet aggregation responses in CKCS and to determine the relationship between the platelet aggregation response and serum magnesium concentration, MVP, mitral regurgitation (MR), and platelet count. In 19 CKCS with MVP and 7 control dogs (not CKCS), the platelet aggregation response to 3 different agonists was compared. The CKCS with >100,000 platelets/microL (n = 10) had a significantly higher maximum aggregation response with regard to all tested agonists than the CKCS with <100,000 platelets/microL (n = 9) and control dogs (n = 7). The CKCS with <100,000 platelets/microL had a platelet aggregation response similar to the control dogs. There was no correlation between degree of MVP and platelet aggregation response. Platelet diameter increased (P = .006) and serum magnesium concentration decreased (P = .04) with lower platelet concentration. In conclusion, CKCS with MVP appeared to separate into 2 groups--1 group with <100,000 platelets/microL, normal platelet aggregation, low serum magnesium concentration, and enlarged platelets, and another group with >100,000 platelets/microL, increased platelet aggregation, and normal serum magnesium concentration and platelet size.  相似文献   

10.
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11.
A 2-year-old spayed female Whippet with membranoproliferative glomerulonephritis and nephrotic syndrome was treated with a specific thromboxane synthetase inhibitor (3-methyl-2[3-pyridyl]-1-indoleoctanoic acid), resulting in decreased proteinuria and resolution of ascites and edema. Glomerular histology, however, appeared unaffected by treatment. Discontinuation of treatment for 10 weeks resulted in increased proteinuria and decreased serum albumin concentrations that were again attenuated when treatment was reinitiated. Thromboxane synthetase inhibitors have been used successfully to treat experimentally induced glomerulonephritis in several species and this treatment appears to hold promise for naturally occurring glomerulonephritis in dogs.  相似文献   

12.
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   

13.
Whole blood platelet aggregation in uremic dogs   总被引：1，自引：0，他引：1  
Whole blood platelet aggregation responses to collagen, arachidonic acid, and adenosine diphosphate were determined by use of the impedance method in 22 dogs with serum urea concentrations greater than or equal to 20 mmol/L, which was attributable to renal disease, and in 25 healthy control dogs. The median changes in impedance for the control dogs were 23 ohms for collagen, 18 ohms for arachidonic acid, and 6 ohms for adenosine diphosphate. The median changes in impedance in uremic dogs were 25 ohms for collagen, 21 ohms for arachidonic acid, and 15 ohms for adenosine diphosphate. There were no significant differences in platelet aggregation responses to collagen, arachidonic acid, and adenosine diphosphate between uremic and control dogs. Hemorrhagic tendencies were not detected in uremic dogs by use of whole blood platelet aggregation. Results of this study suggest that platelet aggregation by use of the whole blood platelet aggregometer is not abnormal in uremic dogs, but does not exclude the possibility of a platelet aggregation defect undetected by the whole blood system.  相似文献   

14.
The influence of heparin on different tests of platelet function was investigated in 5 healthy dogs receiving subcutaneously 1000 I.E./kg BW of a commercial unfractionated Sodium heparin preparation. Blood samples were collected before and 4 hours after heparin injection. Besides plasma activity of heparin platelet count, capillary bleeding time with two different methods, platelet aggregation according to Breddin and to Born with the inductors ADP, collagen, and thrombin as well as in vitro bleeding time were measured. The activity of heparin four hours after the subcutaneous heparin application was 1.20 +/- 0.11 I.E./ml. Compared to the starting values no significant influence of this heparin level could be demonstrated on platelet count, platelet aggregation according to Born with the inductors ADP and collagen, platelet aggregation according to the Breddin method as well as in vitro bleeding time (p > 0.05). Only one of the two methods used for measuring the capillary bleeding time showed a slight prolongation compared to the starting value (mean = 77 sec) to 88 sec (p < 0.05). The most significant influence was seen on the platelet aggregation induced by 1 I.U./ml thrombin, whereby the aggregation maximum decreased from 92.0% (mean) to 12.2% (p < 0.001). Whereas the latter result has to be interpreted primarily as a consequence of the anti-thrombin effect of heparin, the results of the other tests in summary illustrate the clinical unimportant influence of heparin on platelet function in dogs.  相似文献   

15.
Ticlopidine hydrochloride was evaluated for its effectiveness in inhibiting platelet aggregation and serotonin release in 5 laboratory Beagles before and after heartworm implantation with 7 adult Dirofilaria immitis, and after embolization with 7 dead heartworms to mimic what happens after heartworm adulticide treatment. Five other laboratory Beagles, similarly implanted and embolized with heartworms, were used as nonmedicated controls. During the heartworm-negative stage, the dosage of ticlopidine that inhibited adenosine diphosphate (ADP)-induced platelet aggregation in 5 dogs by at least 50% after 5 days of treatment was 62 mg/kg of body weight once a day. In the same dogs implanted with 7 adult heartworms 21 days previously, mean (+/- SD) ticlopidine dosage required to obtain similar results was 71 (+/- 13) mg/kg given once daily. During the 21 days after dead heartworms were implanted in heartworm-infected dogs, mean ticlopidine dosage was 108 (+/- 35) mg/kg (range, 62 to 150 mg/kg). Ticlopidine treatment was associated with increased platelet numbers in all 5 dogs during the heartworm-negative stage and in 4 of 5 dogs during the heartworm implantation and heartworm embolization stages. Mean platelet volume tended to decrease as platelet numbers increased. At necropsy, gross and histologic pulmonary lesions were less severe in ticlopidine-treated dogs than in nonmedicated control dogs.  相似文献   

16.
Platelet aggregation and adenosine triphosphate (ATP) secretion in response to arachidonic acid (10 microM) or collagen (5 micrograms/ml) were compared in healthy, adult female Beagles treated with low-dosage aspirin (3.5 mg/kg of body weight, PO, q 12 h for 7 treatments) or with CGS 12970, a specific thromboxane synthetase inhibitor (10 mg/kg, PO, q 8 h for 10 treatments). Platelet aggregation was assessed in whole blood by use of an electrical impedance method. Baseline values obtained prior to treatment served as controls. Addition of arachidonic acid to blood from nontreated dogs resulted in significantly (P less than 0.001) increased impedance, but had no effect in blood from dogs treated with either aspirin or CGS 12970. Treatment with CGS 12970 or aspirin significantly (P less than 0.001) decreased platelet ATP secretion in response to arachidonic acid, compared with baseline values; however ATP secretion in aspirin-treated dogs was significantly (P less than 0.01) less than ATP secretion in CGS 12970-treated dogs. Differences in platelet aggregation were not observed between control dogs and aspirin- or CGS 12970-treated dogs in response to collagen as an aggregant, however, collagen-induced platelet ATP secretion was significantly (P less than 0.001) decreased in dogs treated with aspirin, compared with control values and values from dogs treated with CGS 12970. In dogs treated orally with 0.1, 0.2, 1.0, or 10 mg of CGS 12970/kg, dose-dependent inhibition of arachidonic acid-induced platelet aggregation was observed, with impedance changes not observed at the 10-mg/kg dosage and normal platelet aggregation associated with the 0.1-mg/kg dosage.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

17.
BACKGROUND: Clinical studies investigating platelet function in dogs have had conflicting results that may be caused by normal physiologic variation in platelet response to agonists. OBJECTIVES: The objective of this study was to investigate platelet function in clinically healthy dogs of 4 different breeds by whole-blood aggregometry and with a point-of-care platelet function analyzer (PFA-100), and to evaluate the effect of acetylsalicylic acid (ASA) administration on the results from both methods. METHODS: Forty-five clinically healthy dogs (12 Cavalier King Charles Spaniels [CKCS], 12 Cairn Terriers, 10 Boxers, and 11 Labrador Retrievers) were included in the study. Platelet function was assessed by whole-blood aggregation with ADP (1, 5, 10, and 20 microM) as agonist and by PFA-100 using collagen and epinephrine (Col + Epi) and Col + ADP as agonists. Plasma thromboxane B(2) concentration was determined by an enzyme immunoassay. To investigate the effect of ASA, 10 dogs were dosed daily (75 or 250 mg ASA orally) for 4 consecutive days. RESULTS: A higher platelet aggregation response was found in CKCS compared to the other breeds. Longer PFA-100 closure time (Col + Epi) was found in Cairn Terriers compared to Boxers. Plasma thromboxane B(2) concentration was not statistically different between groups. Administration of ASA prolonged the PFA-100 closure times, using Col + Epi (but not Col + ADP) as agonists. Furthermore, ASA resulted in a decrease in whole-blood platelet aggregation. CONCLUSIONS: Platelet function is influenced by breed, depending upon the methodology applied. However, the importance of these breed differences remains to be investigated. The PFA-100 method with Col + Epi as agonists, and ADP-induced platelet aggregation appear to be sensitive to ASA in dogs.  相似文献   

18.
OBJECTIVE: To compare platelet aggregation in healthy dogs and dogs with mitral valve regurgitation (MVR) to determine whether regurgitation had an effect on platelet function. ANIMALS: 32 dogs with MVR and 43 healthy dogs. PROCEDURE: Platelet aggregation was measured with an aggregometer, using adenosine 5'-diphosphate as the aggregating agent, and the maximum aggregation and the enhancement of platelet sensitivity (EPS) values were calculated. RESULTS: Platelet count and maximum aggregation were not significantly different between healthy dogs and dogs with MVR. However, EPS values in dogs with MVR were significantly higher than values in healthy dogs. Platelet count and maximum aggregation were not significantly different between dogs classified as New York Heart Association functional class I or II and dogs classified as functional class III or IV; however, EPS values were significantly higher in dogs classified as functional class III or IV. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that platelet aggregation is decreased in dogs with MVR and that the EPS value may be more sensitive to differences in disease severity than in measurement of maximum aggregation.  相似文献   

19.
OBJECTIVE: To evaluate the accuracy of point-of-care tests for the diagnosis of disseminated intravascular coagulation (DIC) in dogs and assess the correlation and agreement of results between point-of-care and laboratory tests in the evaluation of hemostatic function. DESIGN: Prospective case series. ANIMALS: 59 critically ill dogs (affected dogs) with clinical signs of diseases known to predispose to DIC and 52 clinically normal dogs. PROCEDURES: Accuracy of the point-of-care tests (activated clotting time [ACT], estimated platelet count and number of schizocytes from a blood smear, plasma total solids [TS] concentration, and the protamine sulfate test) was evaluated, using receiver operating characteristic curves and likelihood ratios. A strategy, using likelihood ratios to calculate a posttest probability of DIC, was tested with 65% used as a threshold for initiation of treatment. Results of laboratory tests (coagulogram and plasma antithrombin III activity) were used as the standard for comparison in each dog. RESULTS: ACT and estimated platelet count provided the best accuracy for detection of DIC. The plasma TS concentration, schizocyte number, and protamine sulfate test had poor accuracy. The strategy using post-test probability of DIC identified 12 of 16 affected dogs that had DIC. Estimated platelet count was correlated and had acceptable clinical agreement with automated platelet count (r = 0.70). The plasma TS (r = 0.28) concentration and serum albumin (r = 0.63) concentration were not accurate predictors of plasma antithrombin III activity. The ACT did not correlate with activated partial thromboplastin time (r = 0.28). CONCLUSIONS AND CLINICAL RELEVANCE: Strategic use of likelihood ratios from point-of-care tests can assist clinicians in making treatment decisions for dogs suspected to have DIC when immediate laboratory support is unavailable.  相似文献   

20.
Ten adult dogs (5 Beagles and 5 mixed-breed dogs) were inoculated IV with canine platelets containing Ehrlichia platys. Inclusions and morulae of E platys developed in platelets of infected dogs at 10 to 14 days after inoculation, followed by marked thrombocytopenia at 14 to 21 days. Parasitemia and marked thrombocytopenia recurred at 24 to 28 days after inoculation. Increased numbers of megakaryocytes were observed in marrow aspirate smears from infected dogs, indicative of regenerative thrombocytopenia. Prior to infection, platelet-rich plasma from these dogs was determined to have similar aggregatory response to arachidonate. After infection with E platys, the aggregatory response of platelet-rich plasma to collagen or 3 dilutions of adenosine diphosphate was evaluated. A statistically significant (P less than 0.05) inhibition of platelet aggregatory response to the lowest dilution of adenosine diphosphate was detected for mixed-breed dogs, whereas aggregation responses were unchanged in Beagles. Results indicate that platelet activation may occur in dogs with acute ehrlichial infection.  相似文献   

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