Platelet serotonin changes in dogs with prosthetic aortic grafts

The purpose of this study was to elucidate the mechanisms underlying the striking reduction in platelet serotonin found after placement of prosthetic aortic grafts in dogs. Changes in platelet serotonin paralleled changes in platelet survival time. Both were reduced after graft placement, remained depressed for up to a year, and then returned to normal. In vivo release of serotonin was assessed by labeling autologous platelets with ⁵¹Cr (a nonreleasable, cytoplasmic label) and ¹⁴C-serotonin (a releasable, storage granule label). In dogs with grafts, ¹⁴C-serotonin persisted in the circulation beyond the life span of ⁵¹Cr-labeled platelets. The ratio of platelet ¹⁴C/⁵¹Cr activity over 5 days following infusion of double-labeled platelets markedly increased. These data indicated in vivo release and reutilization of labeled serotonin. In vitro platelet uptake of ¹⁴C-serotonin was assessed in separate experiments and was found to be depressed following graft placement. We conclude that the reduction in platelet serotonin stems from platelet interaction with aortic prostheses. Platelets adhere to the prosthetic surface, release serotonin, and recirculate. Reutilization of released serotonin occurs but may be limited by depressed platelet uptake. The net effect is a reduction in platelet serotonin. These findings support our view that platelet interaction with prosthetic surfaces is, in large measure, a reversible phenomenon, with platelets reentering the circulation in an altered state.     

Heparin-induced platelet activation: the role of thromboxane A2 synthesis and the extent of platelet granule release in two patients

Heparin-induced thrombosis is due to an immune-mediated activation of circulating platelets and has significant clinical implications for patients with vascular disease. The purpose of this article was (1) to define the biochemical mechanisms of heparin-induced platelet activation (HIPA) and (2) to determine the relationship between thromboxane A2 (TxA2) synthesis and platelet granule release. In two patients with confirmed HIPA, heparin (3 U/ml) induced extensive platelet aggregation (61.5%), release of 14C-serotonin (81.5% of releasable 14C-serotonin, a dense granule marker) and platelet factor 4 (63.7% of releasable platelet factor 4, an alpha granule marker) and generation of TxB2, a stable metabolite of TxA2 (100% relative to serum control). In one patient heparin did not induce release of n-acetyl-beta-glucosaminadase (N-AC, a lysosomal granule marker), and aspirin (4 mmol/L), which abolished TxA2 synthesis, prevented aggregation and granule release. In the second patient heparin did induce release of N-AC (39.7% of releasable N-AC) and aspirin, despite abolishing TxA2 synthesis, did not prevent aggregation or granule release. In contrast, by elevating intracellular cyclic adenosine monophosphate, iloprost (0.01 mumol/L), a stable prostacyclin analogue, prevented heparin-induced aggregation, granule release, and TxB2 generation in both patients. Thus we show (1) HIPA can proceed independently of TxA2 synthesis; (2) heparin in certain patients can release lysosomal hydrolases, thus mimicking strong platelet agonists such as thrombin; and (3) iloprost but not aspirin prevents HIPA regardless of the biochemical pathways involved.     

High-dose heparin suppresses platelet alpha granule secretion.

Platelet degranulation has been implicated in the pathophysiology of acute arterial thrombosis, intimal hyperplasia, and atherogenesis. Most previous studies that examined the effect of heparin on platelet function have used platelet aggregometry. These studies have resulted in contradictory data and, by the nature of the assay, reveal no information with regard to platelet degranulation. In contrast, flow cytometry allows accurate quantification of the extent of platelet degranulation by measurement of the platelet surface binding of a GMP-140 specific monoclonal antibody (S12). GMP-140 is only expressed on the platelet surface after platelet alpha granule release. In the present study increasing concentrations of heparin were added to whole blood anticoagulated with sodium citrate. Platelets were activated with a panel of agonists, and the extent of platelet degranulation was quantified by whole blood flow cytometry. Heparin concentrations as high as 100 units/ml were found to suppress platelet alpha granule release induced by either a thromboxane A2 analog (U46619) or a combination of adenosine diphosphate and epinephrine. Heparin suppressed alpha granule release induced by thrombin both in whole blood and in washed platelets. The addition of heparin after platelet activation had no effect on S12 binding. In summary, heparin in high concentrations is a potent inhibitor of platelet degranulation, an action that is unrelated to its effect on the coagulation cascade. Although the heparin concentrations used in this study exceed those used clinically by a factor of 10 or more, future studies of heparin fractions may allow the separation of the anticoagulant and antiplatelet properties of the molecule and allow the administration of an agent that selectively suppresses platelet degranulation without the humoral anticoagulant effect.     

Platelet size and function in septic rats: changes in the adenylate pool

Cecal ligation and puncture (CLP) were performed in rats. After 4 hr (early sepsis) and 16 hr (late sepsis), platelet morphology and function were studied. At 16 hr, platelet counts for the CLP group were significantly lower than for the sham-operated control group. Low maximum aggregation rates (MAR) and decreased platelet counts were elicited in platelet-rich plasma with 4 M ADP and 2 micrograms/ml collagen. However, with platelet counts equalized, MAR for the CLP group increased significantly, especially after 16 hr. The platelet-large cell rate and platelet distribution width decreased temporarily at 4 hr, then rose significantly at 16 hr. No significant changes were observed in the mean platelet volume after 4 hr, but there were significant increases after 16 hr. Total adenine nucleotide (TAN) levels within the platelets rose significantly in the CLP group, suggesting the appearance during the late sepsis of large, heavy platelets or adenine nucleotide-rich platelets. The platelet adenylate pool was divided into granular and cytoplasmic fractions, respectively characterized by ADP and ATP increases. However, no septicemia-related differences were noted in the degree of binding between goat antirat fibrinogen and platelet surface glycoprotein IIb/IIIa complex. Internal environment changes in the platelets indicated that during septicemia hyperfunctional or hypersensitive platelets with a latent capacity for active aggregation and release appeared in the circulation. Hypercoagulability in septicemia involves activation of coagulation factors, stimulation of the coagulation cascade, volume changes accompanying increased platelet TAN content, and changes in AN distribution in the two pools. These findings significantly increase our understanding of the transition from the prethrombotic state to thrombosis in septicemia.     

Platelet function tests predict bleeding and thrombotic events after off-pump coronary bypass grafting.

OBJECTIVE: A balanced coagulation system after cardiac surgery minimizes bleeding and thrombotic events. However, the best method to monitor this balance has not been established. We used a series of tests of coagulation and platelet function to define the risk of bleeding and thrombotic events after OPCAB. METHODS: In 76 patients, routine coagulation tests (i.e. prothrombin time, fibrinogen level, d-dimer, and platelet count), thrombelastography, and whole blood aggregometry were obtained perioperatively and on days 1 and 3 after OPCAB. Intra- and postoperative blood loss was determined. Early patency of venous bypass grafts was determined using CT angiography (Philips Medical, Corp.). RESULTS: Chest tube output and red cell volume loss at 24 h were 952+/-475 and 190+/-115 ml, respectively. Early graft failure developed in eight patients. Perioperative changes in routine coagulation tests showed no correlation with either bleeding or thrombosis. However, perioperative decline in platelet function as assessed by the area under the impedance curve for whole blood aggregometry correlated with intraoperative blood loss (R=0.42, P<0.05). A perioperative decline in the maximum amplitude of the thrombelastography trace showed a significant correlation with 24h hemoglobin loss (R=0.45, P<0.05). Compared to those with all patent grafts, patients with early graft failure demonstrated a reduction in platelet sensitivity to aspirin by both thrombelastography and aggregometry on day 3. CONCLUSIONS: In contrast to standard coagulation testing, platelet function predicted both bleeding and thrombosis after OPCAB. Titration of perioperative platelet function according to these tests may minimize thrombosis without increasing bleeding.     

Mechanism of thrombosis caused by sclerotherapy of esophageal varices using sodium tetradecyl sulphate

Summary The mechanism of thrombosis following intravariceal injection of sodium tetradecyl sulphate (S.T.D.) was investigated with respect to effects on the vascular endothelium, the coagulation cascade, and platelet function. Using an umbilical cord model designed to simulate blood flow over the endothelium, it was found that S.T.D. is a potent toxin for endothelial cells in that brief exposure to even low concentrations of the agent were effective in stripping endothelium over a considerable distance, exposing highly thrombogenic endothelium in the process. Effects on coagulation and platelet function were found to be dependent on concentration. Diluted S.T.D. induced a hypercoagulable state, possibly in consequence of a selective inhibition of the physiological anticoagulant, protein C, and promoted platelet aggregation. Higher concentrations inactivated the coagulation cascade and lysed platelets completely. These results suggest that intravariceal infusion of S.T.D. at considerable dilution may be at least as effective in inducing thrombosis as standard dosage, and possibly more so.     

Platelet function and pharmacologic inhibition

Platelets have traditionally been understood within the context of hemostasis and hemorrhagic disorders. However, with increasing procedures being performed in smaller vessels and with an increasing incidence of atherosclerosis, the often critical role platelets play is more evident. Platelets are no longer viewed as "scaffolding" for the events of the coagulation cascade but rather as important catalysts in hemostasis, thrombosis, and fibrinolysis. Improved understanding of platelet physiology has led to developments of pharmacologic adjuncts resulting in improved patency rates and improved patient outcomes. This review addresses the physiology of platelet function and the impact of new pharmacologic agents in percutaneous intervention.     

Hemostasis after open-heart surgery with extreme or moderate hemodilution

Patients who received aortic disc valves during cardiopulmonary bypass (CPB) with extreme hemodilution, obtained with preoperative blood withdrawal, infusion of acetate solution and use of blood-free priming fluid, bled less than patients operated with moderate dilution. One hour after CPB with extreme dilution when the autologous blood had been reinfused, platelet adhesiveness was twice as high as in the moderate dilution group. Other parameters of platelet function, coagulation and fibrinolysis did not differ between the groups. The higher number of reactive platelets may therefore have contributed to the improved hemostasis after extreme dilution. Later, thrombocytosis with hyperreactive platelets and hyperfibrinogenemia developed in all patients. This might predispose for thrombosis.     

Heparin-induced platelet activation in sixteen surgical patients: diagnosis and management

Heparin-induced platelet activation (HIPA) is a syndrome associated with thrombocytopenia, intravascular thrombosis, and arterial emboli. We have evaluated 16 patients for presumed HIPA because of the occurrence of thrombocytopenia or a new thrombotic complication during heparin therapy. In this group, 16 thrombotic events occurred in 10 patients with a mortality rate of 18.8%. Diagnosis was confirmed in vitro by the demonstration of at least 20% platelet aggregation and/or 6% 14C-serotonin release after heparin (0.1 to 3 U/ml) was added to a mixture of patient platelet-poor plasma (PPP, two parts) and aspirin-free donor platelet-rich plasma (PRP, three parts). After heparin was discontinued, seven patients continued to have HIPA in their own PRP although it could no longer be observed in donor PRP. Iloprost, a potent prostacyclin analog that reversibly inhibits platelet activation, completely prevented HIPA and release in all of nine patients. Aspirin, an irreversible cyclooxygenase inhibitor, failed to prevent HIPA in four of these nine patients. In conclusion, HIPA is associated with an extremely high morbidity and mortality rate. Evaluation of the patients' PRP in response to heparin may improve the diagnostic sensitivity of this assay. Aspirin does not reliably prevent HIPA, which suggests participation of thromboxane-independent pathways. Thus, if further exposure to heparin is unavoidable, a more effective platelet inhibitor such as iloprost is required to reliably prevent in vivo HIPA.     

Whole blood platelet aggregation in humans and animals: a comparative study

BACKGROUND. Many animal species are used to evaluate the performance and blood compatibility of cardiovascular devices, but interspecies differences in platelet activity have not been well characterized. This study measures platelet response to six agonists in human, dog, and calf blood. MATERIALS AND METHODS. We used whole blood impedance lumi-aggregometry to measure platelet aggregation and ATP release in blood samples from adult humans (n = 19), mongrel dogs (n = 19), and Holstein calves (n = 7). The agonists were collagen, ristocetin, arachidonic acid, thrombin, and three concentrations of both ADP and epinephrine. RESULTS. Only collagen (1 microg/ml) and ADP (5, 10, and 20 microM) caused aggregation and ATP release in all samples. Canine platelets responded to all six agonists at all doses. Human platelets responded to everything except epinephrine at 2 and 100 microM. Bovine platelets responded only to collagen, ADP, and thrombin. In bovine platelets, aggregation from collagen and ATP release from thrombin were significantly lower than the corresponding responses in human and canine blood. The aggregation induced by 10 microM ADP was significantly higher in canine than in human platelets. CONCLUSION. Human, canine, and bovine platelets have very different responses to agonists. In these models, collagen (1 microg/ml) and ADP (10 microM) are the agonists of choice for investigating whole blood platelet aggregation because they provide the most consistent results between species. For ATP release, 1 U/ml thrombin is the recommended agonist and the dose for all three species.     

Epinephrine enhances platelet-neutrophil adhesion in whole blood in vitro

Previous studies showed that alpha- or beta-adrenoceptor stimulation by catecholamines influenced neutrophil function, cytokine liberation, and platelet aggregability. We investigated whether adrenergic stimulation with epinephrine also alters platelet-neutrophil adhesion. This might be of specific interest in the critically ill, because the increased association of platelets and neutrophils has been shown to be of key importance in inflammation and thrombosis. For this purpose, whole blood was incubated with increasing concentrations of epinephrine (10 nM, 100 nM, and 1 microM). To distinguish receptor-specific effects, a subset of samples was incubated with propranolol (10 microM) or phentolamine (10 microM) before exposure to epinephrine. After incubation, another subset of samples was also stimulated with 100 nM of N-formyl-methionyl-leucyl-phenylalanine. All samples were stained, and platelet-neutrophil adhesion and CD45, L-selectin, CD11b, P-selectin glycoprotein ligand-1, glycoprotein IIb/IIIa, and P-selectin expression were measured by two-color flow cytometry. Epinephrine significantly enhanced platelet-neutrophil adhesion and P-selectin and glycoprotein IIb/IIIa expression on platelets. CD11b and L-selectin expression on unstimulated neutrophils remained unchanged, whereas N-formyl-methionyl-leucyl-phenylalanine-induced upregulation of CD11b and downregulation of L-selectin were suppressed by epinephrine. beta-Adrenergic blockade before incubation with epinephrine increased platelet-neutrophil aggregates and adhesion molecule expression (CD11b, P-selectin, and glycoprotein IIb/IIIa) even further. These results demonstrate that epinephrine enhances platelet-neutrophil adhesion. The alpha-adrenergic receptor-mediated increase in P-selectin and glycoprotein IIb/IIIa expression on platelets may contribute substantially to this effect. Our study shows that inotropic support enhances the platelet-neutrophil interaction, which might be crucial for critically ill patients.     

Human neutrophil cathepsin G is a potent platelet activator

Purpose: Neutrophil activation has been implicated in the pathophysiologic condition of ischemia-reperfusion injury, the formation of arterial aneurysms, the progression of myocardial ischemia, and the initiation of deep venous thrombosis. Activated neutrophils release cathepsin G, a serine protease, from their granules, which may cause platelet activation that leads to intravascular thrombosis, tissue infarction, and systemic release of the thrombogenic products of platelet granules. This study used flow cytometry to quantify the extent of cathepsin G–induced platelet activation and degranulation through changes in the expression of platelet surface glycoproteins.Methods: Increasing concentrations of human neutrophil–derived cathepsin G were incubated with washed platelets or whole blood from healthy human donors. The platelet surface expression of glycoproteins, including P-selectin, a platelet membrane glycoprotein only expressed after platelet alpha granule release, were determined by quantifying the platelet binding of a panel of fluorescently labeled monoclonal antibodies. Results were compared with the effect of a maximal dose of thrombin, the most potent known platelet activator.Results: In a washed platelet system, cathepsin G increased platelet surface expression of P-selectin (an activation-dependent neutrophil binding site), the glycoprotein IIb/IIIa complex (fibrinogen receptor), and glycoprotein IV (thrombospondin receptor), and decreased surface expression of glycoprotein Ib (von Willebrand factor receptor) to an extent comparable to maximal thrombin. However, these effects were not observed in a whole blood system. Further experiments revealed that preexposure to plasma completely inhibited cathepsin G–induced washed platelet activation and degranulation. Prostacyclin treatment of washed platelets markedly inhibited cathepsin G–induced platelet activation.Conclusions: Cathepsin G is a very potent platelet agonist and degranulator, comparable to maximal thrombin, which alters platelet surface glycoprotein expression for enhanced neutrophil binding and effective platelet aggregation. This study helps to elucidate a possible pathway through which neutrophils may directly activate platelets, leading to intravascular thrombosis, irreversible ischemia, and tissue death in cardiovascular disease states. Patients with diseased endothelium that is deficient in prostacyclin production may be particularly prone to the detrimental effects of neutrophil-derived cathepsin G platelet activation. (J VASC SURG 1994;19:306-19.)     

Coagulation disorders following severe trauma: surgeon's role in prevention

INTRODUCTION: Severe trauma must be considered a "systemic disease" that could lead to severe systemic complications. PHYSIOPATHOLOGIC IMPLICATIONS: Coagulation disorders are present in most trauma patients as hemorrhagic disorder, thrombosis, or like in DIC, with both coexistent phenomenon. Trauma determine the activations of intrinsic and extrinsic coagulation pathways, and of platelets. Intrinsic pathway activation induce a pro-coagulant function and the activation of fibrinolytic system. Both system activation explain low incidence of deep venous thrombosis. Post-traumatic activation of extrinsic coagulation lead to thrombin and fibrin production. In trauma patients platelets activation is related to endothelial damage, exposition of collagen, interaction with PAF and presence of microorganisms. Post-traumatic DIC is characterized by procoagulant factors activation, with intravascular deposit of fibrin and thrombosis, and by hemorrhagic disorders due to consumption of platelet and procoagulant factors. Lower levels of antithrombin III, in trauma patients, are strictly related to severity of damage and shock. Coagulation disorders related to sepsis, that often complicate trauma, are added to those determined by trauma, with a negative synergic effect. Medical treatment with massive infusion of colloid and crystalloid solution, and fluid, and massive transfusion of plasma and red blood cells can determine dilutional thrombocytopenia, reduced activity of coagulation factors and reduced haemostatic activity of RBC due to excessive haemodilution--Hct <20%. PREVENTION STRATEGY: To avoid post-traumatic coagulation disorders is important to prevent sepsis, thrombocytopenia and reduced activity of coagulation factors and of RBC, as well as prevent and immediately treat shock. The early use of high dose antithrombin concentrate, is important to prevent DIC and MOFS, and administer subcutaneous or intravenous heparin, in absence of hemorrhagic disorders that contraindicate its use.     

Platelet dysfunction associated with cardiopulmonary bypass.

The clinical significance and pathogenesis of the platelet dysfunction following cardiopulmonary bypass were studied in conjunction with the degree of functional impairment associated with the use of membrane and bubble oxygenators. Forty consecutive patients had the following tests preoperatively and postoperatively: complete blood count (CBC), platelet count, prothrombin consumption time, bleeding time, prothrombin time, partial thromboplastin time, fibrinogen, euglobulin clot lysis, fibrin degradation products, and platelet aggregation tests. Six patients were given 14C-serotonin tests before and after operation, and preoperative and postoperative electron micrographs were made of the platelets of 3 patients. The amount of blood lost, the blood transfused, and plasma hemoglobin levels were also measured. Abnormal aggregation of platelets was found, with no difference between the membrane and bubble oxygenators. In vitro aggregation tests with protamine sulfate and hemoglobin solutions, as well as the 14C-serotonin studies and electron micrographs, suggest that platelets acquire storage pool deficiency and an abnormal membrane during cardiopulmonary bypass.     

Hereditary nephritis,platelet disorders and deafness — Epstein's syndrome

A 14-year-old boy with persistent proteinuria (1.6–4.0 g/day), microscopic haematuria, moderate hypertension, macrothrombocytopenia (giant platelets, platelet number 30×10⁹/l) and a familial sensorineural hearing loss (the father and the brother were also affected) was studied. Kidney biopsy revealed a diffuse mesangial proliferation, and a focal thickening of the glomerular basement membrane was seen on electron microscopy. A normal number of megakaryocytes was observed in bone marrow aspirates. The aggregation response of the platelets to collage, epinephrine and adenosine diphosphate (ADP) was decreased. The platelet number was slightly diminished, platelets were of normal size in both parents and the brother, and showed a decreased aggregability in response to collagen, epinephrine and ADP in the brother and mother. No functional abnormality of the platelets was observed in the father. Urinalysis and kidney function were normal in the family members. This boy with nephritis, platelet disorders and hearing loss corresponds to Epstein's syndrome.     

Abnormalities of aggregation, thromboxane A2 synthesis, and 14C serotonin release in platelets of patients with idiopathic scoliosis

Platelet functions were investigated in 16 patients with idiopathic scoliosis (IS), in seven patients with congenital scoliosis (CS), and in 12 healthy individuals who served as a control group. All were females, aged 11 to 22 years. Platelet aggregation anomalies were observed in all IS patients. These constituted an impaired platelet-release reaction when aggregation was induced with ADP or epinephrine, but not with collagen or arachidonic acid. A decreased thromboxane A2 synthesis and impaired 14C-serotonin release were also observed when platelets were stimulated with ADP or epinephrine. Platelet from CS patients and the controls did not show any functional abnormalities when stimulated with the above four aggregating agents. The platelet function anomaly in IS patients was not associated with prolongation of the bleeding time, spontaneous occurrence of hemorrhagic episodes, or increased bleeding during invasive procedures, including major spinal surgery. The above findings and the recently described platelet structural anomalies in IS may imply that the pathological process operative in idiopathic scoliosis involves not only the axial skeleton, but also cellular blood elements. The similarity between blood platelets and muscle cells, and the anomalies that have been found in both systems in IS, support the notion that a muscle disorder may be involved in the pathogenesis of the disease.     

全麻药对血小板功能的影响

血小板是参与止血、凝血和血栓形成过程的主要效应细胞。血小板功能异常可加剧术中和术后出血。临床麻醉中使用的全麻药物对血小板功能有一定影响。现就全麻药对血小板功能的影响作一简要综述。     

Procoagulant activity in hemostasis and thrombosis: Virchow's triad revisited

Virchow's triad is traditionally invoked to explain pathophysiologic mechanisms leading to thrombosis, alleging concerted roles for abnormalities in blood composition, vessel wall components, and blood flow in the development of arterial and venous thrombosis. Given the tissue-specific bleeding observed in hemophilia patients, it may be instructive to consider the principles of Virchow's triad when investigating mechanisms operant in hemostatic disorders as well. Blood composition (the function of circulating blood cells and plasma proteins) is the most well studied component of the triad. For example, increased levels of plasma procoagulant proteins such as prothrombin and fibrinogen are established risk factors for thrombosis, whereas deficiencies in plasma factors VIII and IX result in bleeding (hemophilia A and B, respectively). Vessel wall (cellular) components contribute adhesion molecules that recruit circulating leukocytes and platelets to sites of vascular damage, tissue factor, which provides a procoagulant signal of vascular breach, and a surface upon which coagulation complexes are assembled. Blood flow is often characterized by 2 key variables: shear rate and shear stress. Shear rate affects several aspects of coagulation, including transport rates of platelets and plasma proteins to and from the injury site, platelet activation, and the kinetics of fibrin monomer formation and polymerization. Shear stress modulates adhesion rates of platelets and expression of adhesion molecules and procoagulant activity on endothelial cells lining the blood vessels. That no one abnormality in any component of Virchow's triad fully predicts coagulopathy a priori suggests coagulopathies are complex, multifactorial, and interactive. In this review, we focus on contributions of blood composition, vascular cells, and blood flow to hemostasis and thrombosis, and suggest that cross-talk among the 3 components of Virchow's triad is necessary for hemostasis and determines propensity for thrombosis or bleeding. Investigative models that permit interplay among these components are necessary to understand the operant pathophysiology, and effectively treat and prevent thrombotic and bleeding disorders.     

磺达肝癸钠预防髋膝关节置换术后下肢深静脉血栓形成

目的：探讨磺达肝癸钠预防髋、膝关节置换术后下肢深静脉血栓形成的有效性和安全性。方法：选择89例连续的行人工髋、膝关节置换手术患者,随机分为对照组45例：给予肢体气压泵预防深静脉血栓;磺达肝癸钠组44例：给予磺达肝癸钠联合肢体气压泵预防。术后观察比较血小板、凝血功能指标变化情况及深静脉血栓形成。结果：两组患者总失血量、血小板、凝血酶原时间及活动度与活化部分凝血酶时间变化比较均无统计学差异（P＞0.05）;磺达肝癸钠组无1例发生深静脉血栓,对照组16例深静脉血栓形成（χ2=19.073,P＜0.01）。结论：使用磺达肝癸钠预防髋、膝关节置换术后深静脉血栓形成对凝血功能、血小板无明显影响,是安全有效的。     

PLATELET FUNCTION IN THE PERI-OPERATIVE PERIOD

Although platelets have an important role in haemostasis and in thrombosis, what happens to platelet function postoperatively is not well understood. We investigated platelet function in the perisperative period by measuring total platelet count and several products released by activated platelets, thromboxane, betathromboglobulin and lyso-platelet activating factor (lyso-PAF). The only changes detected were a significant rise in total platelet count between 48 h and 5 days postoperation, and a progressive fall in lyso-PAF up to 48 h post-operation. It is possible that other changes may have occurred, but were an immediate effect and were not apparent at time of the first blood sample 2–3 h post-operation.