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Platelet function was evaluated in 10 hypertensive and 11 normal subjects. In the placebo phase, the plasma beta thromboglobulin level (an index of platelet activation in vivo) was significantly (p less than 0.01) higher in the hypertensive than in the normal subjects; other tests of platelet function gave similar results in the two groups. After control of blood pressure with lofexidine (a centrally acting imidazoline derivative), plasma beta thromboglobulin levels decreased in 9 of the 10 hypertensive patients, but increased in one who showed no change in blood pressure. These studies suggest that enhanced platelet activation in primary hypertension may be associated with increased vascular resistance.

The roles of fibrinogen and fibronectin were contasted in the responses of human platelets to Staphylococcus aureus and collagen. Congenital afibrinogenemic (CA) platelets and washed normal platelets had delayed aggregation due to a prolonged latent phase in response to contact with the bacteria when fibrinogen was absent from the suspending media. When a physiologic level of human fibrinogen was added to the CA platelets in autologous plasma or to the washed platelets in balanced saline, the times to aggregation were significantly shortened (P < 0.05) and restored to rates comparable to those of normal platelets in whole plasma. In contrast, the presence or absence of fibrinogen in the media had no significant effect on the initial adherence and shape-change response of CA or washed platelets to collagen. Platelets with a demonstrated aberration of fibronectin responded normally to all ratios of S aureus, but they responded only to doses of collagen that were several times the threshold levels for normal platelets. These results demonstrate an important role for fibrinogen as a cofactor in platelet interactions with S aureus and indicate that fibronectin is not a major factor in the responses of human platelets to this microorganism.

In subagglutinating amounts, an IgG antibody isolated from the plasma of a polytransfused thrombasthenic patient (L) inhibited ADP-, epinephrine-, collagen-, and thrombin-induced aggregation of normal human platelets. The inhibition of ADP-induced aggregation was strongly diminished following the prior incubation of the antibody with control human platelet stroma but not with the stroma prepared from the platelets of two different thrombasthenic patients. The IgG(L) did not affect the binding of 14C-ADP to control human platelet membranes and did not inhibit the ADP-induced shape change. Bovine factor VIIIVWF-induced agglutination and ristocetin-induced aggregation of control human platelets were not inhibited in the presence of the antibody. The IgG(L) strongly inhibited ADP-induced retraction of reptilase clot and thrombin-induced clot retraction. This antibody therefore induced a thrombasthenialike state in normal human platelets, suggesting that the antigenic site recognized by the antibody plays a central role in the later stages of the mechanism of platelet aggregation induced by physiologic aggregation-inducing agents.

Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet-rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

To assess the nature of the hemostatic abnormalities associated with chronic liver disease, we have simultaneously evaluated the kinetic of radiolabeled platelets, fibrinogen, and plasminogen, together wit tests of platelet and fibrinogen function, and coagulation factors in 60 patients with documented, severe but stable cirrhosis of the liver. The mean platelet survival was substantially reduced (5.8 +/- 1.7 days compared with 9.5 +/- 0.6 days in normals, p less than 0.0001) and splenic sequestration of platelets was increased (mean recovery was 47% +/- 18 vs. 65% +/- 5 in normals, p less than 0.0001). Nevertheless the mean platelet count was nearly normal because platelet production was increased nearly twice normal values (mean turnover was 64,000 +/- 33,000 platelets/microliter/day; p less than 0.0001). The mean rate of fibrinogen removal was shortened (p less than 0.0001) and fibrinogen turnover increased about 20% (p = 0.008) while the mean fibrinogen concentration was not different from the results in normal control subjects (p = 0.212). Autologous and homologous fibrinogen disappeared from the circulation at equivalent rates (r = 0.751; p = 0.008), indicating that fibrinogen from cirrhotic patients was not kinetically different from normal fibrinogen. The mean plasminogen survival was significantly shortened (p less than 0.0001), but the mean plasminogen turnover was not increased (p = 0.388). Thus the plasminogen concentration was reduced (p less than 0.0001). For platelets, fibrinogen, and plasminogen, the production rate was the most important determinant of the concentration in the circulation. The administration of heparin to cirrhotic patients improved the survival of fibrinogen but not of platelets. LeVeen valve implantation generally resulted in parallel shortening of both the platelet and fibrinogen survivals and concentrations. Platelet function as assessed by template bleeding time, platelet retention by glass bead columns, and aggregation induced by ADP, epinephrine, and collagen was normal. Fibrinogen determinations by the Clauss and Jacobsson techniques were equivalent, indicating that the ability to polymerize fibrin monomer was not detectably altered. Sixty percent of patients had an abnormal prothrombin time and half that number had a prolonged partial thromboplastin time. Although most patients had a modest decrease in the prothrombin complex coagulation factors, fibrin degradation products were, in general, not elevated in the circulation. The wide range of values observed suggests that a number of different and complex processes may be ongoing in different patients. Overall, the kinetic data suggest that platelets are initially consumed, perhaps on incompletely endothelialized endovascular surfaces in the liver, and that fibrin subsequently forms secondary to local stasis. The absence of increased production of fibrinogen and plasminogen despite shortened survival times reflects the reduced capability of the cirrhotic liver to increase protein synthesis.

As knowledge of blood coagulation has advanced we have begun to examine not only the clinical entities associated with hemorrhage but also a group in which thrombosis represents the major problem. Thrombotic disorders believed to be associated with coagulation are recognized clinically but seldom investigated in the laboratory. The present approach to the problem is based on theoretical and experimental knowledge and a rapidly developing body of clinical information related to the role of platelets and antithrombin III in the initiation and control of thrombosis.

Four patients with myeloproliferative diseases and acute hemorrhagic or thrombotic complications of thrombocytosis were treated with plateletpheresis by discontinuous-flow centrifugation. Reduction of platelet counts was achieved rapidly, without complications and was associated with clinical improvement. In all four cases, abnormal platelet aggregation testing was present before pheresis, but improved immediately after pheresis. Platelet-sizing data obtained in one case suggested that during the pheresis procedure, a population of larger volume platelets was selectively removed. The efficacy of plateletpheresis in these clinical situations may be related to the selective removal of a large abnormal platelet population.

The continual remodeling of the artery wall significantly narrows the lumen. It contributes to the development of atherosclerotic plaque through the incorporation of lipid into the arterial intima. The steps in the repair of arterial intima include platelet accumulation followed by leukocyte attachment to denuded areas, smooth muscle migration from the media, deposition of extracellular connective tissue components, and endothelial progression seem related to re-endothelialization, platelets, the pituitary, and unidentified factors.

A new microsurgical procedure for the induction of thrombosis in rat aorta is described. The method is based on the introduction into the vascular lumen of a small piece of the aortic wall, the so called "aortic flap". A long-lived, platelet-rich arterial thrombus invariably forms on the inserted aortic flap. These thrombi closely resemble human arterial thrombi in structure and subsequent development.

Investigation of platelet function in dogs with cyclic hematopoiesis (CH) revealed a platelet aggregation disorder. Collagen-induced aggregation of CH dog platelets was significantly abnormal, although normal aggregation in response to ADP was observed. Aggregation was particularly defective on days 2-4 and 14 of the 14-day neutrophil cycle that is typical of CH dogs. The lack of response to collagen suggested a defect in the arachidonic acid pathway of platelet metabolism, since platelet-generated thromboxane-B2 levels were about 30% (p less than 0.0005) of control values. Platelets from dogs heterozygous for CH demonstrated moderately depressed responses to collagen that were intermediate between the values found for platelets from CH dogs and platelets from normal, mixed-breed dogs. Not only does this work indicate a platelet defect in CH dogs, but this phenomenon may be useful as a genetic marker for identification of dogs heterozygous for the CH gene.

The role of blood platelets in producing early intimal changes in cerebral arteries following subarachnoid hemorrhage (SAH) was examined by using 18 cats. Experimental SAH was produced by a rupture of the proximal portion of the right middle cerebral artery. Following SAH, the scanning electron microscope revealed that structural alterations in the intimal layer of major cerebral arteries occurred as early as 2 hours and became more severe by 48 hours. Vascular alterations, which were predominantly detected in the ruptured vessel, consisted of endothelial cell corrugation, detachment, crater formation, intimal adhesion of platelets and red blood cells, intimal thrombi, and reendothelialization. When cats were pretreated prior to SAH with an anti-platelet-aggregating agent, OKY-1581, the intimal blood elements and thrombi were clearly reduced, and reendothelialization was not observed. However, endothelial cell changes in the OKY-1581-treated group were very similar to those occurring in the nontreated group. While these results suggest that bioactive substances contained within blood platelets, such as growth factors, serotonin, and norepinephrine, have little effect on producing endothelial cell injury, platelets may be important in the initiation of reendothelialization following vessel injury.

Changes in circulating platelets were observed after placement of woven Dacron aortic prostheses in dogs. Platelets had increased sensitivity to aggregating agents for up to 6 months postoperatively, during which period platelet survival was maximally shortened. Platelet survival gradually lengthened but remained less than preoperative values, even at 18 months. Platelet 5HT, consistently reduced after placement of aortic prostheses, closely paralleled changes in platelet survival. Studies with platelets labeled simultaneously with 14C-5HT and 51Cr suggested in vivo platelet release and reutilization of 5HT. In vitro platelet uptake of 14C-5HT, however, was depressed. Urinary excretion of 5HIAA increased slightly, but not significantly, after placement of aortic prostheses. These findings suggested that platelet interaction with the prosthetic surface led to partial release of platelet storage granule contents. Reutilization of released 5HT occurred but was limited because of impaired platelet uptake or storage of 5HT. Platelet damage was suggested by 51Cr-platelet cross-transfusion experiments. Platelets from normal dogs had normal recovery and reduced survival when cross-transfused into animals with aortic prostheses. When platelets from dogs with aortic prostheses were cross-transfused into normal animals, recovery was strikingly reduced and survival very short. Taken together, these studies suggest that, in dogs, platelet interaction in thrombosis on prosthetic surfaces is, in part, a reversible process, with platelets re-entering the circulation in an altered state.

A patient suffering from essential thrombocythemia presented manifestations of digital thromboses and two cerebral ischemic strokes. Anomalies of platelet function are discussed in relation to published data and the efficacy of antiaggregant treatment is stressed.

The survival of 111indium labelled platelets has been determined in a series of 47 subjects comprising nine with cyanotic congenital disease (Eisenmenger's syndrome), seven with congenital heart disease associated with left to right shunts, six with primary pulmonary hypertension, six with peripheral vascular disease, 11 with cardiac disorder associated with low cardiac output and eight normal volunteers. Compared with the value in the normals of 9.5 days, mean survival was significantly shortened in those with Eisenmenger's syndrome (8.4 days) and with peripheral vascular disease (8.5 days). It was normal in patients with left to right shunts (9.5 days). Gamma camera imaging in selected patients failed to reveal any abnormal sites of deposition of labelled platelets except in one patient with peripheral vascular disease who had bilateral abnormal activity in his lower limbs and a shortened platelet survival (8.0 days). From theoretical considerations, it was concluded that the reduction in platelet survival in Eisenmenger's syndrome was such that, had it been the result of pulmonary intravascular platelet deposition, abnormal activity should have been visible on chest scanning with the gamma camera. The absence of scintigraphic evidence of abnormal platelet deposition in the lungs of these patients, combined with the linear configuration of their platelet survival curves, suggests that the accelerated platelet destruction is in the reticuloendothelial (RE) system rather than intravascular. Indirect evidence in favour of increased RE destruction of platelets in Eisenmenger's syndrome was the finding of an approximate doubling of intrasplenic platelet transit time, indicating abnormal platelet pooling within the spleen.

The predilection sites of arterial thrombosis are characterized by local increase in wall shear stress, flow separation with eddy formation and stagnation point flow. The defenders of high shear, as well as those of low shear theory of thrombogenesis, point to correlations of predilection sites and the respective flow abnormalities. Experimental evidence is provided, that high shear rates can damage both red cells and platelets, that lysed red cells constitute a potent platelet stimulant, due to their content of adenine nucleotides, and that platelets do not adhere to surfaces unless transported onto them by convective motion, the effectiveness of the platelet-wall interaction being enhanced by platelet activation. Based on these facts, a resolution of the contrast between high and low shear theory of thrombosis is attempted in a way, that the different flow regimens, with blood cells sequentially passing them, are each considered important and interdependent steps on the way to thrombosis.

Cigarette smoking or a strong family history of coronary disease was present in 46 of 50 symptomatic patients with coronary artery disease who were younger than 50 years of age. We recorded a shortened platelet survival half-life (less than 92 hours) with 51Cr in 60% of these patients, in 56% of apparently normal persons of the same age who smoked or had a strong family history of coronary disease, and in only 14% of normal persons who did not smoke and had no family history (p less than 0.01). Lengthening of the shortened platelet survival toward normal occurred in coronary patients given dipyridamole plus aspirin and in apparently normal smokers who discontinued smoking (p less than 0.01). The study suggests a possible relationship among cigarette smoking, strong family history of coronary disease and platelet activation in the process of coronary atherogenesis in the young adult.

10 consecutive patients fulfilled the diagnostic criteria for lupus anticoagulant. 4 had concomitant systemic lupus erythematosus, 1 Waldenstrom's disease and 5 had no apparent underlying disease. Only the case with Waldenstrom's disease presented a bleeding tendency, with bleeding time greater than 20 min; the others had a history of thrombotic complications. A defect of platelet aggregation induced by ADP, epinephrine, collagen and arachidonic acid was documented in the Waldenstrom's disease case whose lupus anticoagulant was an IgM. In the others, lupus anticoagulant, identified as IgG immunoglobulins, produced no aggregation abnormalities. However, beta-thromboglobulin levels in platelets, plasma and urine were consistent with a pattern of platelet activation in all cases. IgG immunoglobulins separated from sera of 6 patients showed lupus anticoagulant activity, with no effects on platelet aggregation of normal platelet-rich plasma, but they induced secretion of beta-thromboglobulin from normal platelets.

A patient with hairy cell leukemia developed purpura not attributable to thrombocytopenia. We found markedly reduced platelet aggregation responses and malondialdehyde production, decreased serotonin uptake, and depleted dense granule contents. Ultrastructural studies showed that most platelets had few or nor granules. All of the clinical and laboratory studies of platelet function and morphology improved after splenectomy. These findings indicate that qualitative defects in platelet function occurring in hairy cell leukemia may cause clinically important bleeding and that the bleeding diathesis may be ameliorated by splenectomy.

The interactions between platelets and dialysis membranes were studied prospectively in 10 patients undergoing long-term stable dialysis. Transient but significant thrombocytopenia and platelet activation were found during dialysis with the commonly used cuprophane membrane. Platelet counts decreased from 231 +/- 21 X 10(3)/mm3 before dialysis to 127 +/- 28 X 10(3)/mm3 at 90 minutes following initiation of dialysis (p less than or equal to 0.007). Thromboxane B2, an index of platelet activation, also increased from a baseline level of 1.06 +/- 0.2 pg/10(6) platelets to 7.3 +/- 3.0 pg/10(6) platelets at 90 minutes (p less than or equal to 0.04). Cuprophane membranes were also shown to induce complement activation with C3a desArg, the stable derivative of C3 activation, showing a threefold increase from baseline 15 minutes after initiation of dialysis. In contrast, during dialysis with a non-complement-activating dialyzer membrane, polymethylmethacrylate, thrombocytopenia and platelet activation were not observed. These data suggest that platelet activation and thrombocytopenia during hemodialysis are associated with complement activation during hemodialysis in a manner similar to dialysis-associated neutropenia.

This study describes the effects of the beta 2 receptor agonist terbutaline on platelet sequestration in sheep exposed to endotoxin shock. The in vivo behavior of Indium-111-labeled platelets was followed simultaneously in the lungs, liver, spleen, and kidneys. The effects on the respiratory function and the central hemodynamics were also followed. Twelve adult sheep were given endotoxin (10 micrograms/kg bw), and six of those received a continuous intravenous infusion of terbutaline (20 micrograms/kg/hr) during 4 hr, starting 30 min after injection of endotoxin. The other six acted as controls. It was found that a marked pulmonary and hepatic platelet sequestration occurred during and just after the endotoxin infusion and was followed by a marked platelet disaggregation within 30 min in both groups. Three hours after the endotoxin a second wave of platelet trapping occurred in the control animals in both the lungs and the liver, while no such increase was seen in the terbutaline-treated animals. In the spleen, however, there was a decrease in platelet sequestration after endotoxin in both groups, and in the kidneys only minor changes occurred. Furthermore, less marked hemodynamic and respiratory alterations occurred in the terbutaline group compared with the controls. It was concluded that terbutaline decreased sequestration of platelets in the lungs and in the liver of sheep in endotoxin shock, which may be of importance in the development of multiple organ failure.

Blood platelets contain several growth factors and inhibitors. The better known among them are named platelet-derived growth factor (PDGF) and transforming growth factor beta (TGF beta), active as modulators of growth of normal mesenchymal and epithelial cells. Cancer cell growth in vitro seems to be independent of the effects of exogenous peptides, but dependent on the cell ability to release autocrine growth factors, similar to PDGF or TGF beta. In addition, platelet-associated growth factors and inhibitors, which are able to induce a fibrotic response in connective tissue cells, might also play a role to modulate the desmoplastic reaction surrounding the tumor.

A nine-year-old black girl with essential thrombocythemia developed hemoptysis. Only two other cases in the English literature have been described. Ultrastructure and functional characteristics of this patient's platelets were studied. Twenty-six percent of the patient's platelets were very large (megathrombocytes). Spontaneous aggregated from the patient's platelets were not compact, and the pseudopods did not interdigitate. Both qualitative and quantitative defects in platelet organelles were detected. The microtubular system was faulty in organization. Furthermore, the number of granules (especially alpha granules) was reduced. Platelet aggregation studies demonstrated subnormal aggregation in response to ADP, epinephrine, and collagen, but aggregation with ristocetin was normal. It is postulated that a platelet membrane abnormality may be the cause of their defective platelet aggregation.

Studies of platelets from individuals who have experienced a thrombotic event have not yet conclusively demonstrated an active role for platelets in thrombosis. Platelet hyperactivity after myocardial infarction may relate to poor prognosis but further studies are required. Arachidonate metabolism may differ in platelets from different individuals and studies in vascular disease are warranted.

There is considerable evidence that the quantity or quality of plasma lipids influences platelet function tests, and clofibrate reduces high plasma lipids and alters some platelet tests. Clofibrate was accordingly given to patients with vascular disease who were at risk of thrombosis. The heparin thrombin clotting time (HTCT), initially short and thus possibly reflecting increased activation, was regularly returned to normal after about a month's delay. The fibrinogen was also normalized but the initially abnormal anti-thrombic activity became more abnormal. ICI 55,897, an analogue of clofibrate, also normalized the HTCT and the fibrinogen and had no adverse effect on the anti-thrombin levels. This compound has no effect on plasma lipids. If it can be shown that the correction of abnormal tests conveys clinical benefit these findings suggest that ICI 55,897 might clinically be more beneficial than clofibrate. However, direct comparison of clofibrate and ICI 55,897 suggests that clofibrate is more effective in normalizing the HTCT. The mechanism underlying these drug-induced changes are unknown but they cannot be directly related to lipid changes.

Spontaneously hypertensive rats (Okamoto-Wistar) as compared to their normotensive controls (Kyoto-Wistar) presented a markedly higher platelet activity both in coagulation (as evaluated by the recalcification plasma clotting time of platelet-rich plasma) and aggregation, as triggered by thrombin. By comparing animals fed saturated or polyunsaturated fat, it could be observed that the saturated fat diet induced similar results on platelet functions to these observed in hypertension. In addition, the saturated fat diet further increased the platelet response of the hypertensive animals. By contrast, the polyunsaturated fat, could neither reduce the hypertension nor completely abolish the platelet reactivity associated with the hypertension. The most significant change induced by the saturated fat diet in the fatty acid composition of the platelet phospholipids was an increase in 20:3 omega 9, further enhanced in the hypertensive animals. In the polyunsaturated diet-fed rats, it was mostly 20:4 which was more elevated in the platelet phospholipids of the hypertensive. As a result, it was the sum of 20:3 omega 9 + 20:4 in the platelet phospholipids, which appeared to be the most significantly related, in the 4 groups of animals, to the response of platelets to thrombin induced aggregation.

Adrenoceptor function is an important determinant of the physiological control of the circulation and of the response to drugs acting via the sympathetic nervous system and on the vasculature. There is little consistent evidence for an age-dependent change in alpha-adrenoceptor function though the response to various vasoconstrictor agents including alpha 1 agonists has been shown to change with ageing. These changes seem to reflect structural or functional factors and are not specific for receptor types. In the case of beta-adrenoceptor mediated responses there is evidence for both a decrease in response as well as age-related changes in the functioning of various components of the beta-adrenoceptor system, including receptor affinity, which is decreased. It may well be that decreased beta-adrenoceptor function with ageing contributes to altered cardiovascular control and to decreased efficacy of beta-adrenoceptor blocking drugs in elderly hypertensives.

A variety of platelet function tests were performed in patients with four forms of obstructive cerebrovascular disease (CVD); transient ischemic attacks (TIA), reversible ischemic neurological deficit (RIND), cerebral infarct, and cerebral embolism of cardiac source in rheumatic valvular heart disease (RVHD). Platelet studies included platelet aggregation induced by ADP and ristocetin, spontaneous platelet aggregation, von Willebrand factor (VIII:vWF), platelet aggregation enhancing factor (PAEF), and percentage of large platelets (megathrombocytes). Serial testing was carried out in acute stroke patients. The effect of aspirin therapy was also evaluated. A clear difference in results was observed between patients with cardiogenic embolism and those with other forms of CVD. In patients with TIA, RIND, and cerebral infarct, platelet aggregation, both induced and spontaneous, was enhanced along with elevation of plasma VIII:vWF and PAEF, and increased percentage of megathrombocytes. In patients with cardiogenic embolism, however, these studies were negative except for percent megathrombocytes. This value was increased in the embolic patients with RVHD in comparison with non-embolic patients with RVHD. Increase in platelet aggregation to ADP and percent megathrombocytes developed slowly over a week following stroke. Induced and spontaneous platelet aggregation, and percent megathrombocytes could be normalized with 600 mg aspirin p.o. These studies suggest that a systemic increase of hyperaggregable platelets and of plasma activators of platelet function exists in thrombotic CVD and may be related to its pathogenesis, while local hemodynamic factors may be more important in the thrombogenesis of cardiogenic embolism.

Platelets are postulated to have an important role in acute and chronic cardiovascular events. Clinical events may result during the sequence of platelet activation reactions of adhesion, aggregate formation, release of granular constituents, thromboxane A2 formation, microembolization and platelet vascular occlusion. For example, sudden death may occur in patients with increased platelet sensitivity to catecholamine stimulation, platelet aggregate formation and thromboxane A2 generation resulting in ischemic ventricular arrhythmia induced by small-vessel platelet microembolization and local thromboxane A2 vasoconstriction. Whereas angina might be manifest if the microemboli disaggregated and vasospasm were transient, myocardial infarction would follow extensive permanent occlusion of small vessels or localized narrowing by vasospasm and extension of platelet thrombus formation at the site of intimal thickening. Platelets may also have an important role in atherogenesis through the mediation of the platelet-derived growth factor in the proliferative smooth muscle cell intimal lesion. Direct experimental and indirect clinical studies support the concept that platelets are important in cardiovascular events, but the relationship to spasm and to other possibly even more important mechanisms is not clear. Acute myocardial infarction and mural thrombogenesis appear to have the greatest evidence of being platelet-related.

A prospective study was performed on 26 preeclamptic patients and 17 pregnant control subjects relating the platelet count to in vivo platelet function as assessed by the bleeding time and in vitro platelet function as assessed by collagen-stimulated thromboxane B2 biosynthesis. The results of these tests were normal in all control subjects. Nine of the 26 preeclamptic patients (34%) showed thrombocytopenia, and five of these patients had a prolonged bleeding time. Four of the 16 nonthrombocytopenic patients also had a prolonged bleeding time. Eleven patients had impaired thromboxane B2 biosynthesis, and seven of these had a prolonged bleeding time. In all patients, the bleeding time returned to normal, and in most the platelet count returned to normal within five days or after delivery. A significant proportion of patients with preeclampsia develop an acquired defect of platelet function that could contribute to bleeding.

Subendothelium of blood vessel segments from elderly patients was exposed in a perfusion chamber to citrated blood under arterial blood flow conditions. The resulting platelet adhesion and thrombus formation was assessed morphometrically. The results show that the time course and the extent of platelet adhesion and aggregation were similar to the results obtained previously with subendothelium from rabbit arteries. The extent of surface-induced platelet aggregation was furthermore governed by both the properties of the exposed surface as well as those of the blood perfusate. No significant differences with regard to platelet reactivity were found between veins and arteries and the extent of surface-induced platelet aggregation was rather low.