thromboxane-b2 and Syndrome

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blood Circulation; Cerebrovascular Disorders; Coronary Disease; Drugs, Chinese Herbal; Humans; Medicine, Chinese Traditional; Syndrome; Thrombosis; Thromboxane B2

Leukocyte depletion during cardiopulmonary bypass has been demonstrated in animal experiments to improve pulmonary function. Conflicting results have been reported, however, with clinical depletion by arterial line filter of leukocytes at the beginning of cardiopulmonary bypass. In this study, we examined whether leukocyte depletion from the residual heart-lung machine blood at the end of cardiopulmonary bypass would improve lung function and reduce the postoperative inflammatory response. Thirty patients undergoing elective heart operations were randomly allocated to a leukocyte-depletion group or a control group. In the leukocyte-depletion group (n = 20), all residual blood (1.2 to 2.1 L) was filtered by leukocyte-removal filters and reinfused after cardiopulmonary bypass, whereas in the control group an identical amount of residual blood after cardiopulmonary bypass was reinfused without filtration (n = 10). Leukocyte depletion removed more than 97% of leukocytes from the retransfused blood (p < 0.01) and significantly reduced circulating leukocytes (p < 0.05) and granulocytes (p < 0.05) compared with the control group. Levels of the inflammatory mediator thromboxane B2 determined at the end of operation (p < 0.05) were significantly lower in the depletion group than in the control group, whereas no statistical differences in interleukin-6 levels were found between the two groups. After operation, pulmonary gas exchange function (arterial oxygen tension at a fraction of inspired oxygen of 0.4) was significantly higher in the leukocyte-depletion group 1 hour after arrival to the intensive care unit (p < 0.05) and after extubation (p < 0.05). There were no statistical differences between the two groups with respect to postoperative circulating platelet levels and blood loss, and no infections were observed during the whole period of hospitalization. These results suggest that leukocyte depletion of the residual heart-lung machine blood improves postoperative lung gas exchange function and is safe for patients who are expected to have a severe inflammatory response after heart operations.

Topics: Blood Transfusion, Autologous; Cardiac Surgical Procedures; Cardiopulmonary Bypass; Cytapheresis; Elective Surgical Procedures; Female; Filtration; Granulocytes; Heart-Lung Machine; Humans; Inflammation Mediators; Interleukin-6; Leukocyte Count; Leukocytes; Lung; Male; Middle Aged; Oxygen; Platelet Count; Pulmonary Gas Exchange; Syndrome; Thromboxane B2

55 cases of Qi-deficiency and Blood-Stasis syndrome of coronary heart disease (CHD) and angina pectoris (AP) were divided randomly into two groups. Qi Xue granule (QXG) was administered to 30 cases of treated group, while compound Salvia tablet (CST) was administered to 25 cases of control group. Besides, both group were also given one placebo tablet or granule so as to eliminate the patient's psychological effects.. (1) Effects on clinical symptoms: Total effective rate for AP: 90% in QXG group, marked effective rate and effective rate for ischemic ECG changes were 30% and 46.6% respectively. All of these were better than that of CST group significantly (P < 0.05). Besides, QXG group could alleviate symptoms including asthenia. (2) Effects on submaximal paddle work load test: QXG group could prolong the capacity of exercise (from 336.2 +/- 34.7 to 437.5 +/- 43.8 seconds, P < 0.05), magnify the work load (from 73 +/- 7.18 to 94 +/- 8.5 W, P < 0.05) and elevate the ST segment (from 0.218 +/- 0.03 to 0.176 +/- 0.03 mV) significantly in comparison with CST group, which had little change only. (3) Effects on plasma TXB2, 6-keto-PGF1 alpha (6 Kp) level and ration of TXB2/6Kp in 10 normal subjects were 165 +/- 12.1 pg/ml, 142.6 +/- 17.4 pg/ml and 1.16 +/- 0.19 pg/ml respectively, while in 36 cases AP were 390.6 +/- 14.3, 106.0 +/- 7.9 and 3.67 +/- 0.85 pg/ml respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Angina Pectoris; Drugs, Chinese Herbal; Exercise Tolerance; Female; Humans; Male; Medicine, Chinese Traditional; Middle Aged; Panax; Phytotherapy; Plants, Medicinal; Syndrome; Thromboxane B2; Yang Deficiency

The clinical and biochemical effects of a prostaglandin synthesis precursor (Efamol) containing linoleic acid and its metabolite, gamma-linolenic acid, were studied in 30 women with severe, incapacitating premenstrual syndrome. Efamol treatment alleviated the premenstrual symptoms in general and depression especially better than did a placebo. The capacity of platelets to release thromboxane B2 during spontaneous clotting was decreased in patients undergoing Efamol treatment (141 +/- 59 ng/ml, mean +/- SD) as compared to those undergoing placebo treatment (186 +/- 44 ng/ml, p less than 0.01) and control subjects (176 +/- 40 ng/ml, n = 25, p less than 0.05). No changes were found in plasma 6-keto-prostaglandin F1alpha or in FSH, LH, prolactin, progesterone, estradiol and testosterone. The data suggest that prostaglandins might play a role in the pathophysiology of the premenstrual syndrome.

Topics: 6-Ketoprostaglandin F1 alpha; Fatty Acids, Essential; Fatty Acids, Unsaturated; Female; gamma-Linolenic Acid; Humans; Linoleic Acids; Oenothera biennis; Plant Oils; Premenstrual Syndrome; Syndrome; Thromboxane B2

We report a novel case of gray platelet syndrome (GPS). A 14-year-old boy had bleeding diathesis, mild thrombocytopenia, giant platelets with severe defect of alpha-granule secretory proteins, myelofibrosis and splenomegaly.. Platelet function studies showed a marked reduction of aggregation and Ca(2+) mobilization by thrombin, protease-activated receptor 1 (PAR1)-activating peptide (AP) and PAR4-AP, PAR1 expression at 55% of normal levels, and a more than two hundred fold reduction of in vitro whole-blood thromboxane B(2) (TXB(2)) production. Sequencing of coding regions of the PAR1 gene failed to show abnormalities. This patient was initially classified as a sporadic case of GPS, as electron microscopy failed to identify giant platelets and/or alpha-granule deficiency in his relatives. However, further studies on the father and three other relatives showed a relative lack of platelet alpha-granule proteins by immunofluorescence microscopy, a defective platelet response to PAR4-AP, and severely reduced in vitro whole-blood TXB(2) production. On this basis, we suggest that in this family, GPS was transmitted in a dominant fashion with highly variable penetrance.. Our study suggests that current diagnostic criteria fail to identify some patients with a mild GPS phenotype and that such patients might be identified by the methods cited above. It also better characterizes the pathogenesis of defective platelet responses to thrombin, and raises interesting questions on the correlation between abnormal PAR function and the lack of alpha-granule content in GPS.

Topics: Adolescent; Adult; Aged; Blood Platelets; Calcium Signaling; Coagulants; Cytoplasmic Granules; Family; Female; Humans; Male; Microscopy, Fluorescence; Middle Aged; Oligopeptides; P-Selectin; Pedigree; Phenotype; Platelet Aggregation; Platelet Factor 4; Platelet Function Tests; Platelet Storage Pool Deficiency; Receptor, PAR-1; Syndrome; Thrombin; Thrombospondin 1; Thromboxane B2

Stomach physiological effects of channel tropism of stomach, cold & cool Chinese herbal medicine on rats with stomach-heat syndrome were studied.. Using water decoction of warm &heat medicine, Rhizoma Zingiberis to feed rats for 15 days continuously, causing the stomach-heat sydrome model, then decoction of Rhizoma Coptidis, Herba Taraxaci, Fractus Aurantii Immaturus was used to feed rats for 10 days, respectively. Biochemical indexes of blood reflecting the physiological function of stomach, including thromboxaneB2 (TXB2), 6-keto-PGF(1alpha), Gastrin (Gas), Motilin (MTL), and Somatostation (SS) were measured by radioimmunoassay.. Symptom of stomach-heat syndrome prevailed in body of rats after filled with decoction of Rhizoma Zingiberis, values of TXB2/6-keto-PGF(1alpha), MTL, and Gas in blood raised up evidently, compared with the control (P < 0.05), but values of 6-keto-PGF(1alpha). decreased conspicuously (P < 0.05). After treated with decoction of Rhizoma Coptidis, Herba Taraxaci or Fractus Aurantii Immaturus for 10 days, respectively. Symptoms of stomach heat syndrome were eliminated or alleviated, values of 6-keto-PGF(1alpha), and SS in blood elevated at different degrees, and those of TXB2, TXB2/6-keto-PGF(1alpha), MTL, and Gas felled down at different degrees. Difference of efficacy existed at different groups, group of Rhizoma Coptidis was the strongest, group of Herba Taraxaci was the second, group of Fractus Aurantii Immaturus was the third. Efficacy of medicine in groups with high dosage was stronger than those with low dosage.. Channel tropism of stomach, cold and cool Chinese herbal medicine could improve the physiological functions of stomach effectively, and the efficacy concerns with the degree of their cold and cool characteristics.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Citrus; Coptis; Drugs, Chinese Herbal; Gastrins; Male; Medicine, Chinese Traditional; Motilin; Phytotherapy; Plants, Medicinal; Random Allocation; Rats; Rats, Sprague-Dawley; Somatostatin; Stomach Diseases; Syndrome; Taraxacum; Thromboxane B2; Zingiber officinale

To explore the nature of pathology of sluggishness of lung-defensive qi and to offer objective experimental indexes for weifen syndrome (defensive phase syndrome).. According to the completely random design, the plasma levels of vasoactive intestinal peptide (VIP) and thromboxane B2 (TX2) of 19 patients with weifen syndrome and 13 patients with qifen syndrome (qi phase syndrome) were detected by radioimmunoassay. The plasma levels of VIP and TX2 at different stages of weifen syndrome and qifen syndrome were observed.. The plasma levels of VIP in weifen syndrome and in the late stage of weifen syndrome increased greatly at different stages as compared to qifen syndrome and the blank group (P < 0.01), while the plasma level of TX2 of weifen syndrome was higher only at the late stage than the blank group and qifen syndrome (P < 0.01). As for the levels of VIP and TX2 in weifen syndrome with different internal organs infected, there was no significant difference (P > 0.05).. VIP may be an index reflecting the pathology of weifen syndrome, and it is one of the material foundations of sluggishness of lung-defensive qi, but it has nothing to do with the infected internal organs. The level of TX2 increases only after the fever of patients with weifen syndrome subsided, so it can not be the basis for diagnosis of the early stage of weifen syndrome. It doesn't increase in qifen syndrome either, the mechanism remains to be further studied.

Topics: Female; Humans; Lung Diseases; Male; Radioimmunoassay; Syndrome; Thromboxane B2; Vasoactive Intestinal Peptide

These serial clinical and experimental studies were designed to clarify the pathogenesis of postburn MODS. Both animal and clinical studies were performed. In animal experiments, 46 male cross-bred dogs were cannulated with Swan-Ganz catheters and 39 of them were inflicted with 50% TBSA third degree burns (7 were used as controls). The burned dogs were randomly divided into 4 groups: immediate infusion, delayed infusion, delayed fast infusion and delayed fast infusion combined with ginsenosides. All dogs were kept under constant barbiturate sedation during the whole study period. Hemodynamics, visceral MDA, mitochondrial respiratory control rate (RCR) and ADP/O ratio, ATP, succinic dehydrogenase (SDH), organ water content as well as light and electron microscopy of visceral tissues were determined. In the clinical study, 61 patients with extensive deep burns were chosen, of which 16 sustained MODS. Plasma TXB2/6-keto-PGF1alpha ratio, TNF, SOD, MDA, circulatory platelet aggregate ratio (CPAR), PGE2, interleukin-1, total organ water content and pathological observations of visceral tissues from patients who died of MODS were carried out. Results demonstrated that ischemic-reperfusion damage due to severe shock, sepsis and inhalation injury are three main causes of postburn death. All inflammatory mediators increased markedly in both animals and patients who sustained organ damage or MODS. SDH, RCR, ADP/O and ATP decreased significantly. These findings suggested that ischemic damage and systemic inflammatory response syndrome (SIRS) initiated by mediators or cytokines might be important in the pathogenesis of postburn MODS.

Topics: 6-Ketoprostaglandin F1 alpha; Adenosine Diphosphate; Adenosine Triphosphate; Adult; Animals; Body Water; Burns; Central Nervous System Agents; Dinoprostone; Dogs; Female; Fluid Therapy; Ginsenosides; Hemodynamics; Humans; Hypnotics and Sedatives; Interleukin-1; Male; Malondialdehyde; Mitochondria; Multiple Organ Failure; Oxygen Consumption; Panax; Plants, Medicinal; Platelet Aggregation; Random Allocation; Reperfusion Injury; Saponins; Sepsis; Shock; Succinate Dehydrogenase; Superoxide Dismutase; Syndrome; Systemic Inflammatory Response Syndrome; Thromboxane B2; Tumor Necrosis Factor-alpha

Topics: Humans; Myeloproliferative Disorders; Platelet Activation; Syndrome; Thrombosis; Thromboxane B2

As chronic exposure to hand-held vibrating tools may cause endothelial injury, a subsequent sustained platelet activation with the increased release of vasoconstricting thromboxane A2 (TxA2) could be of pathophysiological importance in vibration-induced Raynaud's phenomenon. Therefore, the aim of this study was to elucidate whether or not hand-arm vibration syndrome is accompanied by increased endogenous TxA2 biosynthesis. The study involved 64 men, aged 23-61 years, stratified according to the exposure to vibrating tools, the presence of Raynaud's phenomenon, and smoking habit. Forty of them were car mechanics and 24 were age-matched healthy volunteers who served as controls. The assessment of platelet TxA2 formation in vivo was performed by quantification of the urinary excretion of its major metabolite, 2,3-dinorthromboxane B2 (2,3-dinor-TxB2), employing gas chromatography-mass spectrometry. The average urinary excretion rate of 2,3-dinor-TxB2 in patients with Raynaud's phenomenon was 296 +/- 42 pg/mg creatinine and did not differ significantly from the corresponding values in controls (328 +/- 62 pg/mg creatinine) or individuals exposed to vibrating tools, but without any signs of vasospastic disease (232 +/- 29 pg/mg creatinine). The only statistically significant difference was found between smokers and non-smokers (P < 0.001), a finding confirming the existence of chronic platelet dysfunction in cigarette smokers. The present data indicate that chronic exposure to vibrating tools, with or without Raynaud's phenomenon, is not associated with an enhanced platelet function as monitored by the urinary excretion of 2,3-dinor-TxB2. Hence, a possible vibration-induced vascular injury does not seem to provide a stimulus sufficient to induce a persistent platelet activation.

Topics: Adult; Blood Platelets; Chromatography, Gas; Chromatography, Liquid; Creatinine; Humans; Male; Mass Spectrometry; Middle Aged; Raynaud Disease; Syndrome; Thromboxane A2; Thromboxane B2; Vasoconstriction; Vibration

Hemostasis (HS) in 134 healthy subjects of over 20 years old was investigated. The cases with HS symptom were 45.5%, which increased with age. TXB2, 6-keto-PGF1 alpha and T/K ratio were measured by radioimmuno assay (RIA).. elevation of TXB2 was more significant in the middle age and old age than in the young group (P < 0.01). But the level of 6-keto-PGF1 alpha in various age group didn't changed significantly; while the ratio between TXB2 and 6-keto-PGF1 alpha was more significant in the aged than in the young person (P < 0.01). The results revealed that there was hypercoagulable tendency with the increase of age, and it was correlated with TXB2 and 6-keto-PGF1 alpha. It is significant in theory and practice to prevent and cure the cardiovascular and cerebrovascular disease as well as HS with the traditional Chinese medicine.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Age Factors; Aged; Aged, 80 and over; Blood Coagulation; Blood Viscosity; Female; Hemostasis; Humans; Male; Medicine, Chinese Traditional; Middle Aged; Syndrome; Thromboxane B2

The pathogenesis of the transient neonatal hyperammonaemia syndrome is largely unknown. The role of platelet activation was investigated in three preterm infants with this syndrome by non-invasive methods. In all three infants, urinary concentrations of beta-thromboglobulin and 11-dehydrothromboxane B2 levels were much higher during the hyperammonaemia than those in ten control preterm infants. It is possible that transient platelet activation occurs in the portal system of these infants, thereby causing the hyperammonaemia.

Topics: Ammonia; beta-Thromboglobulin; Catheterization; Evaluation Studies as Topic; Female; Humans; Infant, Newborn; Infant, Premature, Diseases; Male; Metabolic Diseases; Platelet Activation; Syndrome; Thromboxane B2; Time Factors

Topics: Bone Marrow Transplantation; Capillary Permeability; Humans; Leukotriene E4; Pulmonary Edema; Respiratory Insufficiency; SRS-A; Syndrome; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blood Cell Count; Blood Pressure; Cardiac Output; Heart Rate; Hemodynamics; Indomethacin; Liver Transplantation; Reperfusion Injury; Swine; Syndrome; Thromboxane B2

Mesenteric traction syndrome consists of sudden tachycardia, hypotension, and cutaneous hyperemia, and frequently occurs during mesenteric traction in patients undergoing abdominal aortic aneurysm (AAA) reconstructive surgery. The etiology and clinical impact of this phenomenon are unknown, but the symptoms suggest a release of vasoactive materials from the mesenteric vascular bed. Thirty-one patients who underwent AAA surgery were studied. Mesenteric traction was accompanied by a decrease in systolic (p = 0.005) and diastolic (p less than 0.05) blood pressures, and in systemic vascular resistance (p less than 0.005), and was accompanied by an increase in heart rate (HR) (p less than 0.005), and cardiac output (p = 0.01). These hemodynamic changes coincided with an increase (p less than 0.001) in plasma concentrations of 6-keto-prostaglandin F1 (6-K-PGF1). No apparent change was found in prostaglandin E2, thromboxane B2, and histamine concentrations. The concentration of 6-K-PGF1 was correlated with diastolic blood pressure (r = -0.52, p less than 0.005) and HR (r = 0.65, p less than 0.001). Cutaneous hyperemia was observed in 58% of the patients. In an additional six patients, who had taken aspirin daily before AAA surgery, no significant changes were observed in the hemodynamic measurements or 6-K-PGF1 concentrations. These data suggest that mesenteric traction syndrome may be mediated at least in part by a selective release of prostacyclin.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Aged, 80 and over; Anesthesia, General; Aortic Aneurysm; Epoprostenol; Female; Flushing; Humans; Hypotension; Intraoperative Complications; Male; Mesenteric Arteries; Mesenteric Veins; Middle Aged; Syndrome; Tachycardia; Thromboxane B2

The aim of the study was to investigate the urinary excretion of 6-keto-PGF1 alpha (a stable metabolite of PGI2), thromboxane B2 (TxB2; a stable metabolite of TxA2), and PGE2 in 18 normal subjects, 49 cirrhotics with ascites without renal failure (GFR = 90 +/- 4 ml/min, means +/- S.E.M.) and 20 cirrhotics with functional renal failure (FRF) (GFR = 36 +/- 3). The study was made after 5 days on a 50 mEq sodium diet and without diuretics. Plasma renin activity (PRA), plasma norepinephrine concentration (NE) and plasma antidiuretic hormone concentration (ADH) were also measured. Cirrhotics without FRF showed a significantly higher urinary excretion of 6-keto-PGF1 alpha, TxB2 and PGE, (15.9 +/- 1.7 ng/h, 3.0 +/- 0.3 ng/h, and 6.2 +/- 1.0 ng/h) than did normal subjects (9.2 +/- 0.9, 1.3 +/- 0.1 and 2.3 +/- 0.4). On the contrary, the urinary excretion of these prostaglandins was normal or reduced in patients with FRF (5.3 +/- 0.8, 1.3 +/- 0.2 and 1.9 +/- 0.4). PRA, NE and ADH were significantly increased in cirrhotics with FRF (15.2 +/- 3.9 ng/ml/h, 1026 +/- 149 pg/ml and 4.1 +/- 0.3 pg/ml) and in patients without FRF (8.0 +/- 1.4, 667 +/- 67 and 3.9 +/- 0.3) as compared to normal controls (1.3 +/- 0.2, 275 +/- 46 and 2.4 +/- 0.2). These results suggest that renal hemodynamics in cirrhosis depends upon a critical equilibrium between the activity of endogenous vasoconstrictor systems and the renal production of the vasodilator prostaglandins PGI2 and PGE2. In addition, they do not support FRF in cirrhosis being related to an increased renal production of the vasoconstrictor prostaglandin TxA2.

Topics: 6-Ketoprostaglandin F1 alpha; Acute Kidney Injury; Dinoprostone; Female; Glomerular Filtration Rate; Humans; Kidney; Liver Cirrhosis; Male; Prostaglandins E; Renal Circulation; Syndrome; Thromboxane B2

Topics: Animals; Digestive System; Endothelium; Humans; Interleukin-1; Lung; Macrophages; Multiple Organ Failure; Neutrophils; Prostaglandins; Rabbits; Respiratory Distress Syndrome; Shock, Septic; Syndrome; Thromboxane B2

Topics: Bile Ducts, Intrahepatic; Cholestasis, Intrahepatic; Eicosanoic Acids; Humans; Infant; Prostaglandins; Syndrome; Thromboxane B2

Urinary excretion of the vasoconstrictor metabolite thromboxane B2 is increased in some patients with the hepatorenal syndrome. To define the role of thromboxanes in this syndrome and to evaluate a potential treatment for the renal impairment, we administered the thromboxane synthetase inhibitor dazoxiben to 5 patients with alcoholic hepatitis and rapidly progressive renal failure. Dazoxiben 200 mg/day followed by 400 mg/day reduced urinary thromboxane B2 by approximately 50% without altering prostaglandin E2 or 6-keto prostaglandin F1 alpha and without improving creatinine clearance (6 +/- 2 to 6 +/- 3 ml/min). In 3 additional patients, a higher dose of dazoxiben of 600 mg/day reduced thromboxane B2 by approximately 75% without consistent improvement in renal function. Thus, as judged by selective thromboxane inhibition with dazoxiben, thromboxanes are unlikely to be the key renal vasoconstrictor factor in the hepatorenal syndrome.

Topics: 6-Ketoprostaglandin F1 alpha; Acute Kidney Injury; Adult; Creatinine; Dinoprostone; Drug Evaluation; Hepatitis, Alcoholic; Humans; Imidazoles; Middle Aged; Oxidoreductases; Prostaglandins E; Syndrome; Thromboxane B2; Thromboxane-A Synthase; Thromboxanes

Topics: Dinoprostone; Humans; Kidney Diseases; Kidney Failure, Chronic; Liver Diseases; Prostaglandins E; Syndrome; Thromboxane B2; Thromboxanes

Vasodilatory prostaglandins function to maintain renal perfusion in patients with cirrhosis and ascites. To evaluate the potential contribution of the vasodilator prostaglandin E2 and the vasoconstrictor metabolite thromboxane B2 to the development of the hepatorenal syndrome, we measured urinary excretion of these products in 14 patients with hepatorenal syndrome and in control populations with acute or chronic liver or kidney failure. Radioimmunoassay measurements were confirmed by bioassay and by mass spectrometry. Prostaglandin E2 was decreased compared with healthy controls (2.2 +/- 0.3 vs. 6.3 +/- 0.8 ng/h, p less than 0.01) and compared with acute renal failure (9.6 +/- 2.1 ng/h) and with alcoholic hepatitis (9.2 +/- 3.3 ng/h). Thromboxane B2 concentration was normal in patients with alcoholic hepatitis (0.12 +/- 0.02 vs. 0.15 +/- 0.03 ng/ml) and minimally increased in acute renal failure (0.18 +/- 0.15 ng/ml), but markedly elevated in hepatorenal syndrome (0.69 +/- 0.15 ng/ml, p less than 0.001). Urinary thromboxane B2 concentration fell with improved renal function in 3 patients who survived. These data suggest an imbalance of vasodilator and vasoconstrictor metabolites of arachidonic acid in patients with the hepatorenal syndrome.

Topics: Acute Disease; Acute Kidney Injury; Adolescent; Adult; Biological Assay; Chronic Disease; Dinoprostone; Female; Humans; Kidney Diseases; Kidney Failure, Chronic; Liver Diseases; Male; Mass Spectrometry; Middle Aged; Prostaglandins E; Radioimmunoassay; Syndrome; Thromboxane B2; Thromboxanes

Bleeding and abnormal platelet aggregation occur in patients with myeloproliferative disorders. In this study, twenty patients were examined, some sequentially, and a proportion found to have defective aggregation toward adrenaline, adenosine diphosphate (ADP), and collagen. In these seven patients, the abnormality in platelet response with defective collagen-induced [14C]serotonin release correlated with poor collagen-stimulated thromboxane B2 (TXB2) production. In contrast, five of these patients showed a normal threshold aggregation response to arachidonic acid. The combined results suggest that in these patients, there is a defect between receptor-stimulus coupling and the mobilization of arachidonic acid from membrane phospholipid.

Topics: Blood Platelets; Humans; Leukemia, Myeloid; Membrane Lipids; Myeloproliferative Disorders; Platelet Aggregation; Platelet Count; Polycythemia Vera; Serotonin; Syndrome; Thrombocytosis; Thromboxane B2

An IgG antiplatelet antibody found in a multitransfused patient with Bernard-Soulier syndrome (BSS), reacted with a normal platelet surface antigen of 150 000 daltons which was similar to the glycoprotein missing from BSS platelets. The BSS platelet antibody (BSS-Pab) aggregated all control platelets which then released ADP and 5-HT and synthesized thromboxane. When mixed with the antibody, BSS platelets did not aggregate, did not release ADP and 5-HT and failed to synthesize thromboxane. The BSS-Pab was not inactivated by incubation with BSS platelet stroma. While the antibody did not aggregate thrombasthenic platelets, its aggregating activity was lost after incubation with their stroma. The BSS-Pab did not provoke ADP or 5-HT release or thromboxane synthesis in thrombasthenic platelets or in the platelets of a patient with platelet cyclooxygenase deficiency or in normal platelets treated with indomethacin. The aggregating, release and synthetic responses of platelets after binding of BSS-Pab to its membrane antigen (probably glycoprotein I) requires the presence of glycoprotein IIb and/or IIa and the normal metabolism of arachidonic acid.

Topics: Antibodies; Blood Coagulation Disorders; Blood Platelet Disorders; Blood Platelets; Glycoproteins; Humans; Platelet Aggregation; Syndrome; Thromboxane B2