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Biomedical subjects

P Han

Publications and source records attributed to P Han.

At least 109 records · Page 6Linked to original sources
PubMed1985

Haemostasis in children: anything new?

Our understanding of haemostatic mechanisms has increased in the last decades. This knowledge at the cellular and molecular levels has helped us to appreciate the complexity of haemostatic mechanisms and their disturbance in various disorders. The advance in techniques to measure early activation of coagulation and platelets opens hope of treating acquired bleeding disorders e.g., disseminated intravascular coagulation before the full blown picture. More study needs to be done to define what constitutes normal haemostasis in newborns. The better understanding of control mechanisms of haemostasis will help us in diagnosis and treatment.

Antithrombin III↗
PubMed1984

Normal standards of in vitro induced platelet aggregation.

Measurement of in vitro induced platelet aggregation by turbidimetric method is a very important investigative tool when patients are evaluated for bleeding diasthesis due to possible underlying platelet functional disorders. As commercial controls are not available, it is important that each laboratory establishes its own normal pattern of platelet aggregation induced by standard aggregating agents. The aggregation curves in terms of maximal % aggregation, Vmax and lag time in 50 normal Chinese controls are reported. The final concentrations of the aggregating agents used, namely adenosine diphosphate, adrenaline, collagen and ristocetin, are 20 microM, 10 microM, 0.2 mg/ml and 1.0 mg/ml, respectively. 20% of the controls had either no aggregation or only primary aggregation with adrenaline. Lag time by collagen-induced aggregation is significantly longer, but other parameters of platelet aggregation by adenosine diphosphate, adrenaline and collagen in Chinese are comparable to one reported control study. The maximal % aggregation induced by ristocetin in Chinese does not differ significantly from the reported values in whites but is significantly higher than in Blacks at a concentration of 1.0 mg/ml. Interpretation of platelet aggregometry in patients with bleeding tendency should be based on the normal patterns established from a group of normal controls in each laboratory rather than by comparison with a single control alone.

Adenosine Diphosphate↗
PubMed1983

Effect of the calcium-entry blocking agent nifedipine on activation of human platelets and comparison with verapamil.

The effects of the calcium-entry blocking agent nifedipine on the activation of human platelets by various agonists has been studied and compared with verapamil. Like verapamil, nifedipine inhibited platelet aggregation and secretion caused by collagen, the second phase of ADP-induced aggregation, and aggregation caused by the ionophore A23187. Both agents inhibited the formation of TXB2 from endogenous arachidonate, whereas only nifedipine inhibited platelet aggregation and decreased TXB2 formation caused by exogenous arachidonate without inhibiting uptake. These results indicate that both calcium-blocking agents may be inhibiting the release of arachidonate in platelets by phospholipases, and that nifedipine also inhibits the formation and action of thromboxane A2 in platelets. Epinephrine-induced aggregation was inhibited by low concentrations of verapamil while nifedipine only inhibited aggregation by epinephrine at much higher concentrations. It is suggested that low concentrations of verapamil inhibit epinephrine-induced aggregation by interacting with platelet alpha-adrenergic receptors, and that higher concentrations of both calcium-blocking agents inhibit platelet responses to other aggregating agents by preventing intracellular calcium mobilization.

Arachidonic Acid↗
PubMed1983

Verapamil and collagen-induced platelet reactions--evidence for a role for intracellular calcium in platelet activation.

Calcium is considered to have an essential role in various platelet reactions. Using platelets preincubated with chlortetracycline, a fluorescent divalent cation indicator, and suspended in a calcium free medium, it was shown that collagen-induced intracellular calcium redistribution occurred before the platelet shape change, the release reaction and thromboxane B2 formation. Verapamil, at concentrations which affect intracellular calcium movements, inhibited intracellular calcium redistribution in platelets and the subsequent collagen-induced platelet reactions. Low concentrations of the ionophore A23187 overcame the inhibitory effect of verapamil. These experiments provide evidence that intracellular calcium mobilization is involved in the activation of platelets by collagen. Furthermore, calcium may be released from different cellular pools since platelet secretion, aggregation and thromboxane B2 formation were inhibited at lower concentrations of verapamil than was the platelet shape change.

Adenosine Triphosphate↗
PubMed1983

Platelet tests and antiplatelet drugs in coronary artery disease.

This study was designed to clarify discrepancies in the literature concerning platelet survival time and beta-thromboglobulin (beta TG) levels in patients with coronary artery disease (CAD) and the effect of platelet-suppressant drugs on these tests. Platelet survival time and plasma beta TG levels were determined in 48 patients with angiographically documented CAD. The effect of sulfinpyrazone or aspirin/dipyridamole on these measurements was investigated in a double-blind, crossover trial that included a placebo phase. In patients with CAD, the mean plasma beta TG concentration was significantly elevated, but the mean platelet survival time was not significantly different from that in controls. Treatment with sulfinpyrazone or aspirin/dipyridamole did not produce changes in platelet survival time or plasma beta TG concentration that were significantly different from the values during the placebo phase. This study demonstrates that compared with the spontaneous variation in platelet survival time or beta TG concentration, there was no measureable effect of sulfinpyrazone or aspirin/dipyridamole on the results of the tests.

Adult↗
PubMed1982

Inhibition of platelet function of antiarrhythmic drugs, verapamil and disopyramide.

Various cardiovascular drugs such as nitrates and propranolol, used in the treatment of coronary artery disease have been shown to have an antiplatelet effect. We have studied the in vitro effects of two antiarrhythmic drugs, verapamil and disopyramide, and have shown their inhibitory effect on platelet function. Verapamil, a calcium channel blocker, inhibited the second phase of platelet aggregation induced by adenosine diphosphate (*ADP) and inhibited aggregation induced by collagen. Disopyramide similarly inhibited the second phase of platelet aggregation caused by ADP and aggregation induced by collagen. Either drug in synergism with propranolol inhibited ADP or collagen-induced platelet aggregation. Disopyramide at high concentrations inhibited arachidonic acid whereas verapamil was without effect. Verapamil, but not disopyramide, inhibited aggregated induced by the ionophore A23187.

Adenosine Triphosphate↗
PubMed1981

Plasma and urine beta-thromboglobulin concentration in patients with deep vein thrombosis.

Plasma and urine beta-thromboglobulin (BTG) were measured in 52 patients with established deep vein thrombosis (DVT) and in 100 patients with clinically suspected DVT but with a negative venogram. Both plasma BTG (geometric mean 54: 95% range 12--239 ng/ml) and urine BTG (0.25; 0.03--3.1 ng/ml) were significantly elevated (p less than 0.005) in patients with DVT compared to symptomatic patients with a negative venogram (plasma BTG 32, 9--112 ng/ml; urine BTG 0.12, 0.02--0.58 ng/ml). Sensitivity (35%) and specificity (80%) of the plasma BTG assay for the diagnosis of DVT were low. The urine BTG assay had a sensitivity of 37% but a specificity of 100%. There was a significant correlation between plasma and urine BTG (r = 0.68, p less than 0.005). Serial BTG measurements were made in urine (40 patients) and plasma (20 patients) from high-risk neurosurgical cases who were screened with 125I-fibrinogen leg scanning and impedance plethysmography. BTG was elevated postoperatively and returned to normal within 2 or 3 days, but rose again in 10 patients in association with the development of DVT. The rise of BTG preceded the uptake of 125I-fibrinogen and lasted for only a few days. The return to normal of BTG was not related to treatment with anticoagulants. While measurement of BTG in plasma and urine is of limited value in the clinical diagnosis of venous thrombosis, the data indicate platelet activation occurs in venous thrombosis, but is maximal or perhaps limited to the initial phase of thrombus development.

Adolescent↗
PubMed1980

Beta-thromboglobulin radioimmunoassay. A laboratory characterization and evaluation.

Platelets release beta-thromboglobulin from alpha-granules when they are activated by various stimuli. An evaluation and optimization of a radioimmunoassay for beta-thromboglobulin is described. The optimum conditions for the reaction have been characterized, and the use of second antibody and polyethylene glycol allows completion of the assay within 24 hours. Similar BTG concentrations were obtained using a 1-hour non-equilibration assay but the 1-hour assay was inefficient for processing large volumes of specimens and has the potential for cross reactivity. BTG standards were unstable but the shelf-life was prolonged with aprotinin or by storage at -70 degrees C. Plasma BTG concentration in 80 normal individuals was 28 +/- 18 ng/ml. (mean +/- 2 S.D.).

Adult↗
PubMed1979

Plasma beta-thromboglobulin: differentiation between intravascular and extravascular platelet destruction.

To elucidate the usefulness of beta-thromboglobulin (beta TG) in the differentiation of the mechanism of thrombocytopenia, plasma beta TG concentration was measured in one patient with amegakaryocytic thrombocytopenia, four patients with autoimmune thrombocytopenia (ATP), two patients with thrombotic thrombocytopenia (TTP), and one patient with thrombocytopenia secondary to disseminated intravascular coagulation (DIC). Plasma beta TG was not measurable in amegakaryocytic thrombocytopenia, was normal in ATP, and was increased in TTP and DIC. These data indicate that in thrombocytopenic patients, increased plasma beta TG concentration may result from intravascular platelet consumption with release of platelet constituents in contrast to extravascular platelet destruction by the macrophage-monocyte system.

Adult↗