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Biomedical subjects

T H Spaet

Publications and source records attributed to T H Spaet.

At least 19 recordsLinked to original sources
PubMed1986

Platelet hyperactivity in acute myocardial infarction in man--effects of prostacyclin.

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore, an understanding of factors which impact on platelet performance is important. The present study was undertaken 1. to characterize during evolving myocardial infarction (MI) platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and 2. to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving MI were studied. 22 patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 minutes. In 15 of these patients, who had an anterior MI, transcardiac platelet function and response to PGI2 were studied. The results are as follows: Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, are elevated three and ten fold. 6-keto-prostaglandin F1 alpha, the stable end product of PGI2, is less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets, circulating during evolving MI ("ischemic platelets") are hyperaggregable in response to adenosine diphosphate and relatively resistent to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic adenosine monophosphate and the cAMP response to PGI2 are diminished. The platelet hyper-reactivity is most intense early during infarct evolution and decreases with time. Transcardiac measurements indicate that thromboxane is produced across the ischemic/infarcting compartment in ten of 15 patients with anterior MI. The antiplatelet effect of PGI2 is greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving MI characterized by a pro-aggregatory environment, heightened platelet re-activity, both in the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequence of the data are that the infarct patient in the acute phase may benefit from platelet function suppression and requires significantly greater doses of prostacyclin than normal subjects. The data also suggest future directions for therapeutic manipulation of platelet hyper-reactivity in the setting of acute myocardial ischemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Pseudothrombocytopenia masking true thrombocytopenia.

Pseudothrombocytopenia owing to platelet clumping is usually associated with blood specimens anticoagulated with EDTA. It may also be seen if specimens possessing IgM cold agglutinins are processed at room temperature. A patient with a temperature-independent, EDTA-independent agglutinin is reported whose pseudothrombocytopenia was masking true thrombocytopenia. A technique for blood collection when evaluating similar cases is described.

Aged↗
PubMed1985

Systemic and transcardiac platelet activity in acute myocardial infarction in man: resistance to prostacyclin.

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore an understanding of factors that influence platelet performance is important. This study was undertaken (1) to characterize during evolving myocardial infarction platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and (2) to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving myocardial infarction were studied. Twenty-two patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 min. In 15 patients with anterior myocardial infarction, transcardiac platelet function and response to PGI2 were studied. Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, were elevated three- and 10-fold. 6-Keto-prostaglandin F 1 alpha, the stable end product of PGI2, was less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets circulating during evolving myocardial infarction ("ischemic platelets") were hyperaggregable in response to ADP and relatively resistant to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic AMP and the cyclic AMP response to PGI2 were diminished. The platelet hyperreactivity, expressed by plasma beta-TG, platelet aggregation, and PGI2-induced inhibition of aggregation, was most intense early during infarct evolution and decreased with time. The increased platelet performance resulted in "platelet fatigue," indicated by decreased contents of beta-TG of the ischemic platelet and decreased TxA2 production in response to collagen. However, the ischemic platelet produced twice normal TxA2 in response to arachidonic acid (stimulus and substrate), demonstrating a heightened metabolic capacity. TxA2 was produced across the ischemic/infarcting compartment in 10 of 15 patients with anterior myocardial infarction. The antiplatelet effect of PGI2 was greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving myocardial infarction, characterized by a proaggregatory environment, heightened platelet reactivity in both the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequences of the data are that the patient in the acute phase of myocardial infarction may benefit from suppression of platelet function and requires significantly greater doses of PGI2 than normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1984

Platelet cytoskeleton: immunofluorescence studies on ADP and collagen-activated platelets.

Immunofluorescence studies reveal that platelet changes induced by adenosine diphosphate and collagen do not include the reorganization of the cytoskeleton in such a way as to expose actin, alpha-actinin, or vinculin. However, when such platelets were made permeable by saponin, these cytoskeletal proteins were present. In studies with collagen, fluorescence was observed along the fibers at areas of platelet adhesion and where no platelets were seen by phase microscopy. No fluorescence was observed with collagen treated with platelet-poor plasma. Scanning electron microscopy of collagen samples treated with platelet-rich plasma revealed a fibrillar meshwork with single platelets, platelet aggregates, and nodular structures that were smaller in size than individual platelets. These nodular structures may represent remnants of platelets still attached to the collagen after platelet detachment has occurred. These tenacious collagen-platelet membrane-binding sites have associated with them cytoplasmic alpha-actinin and vinculin, proteins that have been proposed by others to anchor actin filaments to the plasma membrane.

Adenosine Diphosphate↗
PubMed1983

Monitoring heparin therapy--a role for the chromogenic assay.

Heparin therapy was evaluated by simultaneous determinations of the activated partial thromboplastin time (APTT), and plasma heparin levels by chromogenic assay. These tests showed good correlation (r = 0.73) in patients on heparin alone. However, in the presence of concurrent warfarin administration, r fell to 0.37, reflecting an additional warfarin effect upon the APTT. Furthermore, the studies confirmed the increased heparin requirement in patients with pulmonary embolization.

Biological Assay↗
PubMed1983

Long-term effects of deendothelialization of rabbit aorta: in vitro synthesis of DNA, protein, and lipid.

To study the long-term local effects of a single balloon catheter deendothelialization of the aorta in the rabbit, the incorporation of [3H]leucine and [3H]thymidine into protein and DNA, respectively, and [14C]acetate and [14C]mevalonate into sterols was measured in incubations of intima-media sections prepared from vessels taken 1 year following the procedure. The uptake of [3H]thymidine by the tissue was essentially the same as in the nonballooned controls, but the incorporation of [3H]leucine and [14C]acetate into tissue residue (proteins and glycoproteins) was approximately nine times and four times control values, respectively. At the same time, sections from the ballooned animals incorporated over six times the amount of radioactive acetate into nonsaponifiable lipids and cholesterol than did controls. In animals ballooned 3 months before sacrifice, when about half of the aortic luminal surface was covered with endothelium, intima-media tissue from both covered and uncovered areas showed increased uptake of labeled precursors into protein, nonsaponifiables, and cholesterol but there was no significant difference in incorporation between reendothelialized and nonendothelialized areas. The persistence of increased metabolic activity in the vessel following the loss of endothelium could be a contributing factor in the atherogenic process.

Acetates↗
PubMed1982

Selective arterial medial injury fails to produce intimal hyperplasia in experimental animals.

The hypothesis was tested, in rats and rabbits, that selective medial injury may lead to arterial intimal hyperplasia. Lesions were produced by passage of a micro-suture through the arterial wall without penetration to the lumen, or controls in which the suture did penetrate. Vessels were examined histologically at intervals up to 2 weeks after suturing. Only vessels with penetrating sutures developed intimal hyperplasia, suggesting that medial injury alone is insufficient for the production of arteriosclerosis.

Animals↗
PubMed1982

Side-chain oxidation of lipoprotein-bound [24,25-3H]cholesterol in the rat: comparison of HDL and LDL and implications for bile acid synthesis.

The purpose of the study was to test the hypothesis that high density lipoprotein (HDL) cholesterol would be more easily oxidized in vivo than low density lipoprotein (LDL) cholesterol. Homologous plasma was incubated with [24,25-3H]cholesterol and fractionated by ultracentrifugation to obtain HDL and LDL each labeled with [3H] free sterol. HDL and LDL labeled with [24,25-3H]cholesteryl esters were prepared by ultracentrifugation of plasma from donor rats injected 24 hr previously with [24,25-3H]cholesterol in propylene glycol. These four labeled lipoproteins were administered to recipient rats. It was found that more tritium oxide (3H2O) was produced after the HDL doses than after the corresponding LDL doses, from 2--3-fold more when lipoprotein free cholesterol was labeled and from 2--6-fold more when lipoprotein cholesteryl esters were labeled. More 3H2O was produced from free cholesterol-labeled lipoproteins than from cholesteryl ester-labeled lipoproteins. Since oxidation of cholesterol is a measure of bile acid formation, it is concluded that under the conditions of the study HDL-cholesterol is a better precursor of bile acids than LDL-cholesterol.

Animals↗
PubMed1980

Heparin therapy.

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Dose-Response Relationship, Drug↗
PubMed1979

Hematology.

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Complement System Proteins↗