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.

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.

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.

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.

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.

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.

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.

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.

In vitro synthesis of DNA, protein, and lipids by the de-endothelialized rabbit aorta.

The uptake of [3H] leucine, [3H] thymidine, [14C] acetate, and [14C] mevalonic acid by aortic intima media from normal rabbits and from rabbits subjected to a single balloon de-endothelialization as measured 6 days, 2 months, and 4 months after treatment to determine how long the injury-induced stimulation of incorporation of these precursors into tissue components persisted beyond 6 days, the time of maximum proliferative response of the smooth muscle cells. We found that [3H] thymidine incorporation (indicative of DNA synthesis and the potential for cell proliferation) was about three times greater in the de-endothelialized tissue than in the control tissue 6 days after vessel injury, but that by 2 months it was normal. Labeled leucine incorporation into the de-endothelialized tissue (a measure of protein synthesis) was eight times higher than normal at the time of maximum proliferative response to injury (6 days), and showed no decrease under identical incubation conditions in ballooned tissue obtained 2 months after de-endothelialization; it continued high at 4 months.

The influence of the pituitary on arterial intimal proliferation in the rat.

The formation of arteriosclerotic fibromusculoelastic intimal thickening following arterial de-endothelialization is well documented. Recent findings, both in vitro and in vivo, suggest that platelets are a major participant in the pathogenesis of this lesion by releasing a mitogen to medial smooth muscle cells (SMC). This mitogen results in SMC migration to and proliferation within the intima.

Delayed consequences of endothelial removal from rabbit aortae.

One year after de-endothelialization of rabbit aorta by a balloon catheter, the damaged areas show arteriosclerotic thickening. In the study described here, aortae from six rabbits were examined 2 years after the single injury. Three had advanced atherosclerotic lesions.