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Biomedical subjects

J Zahavi

Publications and source records attributed to J Zahavi.

At least 37 records · Page 2Linked to original sources
PubMed1980

Enhanced in-vivo platelet release reaction, increased thromboxane synthesis, and decreased prostacyclin release after tourniquet ischaemia.

Plasma beta-thromboglobulin (beta-TG), a marker of in-vivo platelet release reaction, was measured in 27 meniscectomy patients, 10 patients who underwent total knee replacements (TKR) (both procedures performed under tourniquet ischaemia), and 10 herniorrhaphy patients. In 22 meniscectomy and 7 TKR patients plasma-thromboxane-B2 (TxB2), a stable end-product of thromboxane-synthetase activity, was also determined. The mean plasma beta-TG and TxB2 had risen significantly within 5 min of release of the tourniquet, indicating increased in-vivo platelet release reaction and prostaglandin synthesis in these patients. In the herniorrhaphy patients beta-TG and TxB2 did not alter significantly postoperatively. In 6 pigs (weighing 20-30 kg) who underwent meniscectomy under tourniquet ischaemia plasma TxB2 rose significantly 15-30 min after release of the tourniquet, and prostacyclin release was significantly lower from veins exposed to ischaemia than from control veins. Large de-endothelialised areas were seen on scanning electron-micrographic sections of affected veins, and these areas were covered with a monolayer of platelets and platelet clumps. These changes associated with tourniquet ischaemia may explain the high incidence of venous thrombosis seen in patients undergoing meniscectomy and TKR.

Adult↗
PubMed1979

beta-Thromboglobulin, platelet production time and pletelet function in vascular disease.

Plasma beta-thromboglobulin (beta TG) levels were measured in 103 healthy controls and 112 patients suffering from either peripheral vascular disease (PVD), or cerebrovascular disease (CVD) or deep vein thrombosis (DVT). Plasma beta TG was significantly elevated in 46 PVD patients and 24 recent DVT patients compared to controls, but did not differ significantly in 18 chronic DVT and 24 old CVD patients. In addition, heparin neutralizing activity (HNA) and platelet aggregation induced by adenosine diphosphate, 1-epinephrine and thrombin were compared in 33 out of the 46 PVD patients to 33 controls. The mean HNA was significantly shorter in the PVD patients than in controls. The rate and extent of platelet aggregation were increased in PVD patients compared to controls, but the difference was not statistically significant. Platelet production time (PPT) was measured in 20 controls, 35 PVD patients, nine chronic DVT and 12 chronic CVD patients; significantly shorter PPT was only observed in 14 patients with advanced PVD compared to controls, suggesting increased platelet consumption in these patients. All four assays (plasma beta TG, HNA, platelet aggregation and PPT) were performed in 25 patients; no correlation between the four tests was found in these patients suggesting that the tests were measuring various aspects of platelet function. These results suggest that in vivo platelet consumption as well as platelet aggregation and 'release reaction' are presumably enhanced in PVD and recent DVT patients and that plasma beta TG and PPT assays may be better and more specific indicators of in vivo platelet activation than in vitro platelet aggregation test.

Adolescent↗
PubMed1979

A modified non-radioisotope method for measurement of platelet production time.

Platelet production time (PPT), based on the measurement of malondialdehyde (MDA) production prior to and after the intake of acetylsalicylic acid (ASA), was determined in 20 healthy subjects. High MDA levels were produced by stimulating platelet lipid peroxidation with arachidonic acid, resulting in a reliable, sensitive and accurate technique. PPT correlated well with platelet survival time measured by 51Cr autologous labelled platelets when both methods were used simultaneously in the same patients. This modified non-radioisotope method might serve as a useful aid in the diagnosis of platelet disorders, thromboembolic diseases associated with increased platelet consumption and for the evaluation of drugs affecting platelet function.

Aspirin↗
PubMed1979

Subendocardial infarction and thrombocytopenia.

Two female patients who suffered from drug-induced thrombocytopenic purpura and subendocardial myocardial infarction are presented. One of them died from cerebral haemorrhage and diffuse subendocardial punctate haemorrhages were found at post-mortem. The abnormal haemostasis which is associated with thrombocytopenia might induce diffuse damage of the myocardium and might impair heart performance. This finding may be more frequent than hitherto appreciated and calls for serial electrographic tracings in thrombocytopenic patients.

Anti-Inflammatory Agents↗
PubMed1977

Quantitative venographic assessment of deep vein thrombosis in the evaluation of streptokinase and heparin therapy.

A technique of quantitative venography has been developed in which values are assigned to the deep veins of the calf, knee, thigh, and pelvis, based upon the calculated volume and degree of occlusion of these venous segments. A maximum score of 40 units reflects complete thrombosis of all segments. This technique has been applied to a randomized, single-blind study of streptokinase versus heparin treatment. Each group of 12 patients had similar mean inital venographic scores; follow-up venograms were performed 5 days after the start of therapy. Streptokinase patients with high initial scores (larger than 20) showed a mean improvement of 12.1 units, while those with low initial scores(less than 20) were essentially unchanged. Heparin patients with high scores had a minimal mean improvement of 1.1 units, but those with low scores had a significant mean extension of thrombosis of 8.6 units. Patients with symptoms for less than 7 days showed greated mean improvement (12.7 units) with streptokinase that those with a longer duration of symptoms (2.0 units); heparin patients in these subgroups showed a mean worsening of 7.5 units and no change, respectively. Extrinsic venous obstruction by tumor did not prevent an excellent response to streptokinase. No single test of coagulation of fibriolysis was a reliable indicator of the degree of venographic response to lytic therapy. Pyrexia and hemorrhagic complications occurred in over one-half of the streptokinase patients; one had an anaphylactic reaction, and one died of intracerebral hemorrhage during therapy. The data suggest that lytic therapy is best restricted to the patient with acute extensive thrombosis. Also, continuous infusions of heparin according to current guidelines may be inadequate to prevent thrombus growth in some patients.

Adolescent↗