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N Ellison

Publications and source records attributed to N Ellison.

15 recordsLinked to original sources
PubMed1990

Intraoperative management of patients with heparin-induced thrombocytopenia.

For 11 patients with confirmed heparin-induced thrombocytopenia, we used reversible platelet inhibition with iloprost, a stable prostacyclin analogue, to permit safe heparin administration for cardiac (n = 9) or vascular (n = 2) operations. In vitro, iloprost (0.01 mumol/L) prevented both heparin-induced platelet aggregation and 14C-serotonin release in all patients. Therefore, intraoperatively, a continuous infusion of iloprost was started before administration of heparin and was continued until 15 minutes after administration of protamine. For cardiac patients, after heparin administration, the whole blood platelet count did not change (171,000 +/- 29,000/microL versus 174,000 +/- 29,000/microL, mean +/- standard error of the mean); no spontaneous platelet aggregation was observed, and plasma levels of the alpha-granule constituents platelet factor 4 and beta-thromboglobulin increased from 38 +/- 14 and 140 +/- 18 ng/mL to 591 +/- 135 and 235 +/- 48 ng/mL, respectively. Fibrinopeptide A levels actually decreased from 287 +/- 150 to 27 +/- 6 ng/mL. Furthermore, adenosine diphosphate-induced platelet activation was preserved, postoperative bleeding times were unchanged, and no heparin-related deaths occurred. Similar results were obtained in both vascular patients. We conclude that temporary platelet inhibition with iloprost now permits safe heparin administration in all patients with heparin-induced thrombocytopenia who require a cardiac or vascular operation.

Adult↗
PubMed1978

Platelet aggregation following heparin and protamine administration.

The effects of heparin, protamine, and the heparin-protamine complex on the abilities of platelets to aggregate in vitro in response to adenosine diphosphate (ADP) and epinephrine were determined. Citrated blood was obtained from normal volunteers and portions were treated with heparin, protamine, and three different ratios of heparin and protamine. The threshold concentrations of ADP and epinephrine required to produce complete platelet aggregation were then determined. Compared with control citrated plasma, the geometric mean of the threshold concentration for ADP in the heparinized sample was decreased twofold, from 1.88 to 0.94 micrometer; and that for epinephrine more than threefold, from 0.5 to 0.14 micrometer. In contrast, the threshold concentration for ADP was increased to 3.68 micrometer in the neutralized and to 2.78 micrometer in the overneutralized samples and that for epinephrine to 1.62 micrometer in the neutralized and 1.82 micrometer in the overneutralized samples. These data indicate that heparin increases the sensitivity of platelets to ADP and epinephrine as determined by platelet aggregation, and protamine added to heparinized blood not only reverses this effect, but decreases platelet sensitivity when it is added in concentration that neutralize heparin. Additional protamine has no further effect, and protamine alone has no effect on platelet aggregation.

Adenosine Diphosphate↗
PubMed1977

Platelet function.

Basic knowledge regarding platelet physiology has been reviewed and related to clinical situations where platelet function is critically important. Platelet function tests such as aggregation and survival studies, which are research tools now, may soon be available to aid in the diagnosis and management of clinical bleeding problems. A growing understanding of drug-platelet interactions is allowing manipulation of platelets and the clotting system to improve the proganoses for patients who have thromboembolic diseases. Advances in platelet storage and transfusion techniques can save patients who previously might have bled to death. Proper application of the new developments in cardiopulmonary bypass and hemodilution, with attention to platelet and coagulation factor preservation, will contribute to securing hemostasis and conserving blood products.

Blood Coagulation Factors↗