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Biomedical subjects

S H Goodnight

Publications and source records attributed to S H Goodnight.

At least 55 records · Page 3Linked to original sources

The effects of dietary omega 3 fatty acids on platelet composition and function in man: a prospective, controlled study.

The rarity of atherosclerotic vascular disease and a mild bruising tendency in Greenland Eskimos has been linked to their ingestion of omega 3 fatty acids contained in foods obtained from the sea. Previous studies have shown that feeding salmon oil to normal volunteers resulted in reductions of plasma cholesterol and triglycerides. We wished to learn whether salmon oil feeding would result in the incorporation of omega 3 fatty acids into platelets and whether platelet function or platelet-vessel interaction would be altered. Diets containing salmon oils led to the incorporation of eicosapentaenoic acid (C20:5 omega 3) into platelets (6.1%) with a reduction in arachidonic acid (C20:4 omega 6). The ratio of C20:5/C20:4 increased from 0.0045 on the control diet to 0.3 on the salmon diet. Bleeding times were prolonged (from 6.75 to 10 min, p less than 0.005), platelet retention on glass beads was mildly reduced (from 89% to 78%, p less than 0.0005), and platelet aggregation in response to dilute concentrations of ADP was inhibited in the subjects ingesting the salmon oil. We conclude that in normal subjects dietary omega 2 fatty acids derived from salmon oil are incorporated into platelet phospholipids and that these changes are accompanied by alterations in bleeding time and platelet function.

Adenosine Diphosphate↗

Measurement of antithrombin III in normal and pathologic states using chromogenic substrate S-2238. Comparison with immunoelectrophoretic and factor Xa inhibition assays.

Synthetic substrates have recently been developed for the assay of several of the proteolytic enzymes required for blood coagulation, One of these substrates, S-2238, is specific for thrombin and hence can also be used to measure antithrombin-heparin co-factor (AT-III). The thrombin remaining after neutralization by AT-III cleaves a chromophore, p-nitroaniline, from the substrate, which can then te quantified in a spectrophotometer. This new assay for AT-III inhibitory activity was evaluated for normal subjects and for patients who had certain pathologic conditions associated with reduced levels of AT-III. Results from this assay were compared with those from AT-III assays by Laurell immunoelectrophoresis (an immunologic method) and antithrombin inhibition of factor Xa (a biologic clotting method). The chromogenic assay using S-2238 was found to be sensitive, accurate, and easy to perform; its results for both normal subjects and patients correlated extremely well with those of the immunologic and factor Xa inhibition assays (r = 0.94-0.98). Measurement of AT-III using this synthetic substrate should be a valuable addition to routine assays in a clinical coagulation laboratory. These and future substrates may prove extremely useful for assays of factors involved in blood coagulation and fibrinolysis.

Antithrombin III↗

The visual system in thrombotic thrombocytopenic purpura.

Thrombotic thrombocytopenic Purpura (TTP) is a rare, acute usually fatal disease of unknown cause. As the name indicates, it is typified by the abnormal rate of platelet consumption with the deposition of thrombi in many vessels. Approximately 300 cases of TTP have been described in the literature since the first report by Moschowitz in 1925. It may occur at any age, but the peak incidence is during the third decade. Females are affected more frequently than males in the ration 3:2. TTP has occurred in siblings and in a husband and wife. It has been associated with pregnancy in 24 cases. "Visual changes" have been reported in 8% of cases; however, the nature of these visual changes has not been elucidated. It is the purpose of this report to call the attention of ophthalmologists to the severe involvement of the visual system which may occur. We will illustrate with a case report one cause of the blurred vision in TTP, and illustrate other ways the visual system may be involved with a review of the pertinent literature.

Adult↗

Failure of antiplatelet and anticoagulant therapy to improve patency of grafts after coronary-artery bypass: a controlled, randomized study.

Fifty patients who underwent aortocoronary saphenous-vein bypass-graft surgery were randomly assigned to one of three groups to determine the effects of antiplatelet or anticoagulant therapy on graft patency. Twenty-four patients served as controls; 13 patients received aspirin (325 mg three times a day) and dipyridamole (75 mg three times a day); and 13 patients received closely regulated warfarin therapy. Medications were begun on the third post-operative day. Six months after surgery, all patients underwent coronary angiography to assess graft patency. There were no statistically significant differences between groups in various clinical, hemodynamic and angios, 27 of 33 grafts (82 per cent) with aspirin and dipyridamole and 29 of 37 grafts (78 per cent) with warfarin (P less than 0.5), all patients had at least one patent graft. Postoperative treatment either with aspirin and dipyridamole or with warfarin failed to improve the patency of the grafts.

Aged↗

Prednisone-responsive aplastic anemia: a mechanism of glucocorticoid action.

We performed serial agar cultures (CFU-C) using marrow cells from a patient with prednisone-responsive aplastic anemia and from five patients with prednisone-resistant aplasia. Colony growth was decreased in all patients. Cortisol (10(-7)-10(-4)M) significantly enhanced colony growth in the prednisone-responsive patient but fauled to enhance colony growth in the remaining five patients. Further studies in the responsive patient indicated that (1) colony growth was enhanced by depleting T lymphocytes from the marrow cells, (2) colon growth T-depleted marrow cells was inhibited by autologous peripheral blood lymphocytes (PBL), (3) cortisol failed to enhance colony growth of T-depleted marrow cells, (4) PBL and PBL-conditioned medium inhibited colony growth of both autologous and allogeneic marrow cells, but neither cortisol-treated PBL nor T-depleted PBL were inhibitory. Serial cultures in the responsive patient showed that colony growth normalized during remission when "suppressor" cells were absent and that colony growth was subnormal during a later relapse when cortisol-resistant "suppressor" cells were present. Therefore, in this prednisone-responsive patient, cortisol-sensitive T lymphocytes suppressed granulopoiesis in vitro. Our observations suggest that aplastic anemia in this patient is immunologically mediated and that prednisone therapy enhanced hemopoiesis in vivo by inhibiting the "suppressor" T lymphocytes.

Anemia, Aplastic↗

Hemostatic complications in leukemic patients.

With clinical vigilance and laboratory tests of platelet and coagulation factor function, the clinician can promptly recognize and treat hemostatic disorders in leukemic patients. For example, laboratory values are strikingly abnormal in disseminated intravascular coagulation. Prompt neutralization of the underlying cause of the coagulopathy is essential. Platelet and coagulation factors may have to be replaced if the disorder is severe. Diffuse petechiae, purpura, mucous membrane bleeding, and hemorrhage around venipuncture or infusion sites indicate thrombocytopenia. Vigorous platelet replacement is necessary to prevent massive intracranial of gastrointestinal hemorrhage. Platelet dysfunction may cause spontaneous bleeding or immediate or delayed hemorrhage after surgery. The abnormality is often evident in peripheral blood smear or indicated by bleeding time or aggregation studies. If possible, sufficient autologous platelets should be infused to return the bleeding time to normal. Immune thrombocytopenic purpura may be easy to diagnose when the reduction in the circulating platelet count is compared with the normal number of marrow megakaryocytes. But attempts to increase platelet count by platelet transfusions may be frustrating. Treatment involves high doses of corticosteroids, followed by splenectomy if necessary.

Blood Coagulation Disorders↗

The clinical use of fibrinolytic agents.

Two fibrinolytic drugs, streptokinase and urokinase, have undergone extensive clinical evaluation in the past fifteen years. Current evidence suggests that these agents may become the drugs of choice in the treatment of certain patients with venous thrombosis and pulmonary embolism. The ultimate usefulness of fibrinolytic therapy in the treatment of thrombotic conditions other than venous thrombosis and pulmonary embolism has not yet been determined.

Endopeptidases↗

The role of the platelet in coagulation and clinical thrombotic events.

There have been exciting advances in our understanding of platelet function in recent years. Platelet physiology, drugs that inhibit platelet function, and the current evidence supporting the use of platelet-inhibiting drugs in the prevention of clinical thrombotic events are reviewed.

Blood Coagulation↗

Effects of infusion of cardiotomy suction blood during extracorporeal circulation for coronary artery bypass surgery.

The effects of infusion of cardiotomy suction blood during extracorporeal circulation were evaluated in 15 patients undergoing coronary artery bypass surgery without the use of a left ventricular vent. In Group I all cardiotomy suction blood was discarded. In Groups II and III cardiotomy suction blood was reinfused without and with Dacron wool filtration, respectively. Marked hematologic changes were noted in the pericardial samples which also were reflected in oxygenator samples obtained at the end of bypass. Although postoperative bleeding was significantly greater in patients from Group II as compared to Group I, no differences were seen in total intraoperative and postoperative transfusion requirements. No patient required reoperation for bleeding. Recirculation of larger volumes of cardiotomy suction blood potentially could contribute to bleeding problems in the immediate postoperative period.

Blood↗