Search PubMed⌕ Search

Biomedical subjects

E Genton

Publications and source records attributed to E Genton.

At least 55 records · Page 3Linked to original sources
PubMed1976

Clinical and physiologic studies of two siblings with prekallikrein (Fletcher factor) deficiency.

Two siblings with hereditary Fletcher factor (prekallikrein) deficiency were studied for alterations of fibrinolysis, platelet function, skin inflammatory responses, permeability factor (PF/dil) formation and leukocyte chemotaxis. In vivo stimulation of fibrinolytic activity was normal; the bleeding time and platelet functions (adhesivity, aggregation, release reaction) were also normal. Both immediate (wheal-flare reaction to histamine, bradykinin, prostaglandin E1, physical agents) and delayed sensitivity skin test reactions were within normal limits. Migration of subjects' leukocytes to attractants in skin windows and in Boyden-type chambers was the same as that of control leukocytes. Serum complement components were essentially normal. One subject's leukocytes showed normal tissue factor production on stimulation by endotoxin, although prekallikrein deficiency did impair the endotoxin-stimulated generation of serum procoagulant activity. PF/dil caused increased vessel permeability in human skin; in vitro generation of PF/dil required both the Hageman factor and prekallikrein. The Fletcher factor-deficient subjects responded in a normal manner to PF/dil. Based on the Fletcher factor-coagulation assay, the biologic half-disappearance time of prekallikrein (after the transfusion of normal plasma in one of the subjects) was estimated at 35 hours. Therefore, these studies suggest that severe prekallikrein (Fletcher factor) deficiency in man is not associated with any clinically significant impairment in hemostasis, fibrinolysis, inflammatory responses or leukocyte function.

Adolescent↗
PubMed1976

Correlation of platelet survival time with occlusion of saphenous vein aorto-coronary bypass grafts.

Platelet survival time is frequently shortened in patients with coronary artery disease, and it is one of several factors that might contribute to graft occlusion after saphenous vein coronary artery bypass (CAB). In 35 patients with CAB, average platelet survival (autologous labeling with 51Chromium) was shortened in 20 with one or more saphenous vein grafts occluded and normal in 15 with all grafts open. Of 15 with all grafts open, individual levels of platelet survival were normal in 10 while in 20 with one or more grafts occluded platelet survival was normal in only one. Platelet survival was not altered by coronary surgery and nine of ten with shortened platelet survival pre-operatively had graft occlusion. Platelet survival did not correlate with either parent artery occlusion or serum lipoproteins. These findings suggest a relationship between shortened platelet survival and saphenous vein graft occlusion and suggest that platelet suppressant therapy might be useful in preventing graft occlusion.

Adult↗
PubMed1976

Platelets are not essential for the pulmonary vascular pressor response to hypoxia.

The literature suggests that platelets might help mediate the pulmonary vascular pressor response to hypoxia. This study evaluated the hypoxic response in thrombocytopenic dogs. Platet depletion was achieved in five dogs by the use of platelet antiserum. In the normoxic state these dogs had lower cardiac outputs and higher pulmonary and systemic vascular resistances than five control dogs. The pressor response to hypoxia in these dogs was not only preserved but considerably enhanced in comparison to the control dogs. Hypoxia increased the pulmonary vascular resistance 146 +/- 17% above its normoxic value in the thrombocytopenic dogs and 64 +/- 21% in the control dogs. Thus platelets may normally produce a dilator substance or inactivate a pressor substance during hypoxia. The mechanism of the effect is not apparent but it is clear tha the pulmonary pressor response to hypoxia in the dog is not mediated by platelets.

Animals↗
PubMed1975

Platelet survival time following aortic valve replacement.

Thromboembolism continues to complicate the course of patients following aortic valve replacement. In patients with prosthetic and homograft mitral valves, platelet survival time has been shown to correlate with occurrence of thromboembolism. This study extends these observations to patients with aortic valve disease. Platelet survival time was measured (by the chromium-51 method) in 73 patients with aortic valve disease. Eighteen patients were studied preoperatively and had platelet survival times of 3.4 plus or minus 0.14 days (mean plus or minus standard error of the mean), almost the same as normal (3.7 plus or minus 0.4 days). Platelet survival time was shortened (P less than 0.001) following aortic valve replacement with Starr-Edwards prosthesis - Model 1000: 2.5 plus or minus 0.13 days (N = 6); Model 1200-1260: 3.0 plus or minus 0.10 (n = 14); model 2300-2320: 3.0 plus or minus 0.15 days (N = 9) - and with stented aortic homografts: 3.0 plus or minus 0.10 days (N = 16). Platelet survival time was normal following aortic valve replacement in patients with directly sewn aortic homografts 3.7 dats plus or minus 0.24 days (N = 10). Eleven patients with Starr-Edwards prostheses had a history of thromboembolism and all also showed shortened platelet survival time (2.7 plus or minus 0.12 days, P less than 0.001), a measurement which was significantly different (P less than 0.01) from the 18 patients with Starr-Edwards prostheses and no thromboembolism (3.0 plus or minus 0.09 days). Platelet suppressant therapy prolonged platelet survival in eight patients with Starr-Edwards devices, thromboembolism, and shortened platelet survival time. These results suggest that insertion of Starr-Edwards valves and stented aortic homografts alter platelet survival time but that direct homografts do not. A correlation between occurrence of thromboembolism after aortic valve replacement and shortened platelet survival time has been shown.

Adult↗
PubMed1975

Effects of clofibrate and sulfinpyrazone on platelet survival time in coronary artery disease.

Platelet survival time was measured (autologous labelling with 51chromium) in 68 men with coronary artery disease (CAD). Survival was shortened slightly (3.2 +/- 0.04 days; mean +/- SEM) as compared to normal (3.7 +/- 0.04 days; N = 18; P less than 0.001), and 60% had shortened survival (less than 3.3 days). Thirty-seven had hyperlipoproteinemia (36 with Type IV and one with Type III) and platelet survival was shortened (3.1 +/- 0.10 days) and significantly different from survival of men with normal lipoproteins (3.3 +/- 0,12 days; P less than 0.05). Twenty-two with shortened platelet survival and CAD received either clofibrate or sulfinpyrazone. Clofibrate prolonged platelet survival (2.6 +/- 0.09 to 3.4 +/- 0,14 days; P less than 0.001) and ten of 12 had prolongation of survival. Sulfinpyrazone increased survival (2.8 +/- 0.12 to 3.6 +/- 0.21; P less than 0.001) and nine of ten had prolognation of platelet survival. Clofibrate lowered serum cholesterol and tryglyceride but alteration in lipids did not correlate with alteration of survival. Sulfinpyrazone did not alter lipids. Data suggest that survival is shortened in CAD and that clofibrate and sulfinpyrazone alter survival. Platelet suppressant agents may prove beneficial in reducing the extent and complications of atherosclerotic arterial injury.

Adult↗