The phrase "alter platelet function" is correct and usable in written English.
You can use it in contexts related to biology, medicine, or pharmacology when discussing changes to how platelets operate in the body.
Example: "Certain medications can alter platelet function, which may affect blood clotting processes."
Alternatives: "modify platelet activity" or "change platelet behavior."
Therefore, platelet OXPHOS dysfunction observed in sepsis patients probably is not enough to alter platelet function and increase mortality.
This is contrastive to other aspects of platelet function (e.g., expression of P-selectin), where agonists and exercise alter platelet function in a similar manner.
Firstly, all of our patients were being treated with a combination of drugs that may alter platelet function (for example, low-dose aspirin, nifedipine, chronic intravenous iloprost), and thus it would have been unethical to interrupt their ongoing therapy.
Sepsis is characterized by thrombocytopenia and altered platelet function.
This agrees with previous studies highlighting the significance of.O2- in altering platelet function [ 5].
In septic patients disseminated intravascular coagulation is a severe complication whereby an altered platelet function appears contributory.
The effects of hypothermia include altered platelet function, impaired coagulation factor function (a 1°C decrease in temperature is associated with a 10% decrease in function), enzyme inhibition, and fibrinolysis [ 20, 21].
The effects of hypothermia include altered platelet function, impaired coagulation factor function (a 1°C drop in temperature is associated with a 10% drop in function), enzyme inhibition and fibrinolysis [ 206, 207].
The effects of hypothermia include altered platelet function, impaired coagulation factor function (a 1ºC drop in temperature is associated with a 10% drop in function), enzyme inhibition and fibrinolysis [ 196 , 197]
There is convincing evidence linking decreased vascular NO production coupled with the overproduction of reactive oxygen species (ROS) and the generation of potent oxidants such as peroxynitrite (ONOO−) to altered platelet function.
This increased risk of atherosclerosis in diabetic subjects has been attributed to diverse mechanisms such as endothelial dysfunction [ 30] or altered hemostatic factors (higher levels of fibrinogen [ 31], plasminogen activator-inhibitor-1 [ 32, 33] or VonWillebrand factor [ 34]), or altered platelet function [ 35- 38]).
