Mannitol upregulates monocyte HLA-DR, monocyte and neutrophil CD11b, and inhibits neutrophil apoptosis.

D-Mannitol is a substance widely used for both clinical applications as a strong diuretic and in basic research as a purportedly inert osmotic control substance. However, recent experiments have shown that mannitol is able to decrease neutrophil apoptosis in vitro by more than 25%. The aim of the current study was to assess mannitol's effects on two immune cell activation markers; CD11b on neutrophils and monocytes, and HLA-DR on monocytes.

Short-term hyperglycemia in surgical patients and a study of related cellular mechanisms.

Objective: To examine cellular mechanisms by which short-term elevations of glucose or insulin impair leukocyte functions and to assess the occurrence of perioperative hyperglycemia in surgical patients.

Summary Background Data: A major factor in the contemporary management of the critically ill surgical patient is the progressively exact control of blood glucose. However, the separate role of insulin and underlying immunologic mechanisms are not well understood.

Effects of hyperglycemia, hyperinsulinemia, and hyperosmolarity on neutrophil apoptosis.

Background: Hyperglycemia is an independent risk factor for increased mortality of critically ill surgical patients, but despite the recognized clinical benefits of early insulin treatment, there is a lack of understanding of the cellular and molecular mechanisms behind this phenomenon. We hypothesized that polymorphonuclear neutrophils, the first line of the innate immune defense system, suffer from altered apoptotic turnover when exposed to hyperglycemic conditions, ultimately decreasing the number of viable cells active at a site of infection.

Methods: Venous blood samples were drawn from 10 volunteers and incubated for 0.

Endotoxin inhibits apoptosis but induces primary necrosis in neutrophils.

Lipopolysaccharide (LPS) is known to prolong the functional lifespan of neutrophils at a site of infection by preventing apoptosis through inhibitor of apoptosis proteins (IAPs). We hypothesized that the increased neutrophil lifespan ultimately leads to a larger fraction of cells undergoing uncontrolled, primary necrosis. Diluted venous whole blood was incubated with increasing concentrations of LPS for up to 36 hr.

Role of PKC in the late phase of microvascular protection induced by preconditioning.

Introduction: We hypothesized that the late phase of microvascular protection induced by ischemic preconditioning or by adenosine is protein kinase C (PKC) dependent.

Materials And Methods: The cremaster muscle of male Sprague-Dawley rats underwent 45 min of ischemic preconditioning and, 24 h later, 4 h of warm ischemia followed by 60 min of reperfusion. To mimic the effects of IPC, adenosine (ADO; an adenosine receptor agonist) or 4-phorbol 12-myristate 13-acetate (PMA; a PKC activator) was delivered to the vascular network of the cremaster 24 h before the prolonged ischemia via local intra-arterial infusion.