PAF molecular heterogeneity: pathobiological implications.

The existence and potential (patho)physiologic significance of PAF molecular heterogeneity can no longer be summarily dismissed or ignored. While significant advances in the chemistry of PAF have been made, the (patho)physiologic behaviors of most of the PAF molecular species of biologic origin await further study. This is because to date, investigators have studied the biologic activities of what was previously thought to be PAF, i.

Cardiopulmonary and intravascular alterations during the sustained infusion of PAF.

The physiologic responses during prolonged exposure to platelet activating factor (PAF) are largely unexplored. Thus, the cardiopulmonary and intravascular effects of a sustained infusion of 1-O-hexadecyl-2-acetyl-sn-glycero-3- phosphocholine (C16:0-AGEPC; 0.159 nmole/kg/min for 120 min) were characterized in anesthetized rabbits.

Platelet activating factor in pulmonary pathobiology.

Platelet activating factor (PAF) is a potent phospholipid mediator of inflammation that has been gaining increasing attention because of its pathophysiologic effects upon the lung. In particular, PAF stimulates pulmonary hypertension, ventilatory alterations, bronchoconstriction, airway hyperreactivity, and pulmonary inflammatory cell accumulation and edema in a variety of experimental animals and in humans. These observations promote the speculation that this unique phospholipid likely is involved in similar tissue responses during the course of human lung disease.

Mechanism of functional residual capacity increase in haemorrhagic shock.

Shock was elicited in anaesthetized dogs by maintaining a haemorrhagic hypotension of 4 kPa until 30 per cent spontaneous refusion, followed by total reinfusion. Functional residual capacity (FRC) and minute ventilation increased considerably similarly to our previous experiments. Lactate content in both the external intercostal and the biceps femoris muscles increased significantly in advanced shock.

Increase of functional residual capacity in hemorrhagic shock.

Functional residual capacity (FRC) was measured by body plethysmography in anesthetized dogs subjected to hemorrhagic shock. This was elicited by bleeding the animals to a mean arterial blood pressure of 4 kPa. Reinfusion was done at 30% spontaneous uptake of the maximal bleeding volume.