Mutsu Takamatsu

Activity of platelet-activating factor (PAF) acetylhydrolase in plasma from healthy habitual cigarette smokers

SummaryThe activity of platelet-activating factor acetylhydrolase, a specific metabolizing enzyme of platelet-activating factor (PAF), in plasma of 39 male subjects was determined radiochemically by the method of Stafforini et al., (1987) J Biol Chem 262: 4223–4230, to clarify to what extent PAF affects atherosclerotic disorders induced by habitual smoking. The subjects examined included 18 habitual smokers (mean age: 62±10.6 years) and 21 age-matched nonsmokers. Plasma PAF acetylhydrolase activity was higher in the smokers than in the nonsmokers. There was no difference between smokers and nonsmokers in platelet aggregability in response to PAF or ADP. A higher apoprotein B/apoprotein A-I ratio in smokers as compared to nonsmokers was the only manifestation of abnormal lipoprotein metabolism in the former group. In the smokers, plasma PAF acetylhydrolase activity was directly proportional to total cholesterol, LDL-cholesterol, triglyceride, apoprotein B, LDL-cholesterol/HDL-cholesterol or apoprotein B/apoprotein A-I, and inversely proportional to HDL-cholesterol or apoprotein A-I. The results obtained suggest that alterations in PAF acetylhydrolase levels result from a slightly abnormal lipoprotein metabolism. Determination of plasma PAF acetylhydrolase activity is useful to study the role of PAF in atherosclerotic changes induced by smoking.

Platelet‐activating factor acetylhydrolase activity in red blood cell‐stroma from patients with cerebral thrombosis

Platelet‐activating factor (1‐O‐alkyl‐2‐acetyl‐sn‐glycero‐3‐phosphocholine, PAF) is a bioactive phospholipid and inactivated by a specific enzyme, PAF acetylhydrolase (PAF‐AH). We have measured PAF‐AH activity in red blood cells (RBCs) from patients with a history of cerebral thrombosis and age‐matched healthy controls. The activities in 34 patients and 34 controls were 1.29 ± 0.28 and 1.64 ± 0.26 nmol/109 RBCs/min (or, 30.0 ± 5.8 and 35.1 ± 4.7 nmol/g protein/min) (mean ± SD), respectively, and the difference was significant (p < 0.001). In patients, RBC PAF‐AH activity correlated positively with RBC filterability, an index of RBC deformability (r = +0.501, p < 0.05). The RBC activity may play a role in scavenging oxidation products of membrane phospholipids. Lower RBC PAF‐AH activity may predispose to ischemic diseases by disturbing microcirculatory behavior of the RBCs.

Fibrinogen/Albumin Ratio: A Useful Indicator of Hemorheological Abnormalities in Observation of Cerebrovascular Disorders

Although the importance of local microcirculatory disturbances in thrombotic disorders has been generally recognized [1, 3, 5], clinical observations from the viewpoint of hemorheology have not been made intensively because of difficulties in the detection of changes occurring in the microcirculation. A high ratio of fibrinogen to albumin accelerates the erythrocyte aggregation in capillaries which is responsible for the occurrence of thrombotic diseases [1]. This study aims to establish the usefulness of the ratio of fibrinogen to albumin for observations of cerebrovascular disorders.