International comparison of odor threshold values of several odorants in Japan and in The Netherlands.

The purpose of this paper is to compare the published odor threshold values of six odorants. In Japan, all of the odor threshold values used in the Offensive Odor Control Law (enacted in 1972) were determined in an odor-free room (4 m3) by a trained panel (20 men, ages 30-45 years who were perfumers) who sniffed the odors directly and made absolute judgments of odor quality and intensity. In The Netherlands, sensorial odor concentration measurements were made with an olfactometer in a mobile sniffing car with eight panelists, four men and four women, ages 18-40 years. Such presentations are repeated with different dilution ratios. Comparison of the threshold data for the six different compounds given as the barely perceptible concentration level revealed striking similarities for hydrogen sulfide (in Japan 0.0005 ppm/in The Netherlands 0.0003 ppm), phenol (0.012/0.010), styrene (0.033/0.016), toluene (0.92/0.99), and tetrachloroethylene (1.8/1.2) but not for m-xylene (0.012/0.12). Such a similarity was not found with any other literature sources.

Normalization by dietary cod-liver oil of reduced thrombogenesis in essential fatty acid deficient rats.

Rats, deficient in essential fatty acids (EFA), were given diets containing 5 energy% sunflowerseed oil (SO, rich in linoleic acid), cod-liver oil (CLO, rich in timnodonic acid and cervonic acid), or hydrogenated coconut oil (HCO), containing no EFAs at all. SO and CLO feeding resulted in normalization of the reduced arterial thrombus formation in EFA-deficient animals. SO feeding was associated with the normalization of the arachidonic acid content of platelet phospholipids. CLO feeding did not have this effect but greatly increased the availability of timnodonic acid (EPA) and cervonic acid (DHA). Further research is required to investigate whether these changes in fatty acid composition can be hold responsible for the normalizing effect of dietary CLO on the disturbed arterial thrombosis tendency in EFA deficient rats, possibly via the formation of eicosanoids.

Prostacyclin-formation by the rabbit aorta: relation to atherosclerosis.

The Prostacyclin (PGI2)-formation of the aortic vessel wall of normal and of atherosclerotic rabbits was measured by punching out and incubating small pieces of the vessel wall. In atherosclerotic rabbits the pieces taken from plaques produced more PGI2 than pieces taken from normal areas nearby. In addition, distinct differences were seen between different regions of the aorta. An investigation in normal rabbits of the regional distribution of the PGI2-producing capacity between the aortic valve and the bifurcation showed the highest production at places where the earliest and most severe atherosclerotic changes were observed in the atherosclerotic animals.

Normal Hoffmann reflex latencies (H-M interval) in relation to age and body length.

The effects of age and body length on the Hoffmann reflex (H-M interval) was evaluated. 179 normal subjects (15-75 y, 150-200 cm) were tested. The normal upper limit (M + 2SD) of the H-M interval ranges from 22.0 ms (male, 155 cm, 20 y) to 34.3 ms (female, 195 cm, 70 y). The limit of 28 ms, that is often mentioned, holds only for young adults with a body length of less than 175 cm. Moreover it proved that a normal limit of the H-M interval asymmetry of less than 2 ms is too strict. For a mixed population less than 3 ms seems to be a safer upper limit for normal asymmetries.

Influence of dietary linoleic acid on the prostacyclin-production of the isolated pulsatingly perfused rabbit aorta.

Dietary prevention of atherosclerosis and its risk factors by linoleic acid is an easy, safe and important way. In the rabbit, which develops an atherosclerosis similar to the human disease, we looked for effects of a linoleic acid-rich diet (25 en percent) on the formation of arachidonic acid metabolites in the vessel wall and in blood platelets because atherosclerosis is thought to be caused by a change in this balance. For measuring the PGI2-release of the vessel wall we used the model of the isolated pulsatingly perfused aorta, which is described in detail. Both dietary groups of healthy male Dutch rabbits did not show any difference in the formation of arachidonic acid metabolites or in their balance. With 25 en percent linoleic acid the phospholipids contained more linoleic acid and less oleic acid, while arachidonic acid tended to decrease.

The role of arachidonate lipoxygenase and fatty acids during irreversible blood platelet aggregation in vitro.

Arachidonic acid is converted by blood platelets into thromboxane A2 (TXA2) and 12-hydroxyeicosatetraenoic acid (12-OH-C20:4). TXA2 causes platelet aggregation, but the physiological role of 12-OH-C20:4 on blood platelets is not known. The formation of 12-OH-C20:4 by washed platelets can be inhibited by eicosatetraynoic acid at a concentration of 0.7 mumol/l; TXA2-formation is not yet influenced at this low inhibitor concentration. Under these conditions, the irreversible 1-14C arachidonic acid-induced blood platelet aggregation is converted into a reversible type of aggregation. Similar results are obtained by addition of any long-chain fatty acid (20-30 mumol/l), including 12-OH-C20:4 and arachidonic acid, as well as by addition of sulfhydryl reagents. However, in these experiments no inhibition of the arachidonic acid conversion is observed. The results can be explained by a "sticking together" of the blood platelets caused by 12-OH-C20:4 generation. This effect is based on the same principle as that of the chemotactic effect of 12-OH-C20:4 on leucocytes as described by Turner et al. (Nature 257; 680-681, 1975). The explanation is supported by experiments with platelets obtained after ingestion of aspirin. ADP-induced reversible aggregation of three platelets becomes irreversible after addition of arachidonic acid. Irreversible platelet aggregation occurs only during endogenous 12-OH-C20:4 generation in consequence of a "sticking-together" process. This process coincides with a stimulation of the platelet guanylate cyclase.