Breath-holding pulmonary diffusing capacity was measured in four sub-jects at rest and during exercise in order to clarify the magnitude and the pattern of increase in diffusing capacity. Diffusing capacity increased from 29.5 m//min/ Torr at rest to 45.2 ml/min/Torr at the load of 130 watts in a linear fashion. In-crease in diffusing capacity per unit increase in energy expenditure was almost constant among subjects whether work intensity was expressed either in mechanical units or in terms of oxygen intake. In addition, the slope of diffusing capacity on oxygen intake was found to be approximately the same among subject groups, by comparison with other reports. This equation was described by DL (ml/min/Torr)=27.5 +0.008 Vo2 (ml/min) r=0.955 N=40 The slope of DL on Vc was also uniform among subjects and subject groups and the equation was as follows, <BRS> DL (ml/min/Torr)=14.2 +0.272 Vc (ml) r=0.885 N=39 This means that the unit change in DL caused by exercise always reflects the same unit change in Vc. The data on diffusing capacity and alveolar 02 tension obtained after a 4-s and an 8-s breath-holding period implied that effects of the hypoxic breath-holding on the uniform relations of diffusing capacity on energy expendi-ture and on pulmonary capillary blood volume were little even at a heavy work load. Although the mechanism by which diffusingcapacity increases during exer-cise was not made clear, it was suggested that a change in diffusing capacity re-flects the distensibility of pulmonary capillaries. It was concluded that the uniform slope of diffusing capacity on energy expenditure with a relatively wide range in intensity could be a basis for evaluation of the potential increase in pulmonary caPillary blood volume, instead of the traditional methods.
Polygraphic recordings of circadian sleep-waking rhythms of rats were made before and after swimming exercise which was loaded to the animals in the dark period. By visual inspection of the recordings, an exercise-induced increase in the amount of slow-wave sleep (SWS) was observed in the next dark period. In the dark period, 15 hours after the swimming, tryptophan (TRP), serotonin and 5-hydroxyindoleacetic acid (5-HIAA) in several regions of rat brain were measured to clarify the mechanisms of the exercise-induced increase in SWS. The concentrations of TRP and 5-HIAA in the midbrain of the exercised rats were significantly higher than in the control ones. The cortical level of 5-HIAA was also high in the exercise group. The serotonin levels in both the brain regions of the exercised rats were nearly the same with the control. From these results, it is inferred that the increased amount of SWS after the swimming exercise might be attributable to enhanced activity of serotonergic neurons in the midbrain and the cerebral cortex.
Cold-induced vasodilatation (CIVD) and systemic cardiovascular re-sponses due to local finger cooling were studied in 10 healthy subjects at different room (22 and 30°C), water (0, 5, and 10°) temperatures and immersion times (5to 30 min). The skin temperature of the immersed finger, blood pressure, and heart rate were measured before and during the experiments. Conspicuous CIVD com-parable to that at the 0°C test could be obtained even at a water temperature of 5 or 10°C by a rise in room temperature. Under such room and water temperature conditions where marked CIVD appeared, the order of the degree of CIVD in the individuals was almost the same, although the CIVD response was influenced by changes in the room and water temperatures. Furthermore, the order of the mean skin temperature (MSTi) calculated by shortening the immersion time every 1 min remained extremely stable (r > 0.90) even by more than a 20-min reduced immersion time, especially at a water temperature of 5°C. During several minutes after the start of immersion, maximal changes in blood pressure and discomfort due to cold were observed. The degree of these systemic loads in the subjects was reduced with rise in the water temperature. It is concluded that the current local cold tolerance test for 30 min at 0°C can be substituted sufficiently by a 5°C test for 10 to 15 min, and partly even by the 10°C test with the limitation that only MSTi and AT are available as an indicator of the local cold tolerance at higher environ-mental temperatures.
Hexane neuropathy is thought to be produced through the direct action of its metabolite, 2, 5-hexanedione (2, 5-HD), on nervous tissues. 7-Diketones in-cluding 2, 5-HD are reported to be neurotoxic, whereas α, β, and δ-diketones are reported to be not. Experiments were designed to investigate the specificity of the y-diketones in terms of pharmacokinetics. 2, 3-HD (a-diketone), 2, 4-HD (α-diketone), and 2, 5-HD (7-diketone) were tested in this study. Aqueous solutions containing 0.5% of each HD were administered to rats by gavage. HDs in blood, brain, and sciatic nerve were determined at specific intervals after gavage by the extraction method with chloroform or the direct injection method using gas chromatography-mass spectrometry. Examination of tissue distribution revealed that 2, 5-HD was not selectively re-tained by nervous tissues. However, 2, 5-HD had higher concentrations and much longer elimination times in both blood and nervous tissues than 2, 3-HD and 2, 4-HD. Therefore, for an identical dose, 2, 5-HD has a much larger effective dose (con-centration in tissue x time retained by tissue) than 2, 3-HD and 2, 4-HD. These results suggest that the specific neurotoxicity of the 7-diketones is due to their pharmackinetic specificity.
ECoG and AEP of male Sprague-Dawley rats were recorded to elucidate the effect of lead acetate on the central nervous system. Lead acetate (1.0 x 10-2M) in distilled water, 1 m//100 g body weight, was administered intraperitoneally for four consecutive days to an experimental group of rats. On the 11th day after injection, the rats were decapitated and the content of lead in the whole brain was measured in addition to the blood lead concentration and the hematocrit. The body weights and hematocrit values of rats in the experimental group decreased remarkably although they tended to recover by the end of the experimental period. The blood lead concentration of rats in the experimental group increased through-out the experimental period and their whole brain lead amount was twelve times that of the control group. No changes in the ECoG of rats given lead acetate were found in this experiment, but the changes in AEP of the rats in the experi-mental group were delayed P2 peak latency and increased P1-N1 peak to peak amplitude.
To study the effects of occupational exposure to Dichlorodiphenyltrichloroethane (DDT), 29 workers engaged in regular spraying of DDT were subjected to clinical evaluation, Bhatia battery performance test of intelligence, Wechsler memory scale and Bender visuomotor Gestalt test (BGT). DDT level in the sprayers was 8.5 times higher than the controls, suggesting heavy exposure. Visuomotor functions in the sprayers were significantly impaired and were suggestive of dominant frontoparietal lobe involvement. 55.5% sprayers with poor BGT performance had diffuse electroencephalographic (EEG) changes. BGT scores had a moderately significant relationship with DDT level in the sprayers. A possible role of DDT in the impairement of cognitive functions is suggested.
The effect of 54Mn and lead (Pb) interaction on their binding with various tissue proteins have been investigated. Pb was found to bind with low molecular weight glycoprotein in liver, brain and serum. The interaction of 54Mn+ Pb with the proteins in serum, liver and brain resulted in increased binding of both the metals, in comparison with that observed in the presence of either metal alone. Polyacrylamide gel electrophoresis patterns of serum, liver and brain pro-teins interacted with 54Mn+ Pb showed two distinct bands, one corresponding to 54Mn binding protein and the other to lead binding protein. There appears to be no competition of 54Mn and Pb for common binding sites, however, their combi-nation altered the affinity of tissue proteins to bind 54Mn and Pb, the mechanism of which remains to be clarified.