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Biomedical subjects

Y Mizoi

Publications and source records attributed to Y Mizoi.

At least 73 records · Page 4Linked to original sources
PubMed1983

Acetaldehyde-mediated alcohol sensitivity and elevation of plasma catecholamine in man.

According to the presence and absence of aldehyde dehydrogenase (ALDH) I isozyme which had low Km for acetaldehyde, subjects were divided into two groups: the former, the usual ALDH group and the latter, the unusual ALDH one. Blood alcohol and acetaldehyde levels, plasma norepinephrine and epinephrine levels, and urinary excretion of norepinephrine, epinephrine, dopamine, vanillylmandelic acid (VMA) and 3-methoxy-4-hydroxyphenylglycol (MHPG) were determined; and the differences in these values and cardiovascular symptoms after alcohol intake between the two groups were investigated. Fifty-six healthy male volunteers were studied after they ingested 0.4 g of alcohol per kg of body weight. There was no difference in blood alcohol level between the two groups. In the unusual ALDH group, facial flushing, increase of pulse rate and decrease in diastolic blood pressure associated with accumulation of blood acetaldehyde were shown. In addition, rises in plasma catecholamine and urinary excretion of catecholamine were also observed. However, in the usual ALDH group, in which blood acetaldehyde level scarcely increased, these changes were not significant. The alteration of catecholamine metabolism, decrease in urinary VMA and increase in urinary MHPG was recognized in both groups.

Acetaldehyde↗
PubMed1980

Individual differences in blood and breath acetaldehyde levels and urinary excretion of catecholamines after alcohol intake.

Sixty three male Japanese, aged 20-40 yr were evaluated as to the degree of facial flushing following a controlled dose of ethanol either as Japanese rice wine or ethanol 0.4 g kg body weight. Thirty four subjects responded with overt facial flushing. The acetaldehyde levels in blood and expired air were significantly higher in the flushing group without a change in ethanol elimination rate. Urinary excretion of Vanilmandelic acid (VMA) and 3 methyoxy-4-Hydroxyphenylglycol (MHPG) are reported.

Acetaldehyde↗
PubMed1979

Relationship between facial flushing and blood acetaldehyde levels after alcohol intake.

Normal subjects were divided into two groups, i.e., those showing, and those not showing, facial flushing after consuming a small amount of alcohol. In the flushing group, increases of pulse rate, facial skin temperature and carotid arterial pressure and blood flow rate, as well as changes of digital plethysmogram and electrocardiogram, were found together with a conspicuous rise in blood acetaldehyde levels after the drinking. However, significant changes of the signs as mentioned above and elevation of blood acetaldehyde did not occur in the non-flushing group. The maximum blood alcohol levels and the rate of alcohol elimination showed not difference between these two groups. Furthermore, urinary excretions of epinephrine and norepinephrine increased in the flushing cases after the drinking.

Acetaldehyde↗
PubMed1976

Isolated corticotrophin-deficiency found through alcohol-induced hypoglycemic coma.

A case of hypoglycemic coma after alcohol ingestion was observed in a chronic alcoholic. Upon close examination isolated corticotrophin-deficiency was found. It is suggested that ethanol-induced hypoglycemia may be consistent with dysfunction of mitochondria in hepatic cells and that there may be disorder of the hypothalamus in the chronic drinker.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Impairment of cerebral bloodflow by chest compression.

A 5-year-old boy had his chest compressed by the moving belt of an escalator for about 10 to 15 minutes. The patient suffered seizures and was unconscious for eight months. The clinical and histological findings are reported, and compared with the findings of experiments on fatal chest compression in rabbits.

Accidents↗
PubMedDate not supplied

Impact-induced intracranial pressure caused by an accelerated motion of the head or by skull deformation; an experimental study using physical models of the head and neck, and ones of the skull.

An impact incurred by the movable head may bring about a change in intracranial pressure and this change may play an important part in the occurrence of the cerebral contusion. We have carried out the following experiments to determine whether the intracranial pressure change was attributed to an accelerated motion of the head or to a skull deformation. In the blow experiment in which the head was accelerated, a positive peak in the intracranial pressure was recorded immediately after impact at the impact site and a negative one at a site opposite the impact. In the one in which the skull could be deformed, the intracranial pressure curves at both sites contained harmonics. The modal analysis revealed an inbending in the frontal and occipital regions of the skull and an outbending in the parietal and temporal regions immediately after impact, followed by a reverse deformation. Regarding the intracranial pressure change, positive pressures were recorded in the frontal and occipital regions immediately after impact, followed by a negative one. This study demonstrated that the positive and negative peaks were caused by the accelerated motion of the head, and that the curve of the intracranial pressure changes contained harmonics which were caused by the deformation of the skull.

Acceleration↗
PubMedDate not supplied

Differences in the intracranial pressure caused by a 'blow' and/or a 'fall'--an experimental study using physical models of the head and neck.

In cases of a severe head injury caused by a fall, coup contusions are either absent or very minor, in contrast to presence of extensive contre-coup damage. In cases of a severe blow to head, however, the reverse occurs, with contre-coup lesions a rarity and coup damage extensive. To investigate this further, head injuries caused by a 'blow' or a 'fall' have been studied, using physical human models of the head and neck, both filled with distilled, degassed water and fixed onto a dummy torso. An impact of a constant magnitude was applied to the midoccipital region in 'blow' and 'fall' experiments, and the acceleration of the head and changes in the intracranial pressure were measured, with the resulting data analyzed by a computer. In both experiments, the peak amplitude of the acceleration pulse were almost the same. Similarly, the intracranial pressure curve at the impact site consisted of a positive pulse that hardly differed, nor did the peak amplitude of that pulse vary significantly. In the 'blow' experiment, however, the intracranial pressure curve at the site opposite the impact consisted of a negative pulse, whereas in the 'fall' experiment, the intracranial pressure recorded at the same area was negative but of a longer duration, with an absolute value that was slightly greater. Our results indicate that an impact to the head triggers a different response in the intracranial space, dependent on whether that impact force was caused by a 'blow' or a 'fall'.

Acceleration↗
PubMedDate not supplied

Polymorphism of aldehyde dehydrogenase and ethanol elimination.

The influence of polymorphism of aldehyde dehydrogenase (ALDH) on ethanol elimination was investigated. Japanese healthy male volunteers were divided into two groups, i.e., a normal ALDH group of 52 subjects with the low Km isozyme of ALDH, and a deficient group of 48 subjects without it. The subjects of the normal group were given 0.4, 0.8, 1.2, 1.6 or 2.0 g/kg of ethanol, while those in the deficient group ingested 0.4, 0.8 or 1.2 g/kg of ethanol. Widmark's factors (beta 60, Co and r) and ethanol elimination rate (ER) were compared between the two groups. In the deficient group, beta 60 and ER were not clearly elevated with the increase of ethanol dose, while those in the normal ALDH group increased depending on the blood ethanol level. Blood acetaldehyde level was elevated with the increase of the ethanol dose in the deficient group, but not in the normal group. In the experiment of the repeated ingestion of ethanol in the deficient group, the second peak of blood acetaldehyde level was lower than that of the first one.

Acetaldehyde↗