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Biomedical subjects

Y Kamiyama

Publications and source records attributed to Y Kamiyama.

At least 217 records · Page 12Linked to original sources
PubMed1981

Differences in predominant energy substrate in relation to the resected hepatic mass in the phase immediately after hepatectomy.

Changes in the energy substrate utilized by the remnant liver after hepatectomy were studied in relation to the hepatic energy status in 25%, 70%, and 93% hepatectomized rabbits. In 25% hepatectomized rabbits, the energy charge ((ATP + 1/2ADP)/(ATP + ADP + AMP)) level of the remnant liver remained unchanged after hepatectomy and was not affected by portal infusion of (+)-octanoylcarnitine, an inhibitor of fatty acid oxidation. In contrast, the energy charge level of the remnant liver decreased rapidly after 70% hepatectomy and reached the lowest level of 0.77 at 12 to 24 hr after hepatectomy (p less than 0.01). At this time, the energy charge level was further decreased to 0.45 by (+)-octanoylcarnitine (p less than 0.001). It returned to near normal 4 days later. At this time, the effect of (+)-octanoylcarnitine was less evident, with the restoration of the energy change. In 93% hepatectomized rabbits, the energy charge level of the remnant liver decreased rapidly and steeply in the phase immediately after hepatectomy. It is suggested that the remnant liver metabolism switches to predominant utilization of fatty acid as an energy source when the energy charge decreases; it then becomes able to utilize glucose with the restoration of energy charge level. In addition, it is emphasized that hyperosmolar glucose solution or insulin administration during the early period after major hepatectomy should be reconsidered because of their inhibition of the mobilization of free fatty acid from adipose tissue.

Animals↗
PubMed1981

Pathophysiology of hemorrhagic shock. II. Anoxic metabolism of the rat liver following acute blood loss in the rat.

Changes in energy metabolism of rat liver in hemorrhagic shock were investigated. The hepatic energy charge level (0.24-0.693) correlated significantly with the mean arterial blood pressure (20-75 mmHg) (r = 0.931, P less than 0.001), as well as the blood volume withdrawn (2.43-2.82 ml/100 g body weight) which, in turn, correlated with the various mortality rates (LD16, LD50, and LD84) (r = -0.728, P less than 0.01). As shown by the changes in adenylate energy charge levels, the liver was very sensitive to acute blood loss. There was no significant difference between the energy charge levels of liver obtained in situ from rats with 84% mortality after hemorrhage and that of the same liver further incubated in vitro in the absence of O2 (0.304 versus 0.235). From these results, it appears that the energy status in the liver of rats dying from severe hemorrhagic shock has changed to anaerobic metabolism, which may not be sufficient to maintain adequate liver function or support individual survival.

Acute Disease↗
PubMed1981

Pathophysiology of hemorrhagic shock. A role of arterial ketone body ratio as an index of anoxic metabolism of the liver in acute blood loss.

The changes in the oxido-reduction state and the adenylate energy charge of the liver were investigated in rats having 16%, 50%, and 84% mortality rates after acute hemorrhage. In the arterial blood, concentrations of ketone bodies, pyruvate, lactate, and the ratios (acetoacetate to beta-hydroxybutyrate and pyruvate to lactate) were measured after hemorrhage and reinfusion of the shed blood. The mitochondrial oxido-reduction state and the blood ketone body ratio decreased 15 minutes after hemorrhage. The values of these parameters of rats having the higher mortality rate were lower than those rats having the lower mortality rate. In addition, the changes in both the adenylate energy charge and the mitochondria oxido-reduction state of the liver were closely correlated with the changes in the ratio of acetoacetate to beta-hydroxybutyrate in the arterial blood (P less than 0.001). Thus, it is suggested that the decreased oxygen supply to the liver mitochondria may play an important role in determining the mortality rate after acute hemorrhage and is reflected in the ratio of acetoacetate to beta-hydroxybutyrate in the arterial blood.

Acute Disease↗
PubMed1978

Ultrastructural study on kidney cell injury following various types of shock in 26 immediate autopsy patients.

In acute renal failure in man following shock and trauma, an amazing discrepancy was found between the complete breakdown of renal function and the very modest histological and ultrastructural changes in "immediate autopsy" patients, even in those who sustained septic shock. Although, from this limited number of studies no satisfactory interpretation of the pathogenesis of acute renal failure can be deduced from the structural changes found, the findings do indicate that hypoxia plays a key role in aggravating the structural changes that induce permanent cell damage in man following shock of various etiologies including septic shock.

Adolescent↗
PubMed1977

Comparison of subcutaneous and intraportal insulin administrations on adenylate energy charge of the liver in diabetic rats.

Effects of subcutaneous and intraportal administrations of insulin on adenine nucleotide metabolism of the liver and oxidative phosphorylation of the isolated mitochondria were investigated in alloxan-diabetic rats. The diabetic rats were classified into two groups according to the severity of impaired insulin response to oral glucose: diabetic rats with only minor impairment of insulin response and those with severely defective response. The energy charge levels (ATP + 1/2ADP)/(ATP + ADP + AMP) of the liver both groups were not significantly different from those of controls. In the first group, the oxidative phosphorylation of liver mitochondria was within normal limits and was enhanced significantly by subcutaneous administration 4 U. of insulin (p less than 0.005). In the secong group, the mitochondrial oxidative and phosphorylative activities were inhibited severely and did not recover even with subcutaneous administration of 20 U. of insulin. Intraportal administration of insulin doses (4 to 8 U.) insufficient for normalization of hyperglycemia produced a decrease in the energy charge of the liver to a considerably lower level than normal (p less than 0.01), whereas larger doses (20 U.) of insulin raised the energy charge to normal levels, with a concomitant recovery of mitochondrial oxidative phosphorylation. It is suggested that subcutaneous administration of insulin is effective for hepatic energy metabolism only if insulin response to glucose loading is still present but that only intraportal administration of insulin can exert a beneficial effect in diabetic rats without insulin response.

Adenine Nucleotides↗