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Biomedical subjects

T Omae

Publications and source records attributed to T Omae.

At least 379 records · Page 21Linked to original sources
PubMed1976

Congenital oculoskeletal myopathy with abnormal muscle and liver mitochondria.

We report a 22-year-old very thin man, who showed various symptoms and signs of oculoskeletal muscle weakness, episodes of myalgia, prolonged diarrhea, severe myopia, perceptive deafness, electrocardiographic and electroencephalographic abnormalities, and endocrinological abnormality. The onset was at about 3 months of age and a positive family history was strongly suggested. The light-microscopic, histochemical and electron-microscopic findings showed abnormal mitochondria not only in the skeletal muscle, but also in liver cells. From the clinical as well as morphological points of view, this case was suspected to be one of congenital oculoskeletal myopathy probably due to an unidentified systemic metabolic disorder.

Heart↗
PubMed1976

Cerebral lactate, pyruvate and ATP concentrations, and arterial acid-base balance at various time intervals following bilateral carotid artery occlusion in normotensive and spontaneously hypertensive rats.

Cerebral lactate, pyruvate and adenosine triphosphate (ATP), and arterial acid-base balance were measured in normotensive rats (NTR) and spontaneously hypertensive rats (SHR) at various time intervals following bilateral carotid occlusion. In SHR, a great and progressive increase in cerebral lactate and lactate/pyruvate ratio (L/P) ratio) during the first 5-6 hours after occlusion was followed by a gradual decrease as the time interval increased. Cerebral ATP in SHR decreased as cerebral lactate increased, and an inverse relationship was observed between lactate and ATP. On the other hand, in NTR, there were minimal changes in cerebral lactate and L/P ratio following carotid occlusion. These results suggest that bilateral carotid occlusion might cause severe ischemic damages of the brain in SHR, but not in NTR. The hemodynamic factor as a cause of cerebral ischemia in hypertensives is discussed.

Acid-Base Equilibrium↗
PubMed1976

Mortality and cerebral metabolism after bilateral carotid artery ligation in normotensive and spontaneously hypertensive rats.

Mortality and cerebral glycolytic metabolism were studied after bilateral ligation of the common carotid artery in normotensive Wistar rats (NTR), and spontaneously hypertensive rats (SHR) derived from Wistar strain. In the first 24 hours after occlusion of carotid arteries, 72 per cent of 108 SHR died, whereas it was fatal in only 16 per cent of 43 NTR. In SHR, cerebral lactate and cerebral lactate/pyruvate ratio (L/P ratio) increased by 12.4 and 12.1 times the control, respectively at five to six hours after ligation, and remained raised even in rats surviving for two to three days thereafter. Changes in cerebral lactate and L/P ratio were minimal in NTR. Cerebral ATP decreased markedly at five to six hours after ligation in SHR studied. These results indicate that bilateral carotid artery ligation causes severe brain damage in SHR but not in NTR, suggesting hypertension per se to be operative for the development of cerebral ischaemia.

Acid-Base Imbalance↗
PubMed1976

Blood fibrinolytic activity and fibrinoid necrosis of small arteries in the rats treated with renal cortical extract.

In order to determine the role of fibrinolytic system in the production of fibrinoid necrosis, blood fibrinolytic activities were measured in the rats nephrectomized and administered with the subcellular fractions (lysosomal or microsomal fraction) of the rat kidney cortical extract. Tissue plasminogen activator was present in both fractions and blood fibrinolytic activity was increased in the rats so treated. But fibrinoid necrosis in pancreatic and mesenteric small arteries was observed only in those administered lysosomal fraction. Direct relationship between the increase of blood fibrinolytic activity and the aggravation of the vascular degeneration could not be observed in this experiment.

Animals↗