Search PubMed⌕ Search

Biomedical subjects

M Fujishima

Publications and source records attributed to M Fujishima.

At least 847 records · Page 47Linked to original sources
PubMed1980

Response of cortical and pial arteries to changes of arterial CO2 tension in rats--a morphometric study.

Changes of the internal (d) and external diameter (D) of cerebral arteries in response to the various levels of arterial pCO2 were studied in anesthetized rats, of which brains were frozen in situ with isopentane cooled in liquid nitrogen. The parietal cortex was fixed with osmium tetroxide and stained with toluidine blue for morphometry of the cerebral arteries. In comparison with control animals (pCO2 = 41.2 mm Hg), the d/D ratio in animals with hypercapnia (pCO2 = 69.9 mm Hg) was increased by 11.7% in the pial arteries and 7.9% in the cortical arteries, indicating vasodilatation. In contrast, the d/D ratio in those with hypocapnia (pCO2 = 27.7 mm Hg) was decreased by 6.2% and 13.0%, respectively, indicating vasoconstriction. There was a significant linear correlation existing between the d/D ratio of either pial or cortical arteries and pCO2. It is concluded that the cortical arteries respond to changes of arterial pCO2 in a similar manner to the pial arteries.

Animals↗
PubMed1980

Stroke-prone spontaneously hypertensive rats as an experimental model of malignant hypertension. I. A light- and electron-microscopic study of the brain.

A pathological study of the brain of the stroke-prone spontaneously hypertensive (SHRSP) rats revealed development of fibrinoid necrosis of the wall of the intracerebral arterioles. These arterioles were frequently accompanied by occlusion of the lumen, and occasionally intracerebral hemorrhages and mincroinfarcts. The predominant tissue alteration consisted of rarefaction and cyst formation in the white matter, and rarefaction of the neuropil and preserved neurons in the neocortex at the paramedian region of the cerebral hemispheres. Edema fluid was present in and around the lesions. The tissue degeneration can be interpreted to be the sequela of brain edema. Microinfarcts or hemorrhages are only focal lesions, and are assumed to have minor contribution to the brain swelling. Widespread expansion of the extracellular space is assumed to be responsible for the brain swelling. Overall vascular changes of the brain, kidney, and other organs were consistent with those found in malignant hypertension.

Animals↗
PubMed1980

Brain blood flow and mean transit time as related to aging.

Brain blood flow and mean transit time were measured in 41 normotensive control subjects aged from 21 to 76 years by using the intravenous 131I-RISA external counting method. The results showed a significant prolongation of mean transit time and a tendency to increase in brain blood volume relating to advancing age but no change in the blood flow. This indicates that prolonged transit time in the aged is probably due to the increased brain blood volume.

Adult↗
PubMed1979

Effects of long-term antihypertensive treatment on brain metabolism after bilateral carotid artery occlusion in spontaneously hypertensive rats.

The effects of antihypertensive treatment on brain metabolism after bilateral carotid occlusion were studied in spontaneously hypertensive rats. The results indicate that an increase in metabolites of ischaemic brain such as lactate and the lactate/pyruvate ratio after carotid occlusion in spontaneously hypertensive rats is apparently suppressed by treating hypertension. This suggests that hypertension may play an important role in susceptibility to cerebral ischaemia.

Adenosine Triphosphate↗
PubMed1978

Brain metabolism and arterial acid-base balance following bilateral carotid occlusion in normotensive and experimental hypertensive rats.

The effects of bilateral common carotid artery occlusion on brain metabolism and arterial acid-base balance were studied in normotensive and experimental renovascular hypertensive rats. One hour after carotid occlusion in hypertensive rats, supratentorial lactate increased to 383% and lactate-pyruvate ratio to 280% of the controls, while adenosine triphosphate (ATP) decreased to 69%. These metabolic changes were thought to be due to cerebral ischemia. Arterial pCO2 was lowered and the pH was raised in the hypertensive animals due to cerebral ischemia induced hyperventilation. In the normotensive rats, carotid occlusion had minimal effects on cerebral metabolism and arterial acid-base balance. These results suggest that hypertensive rats are more susceptible to cerebral ischemia caused by carotid occlusion than normotensive rats. Increased cerebrovascular resistance in hypertension is discussed as a causal factor in cerebral ischemia.

Acid-Base Equilibrium↗
PubMed1977

An ultrastructural study of developing cerebral infarction following bilateral carotid artery occlusion in spontaneously hypertensive rats.

An ultrastructural study of cerebral infarcts in spontaneously hypertensive rats 1--5 h after bilateral carotid artery occlusion was performed. The alteration of the neocortex consisted of shrinkage of the neurons surrounded by swollen astrocytic processes. Distension of the rough endoplasmic reticulum of the neuronal cytoplasm appeared early, while changes of the mitochondria were slight. Though there appeared slight to moderate perivascular astrocytic swelling, endothelial swelling was rare and there was no severe narrowing of the capillary lumen. There were no filling defects of colloidal carbon injected to the blood vessels of the ischemic brains. Ischemic neuronal alterations were proved to develop in the absence of severe morphological changes of the microvasculature in the developing cerebral infarcts in the present experimental model.

Animals↗
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↗