PubMed Health⌕ Search

Biomedical subjects

K Imataka

Publications and source records attributed to K Imataka.

At least 55 records · Page 3Linked to original sources
PubMed1987

Reflectance spectrophotometric measurement of in vivo local oxygen consumption in the cerebral cortex.

A simple method was developed to measure in vivo local oxygen consumption quantitatively in the brain cortex. Reflectance spectra of tissue hemoglobin at the brain's surface were measured for assessment of both local tissue hemoglobin content and its oxygen saturation. Local oxygen consumption was calculated from the spectral changes of tissue hemoglobin during complete cessation of blood flow by compression of the cortical surface in the suprasylvian gyrus with the tip of an optic probe. This procedure was performed without any brain damage and only took approximately 5 s. The calculated local oxygen consumption during this short period of compression remained constant for a few seconds. Then, it decreased rapidly, although the local tissue hemoglobin was not completely deoxygenated. The value of local cerebral oxygen consumption obtained by this method was 3.02 +/- 0.61 mL O2/100 g brain/min; it was not influenced by the change in systemic blood pressure. The effect of pentobarbital on cerebral oxygen consumption was also studied. At the stage of burst and suppression on electrocorticogram, cerebral oxygen consumption decreased significantly (p less than 0.001) to 1.03 +/- 0.07 mL O2/100 g brain/min.

Animals↗
PubMed1987

Effect of beta-adrenergic receptor blockade on atrial natriuretic peptide in essential hypertension.

Plasma levels of atrial natriuretic peptide (ANP) were measured in 32 untreated subjects with essential hypertension and in 31 patients undergoing long-term treatment with beta-blockers. Patients receiving beta-blockers had significantly higher mean plasma ANP levels (72.0 +/- 36.0 [SD] pg/ml) than did untreated hypertensive subjects (39.8 +/- 15.8 pg/ml; p less than 0.01) and healthy normotensive controls (33.9 +/- 16.6 pg/ml; n = 61, p less than 0.01), while the mean plasma ANP concentration in untreated hypertensive subjects was not statistically different from that in control subjects. Administration of atenolol, 50 mg/day, for 4 weeks to 10 untreated subjects resulted in a significant (p less than 0.001) rise in plasma ANP levels (from 38.8 +/- 9.5 to 68.7 +/- 20.6 pg/ml). In 31 patients undergoing long-term treatment with beta-blockers, multivariate regression analysis revealed that age, pretreatment mean blood pressure, and plasma concentration of cyclic 3',5'-guanosine monophosphate (cGMP) were significant predictors of plasma ANP levels. These results suggest that beta-adrenergic receptor blockade in patients with essential hypertension elevates plasma ANP levels with a concomitant rise in cGMP concentrations, and that increased ANP in plasma may play a role in the compensatory mechanism that operates in response to beta-adrenergic receptor blockade.

Acebutolol↗
PubMed1987

[Experimental production of mitral valve and papillary muscle lesions by cervical vagus stimulation in rabbits].

Mitral valve and papillary muscle lesions were experimentally produced in rabbits by cervical vagal stimulation or compression of the abdominal aorta. The involvement induced the similar findings to mitral valve prolapse in human beings including mid-systolic clicks and a late systolic or holosystolic murmur. Extrasystoles were also common. Necropsies disclosed papillary muscle swelling, bleeding and edematous change in the mitral valve, swelling of the myocardial cells and interstitial fibrosis. Further, bacterial endocarditis was induced in such rabbits by injecting pseudomonas alkaligenes. Possible connection of experimentally-induced lesions of the mitral complex and mitral valve prolapse in human beings was discussed.

Animals↗
PubMed1987

[The sequential changes of energy metabolism following cold-induced brain edema--a histochemical study].

The changes of energy metabolism on vasogenic edema have been largely examined using biochemical quantitative assay. However, the relationship between the sequential changes and blood-brain barrier (BBB) breakdown is not well understood. In the present study, the sequential changes of energy metabolism and potassium in relation to BBB breakdown following the cold-induced brain edema were investigated histochemically. Adult male Wistar rats, weighing 200-250g, were anesthesized with pentobarbital and a burr hole was made in the left parietal region. For evaluating the breakdown of BBB, 2.5% Evans blue (EB) was injected 30 min. before injury, except in the 5 min. model in which it was injected at the time of cold injury. An iron-bar precooled in liquid N2 was placed over the surface for 30 seconds and they were frozen in situ in liquid N2 at 5 min., 2 hrs., 6 hrs., 12 hrs., and 24 hrs., after producing the lesion. The frozen brain was sectioned using a precooled saw in the coronal plane. The brain section was placed in liquid N2 bath and illuminated with 366 nm light (UV) from a 200 watt mercury lamp and Corning filter 5840. NADH fluorescence was recorded photographically through Corning filter 3387 and 5562. Regional ATP and potassium content were investigated histochemically in thin sections with luciferine-luciferase method and Macallum's technique, respectively. At 5 min. after cold injury, leakage of EB was limited within the lesion. Potassium and ATP were decreased in the lesion. NADH fluorescence was increased slightly in the cortex around the lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1987

[Clinical validity of lumbar subarachnoid pressure measurement].

To evaluate the clinical usefulness for measuring lumbar subarachnoid pressure (LSP) as an index of intracranial pressure, the relation between LSP and epidural pressure (EDP) was studied by the cisternal saline infusion and bolus injection in 12 cats at the range of pressure up to 50 mmHg. In the steady state infusion (0.238 ml/min, 0.476 ml/min), the data from LSP and EDP were correlated very well and the LSP value was at least above 80-90% of EDP value at any pressure level. In the bolus injection (0.4 ml), the degree of pressure rise and the time course of both LSP and EDP were quite similar at any pressure level. However, the compliance calculated from the pressure change of LSP and EDP revealed to have a different tendency according to the baseline pressure level at bolus injection. Below 10 mmHg of EDP, the compliance calculated from LSP was usually higher that of EDP. This was considered due to the distensibility of spinal theca. But above 10 mmHg of EDP, the compliance of both LSP and EDP became almost equal and then gradually decreased as the elevation of baseline pressure at bolus injection. This was considered to be the result of disappearance of the distensible effect of spinal theca. In this study, two polyethylene tubes of different size (I. D. 0.45 mm, 0.58 mm) were used for spinal drainage tube to compare the pressure dumping effect of tube. However, on both tubes, the pulse pressure of LSP was usually smaller than that of EDP, with each having almost constant difference.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Exercise-induced QRS axis shift and its clinical significance.

Exercise tests occasionally induce a QRS axis shift. Reviewing single Master's two-step test electrocardiograms of 1810 patients, we examined the incidence of the QRS axis shift and the relations of the QRS axis shifts to ischemic heart disease. The QRS axis shift was 30 degrees or more to the right in 38 (2.1%), 15 to 29 degrees to the right in 304 (16.8%), less than 15 degrees to the right or to the left in 1375 (75.9%), 15 to 29 degrees to the left in 81 (4.5%), and 30 degrees or more to the left in 12 patients (0.7%). The frequency of positive Master's tests and clinical ischemic heart disease were both significantly greater in the patients with QRS axis shifts of 30 degrees or more to the right (15.8% and 26.3%, respectively) and the patients with those of 30 degrees or more to the left (33.3% and 50.0%, respectively) than in the patients with shifts less than 15 degrees (6.5% and 8.5%, respectively). These results indicate that the exercise-induced QRS axis shift is a useful clue for the diagnosis of ischemic heart disease.

Adolescent↗
PubMed1986

Peculiar mitral valve and papillary muscle lesions induced by vagus manipulations in rabbits. An experimental model for nonrheumatic mitral regurgitation.

Peculiar lesions of mitral valves and papillary muscles developed in 50 to 80% of rabbits after clipping (N = 38), crushing (N = 15) or electrical stimulation (N = 44) of their cervical vagi. Both right and left vagus manipulations induced similar cardiac lesions. The earliest manifestation was bleeding of the mitral leaflets, which was followed by swelling and fibrosis of the papillary muscles. Ventricular arrhythmias and systolic murmurs were frequently associated with the vagus manipulations. During or just after electrical stimulation of the vagus, ventricular premature contractions (VPCs) were observed in 30 of 44 animals. Twenty-nine of these 30 animals with VPCs (96.7%) were found to have mitral valve and/or papillary muscle lesions at autopsy, whereas only 5 of 14 animals without VPCs (35.7%) had the cardiac lesions. These results indicate that the occurrence of these ventricular arrhythmias during vagus manipulations was closely related with the mitral valve and papillary muscle lesions.

Animals↗
PubMed1984

Effects of steroid treatment on release of cardiac myosin light chain II in acute myocardial infarction in dogs.

The effect of methylprednisolone sodium succinate (MP) on release of myosin light chain II (LCII) from the myocardium was studied in experimental myocardial infarction (MI). Acute MI was produced in conscious, closed-chest dogs by ligating the left anterior descending coronary artery beyond the first diagonal branch. MP, 30 mg/kg, was administered intravenously just before and 24 hours after MI. After MI, LCII levels in the serum were determined serially up to 240 hours. MI size was determined histologically 10 days after MI. In the MP group, LCII levels in the serum within 72 hours were lower than in the control, and cumulative LCII release for 3 days decreased from 530 +/- 159 to 310 +/- 101 ng/ml (mean +/- standard deviation) (p less than 0.001). However, the peak LCII level appeared later (control vs MP, 63 +/- 27 vs 122 +/- 25 hours, p less than 0.001), and the peak LCII level and cumulative LCII release for 10 days were not decreased by MP treatment. MI size also was not reduced by MP (11.0 +/- 4.4% vs 11.8% +/- 4.5% of the left ventricle, difference not significant). Since the rate of disappearance of LCII is rapid and was not affected by MP, these results suggest that MP treatment early after acute MI delays breakdown of myosin filaments, but cannot prevent it.

Acetylglucosaminidase↗