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Biomedical subjects

B Takase

Publications and source records attributed to B Takase.

69 records · Page 4Linked to original sources
PubMed1988

The role of prostacyclin during exercise in patients with chronic angina pectoris.

To determine changes in platelet activity, prostaglandin metabolism and catecholamine release along with changes in hemodynamics during exercise, we measured these parameters before and immediately after treadmill exercise. Measurements were made on peripheral arterial blood simultaneously with a direct aortic pressure recording in 30 patients with coronary artery disease (Group 1), in 20 patients without significant coronary disease (Group 2), and in 11 young healthy volunteers as controls. At the peak of the exercise regimen, the ST segment depression was found to be significantly lower in Group 1 than in Group 2, whereas the changes in the DPTI/TTI ratio in Group 2 and the controls decreased with the increase in the duration of exercise. The increased serum lactate level at the intermediate level of exercise (420 +/- 20 sec) was significantly lower in the controls than in the other 2 groups. Changes in beta thromboglobulin, platelet factor 4, and plasma norepinephrine were similarly increased in all 3 groups by exercise. At the termination of exercise, however, 6 keto-prostaglandin F1 alpha in Group 1 was insignificantly elevated, whereas it increased from 42.9 +/- 7 pg/ml to 55.7 +/- 7.1 (p less than 0.05) in Group 2 and from 38.2 +/- 5.7 pg/ml to 45.1 +/- 6.8 (p less than 0.01) in the controls. These results suggest that decreased prostacyclin production in the vessel wall might be an indicator of myocardial ischemia, and that the administration of prostacyclin may modulate the coronary vascular tone exaggerated by exercise.

Adult↗
PubMed1987

Effects of treadmill and pacing stress testing on peripheral arterial thromboxane, platelet function and catecholamine activities in patients with chronic coronary artery disease.

Two different methods of causing myocardial oxygen demand and supply imbalance; symptom limited treadmill exercise and right atrial pacing stimulation, were used to examine the alteration of hemodynamics and the effects upon sympathetic nerve activities, platelet functions and prostaglandin synthesis in patients with coronary artery disease (CAD). Age and sex distributions, the cardiothoracic ratio, left ventricular end-diastolic pressure, ejection fraction and coronary artery obstructions of the patients did not differ significantly between the two tests. Arterial blood samples were obtained to assay for plasma catecholamine, beta-thromboglobulin (beta TG), platelet factor 4 (PF4), TXB2 (thromboxane B2) and 6 keto-PGF1-alpha (6 ketoprostaglandin F1-alpha) without any difficulties before and immediately after testing. The arterial systolic pressure and pressure rate product (PRP) were changed more significantly by treadmill exercise than pacing, while the DPTI/TTI (diastolic pressure time index/tension time index) ratio and ST segment deviations showed similar changes with both tests. The plasma NE (norepinephrine) level, beta TG, PF4, and TXB2/6 keto-PGF1-alpha were significantly elevated by treadmill exercise, but not by pacing. 6 keto-PGF1-alpha was not markedly affected by either tests. There were no significant differences between the patients with and without anginal pain either in hemodynamics or metabolites. Significant relationships were observed between changes in plasma NE levels and the PRP (r = 0.76, n = 26, p less than 0.01) and also changes in the arterial systolic pressure (r = 0.64, n = 26, p less than 0.01), but there were no significant correlations between any other hemodynamic parameters with plasma NE, platelet function, prostaglandin activity, or between each metabolite.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[Regional coronary outflow and coronary reserve assessed by the thermodilution technique: an experimental study].

Coronary blood flow distribution and coronary flow reserve were experimentally evaluated by the thermodilution technique. Using a special catheter with two external thermistors 5 cm apart, the great cardiac vein (GCV) outflow and coronary sinus (CS) outflow were measured. Coronary inflows in the left anterior descending (LAD) and circumflex (LCX) arteries were measured by electromagnetic flow probes during arterial occlusion or bolus arterial injection of nitroglycerin and dipyridamole injection in a peripheral vein. On the LAD side, the venous flow due to the interventions increased both GCV and CS outflows, while the interventions in the LCX increased CS outflow without significant changes in the GCV flow. LAD inflow and GCV outflow, and LCX inflow and (CS-GCV) flow correlated well, and there were significant close correlations between each inflow and outflow. Coronary reserve in the LAD and LCX was studied in successive 70% and 90% stenoses produced by a calibrated constrictor. Maximal coronary flow was obtained during reactive hyperemic response after coronary artery occlusion. Although there was no significant coronary reserve in the coronary inflow or outflow in the basal state, coronary reserve in the GCV and CS decreased significantly in stenoses of the LAD and LCX. These results suggest that this method allows practical assessment of drainage from the LAD and LCX areas and that stenosis greater than 70% can be estimated from the changes in regional venous outflows. This method may be helpful in evaluating regional coronary hemodynamics clinically.

Animals↗
PubMed1985

[Effects of percutaneous transluminal coronary angioplasty on left ventricular function at rest and during exercise].

The effects of percutaneous transluminal coronary angioplasty (PTCA) on left ventricular function at rest and during stress test were examined. Effect of PTCA at rest We studied 10 patients who fulfilled the following criteria, 1) single vessel disease, 2) high grade stenosis in the left anterior descending artery, 3) successful PTCA, 4) no restenosis, 5) without electrocardiographic evidence of previous myocardial infarction, and 6) technically adequate left ventriculograms in both pre and post PTCA studies. Follow-up studies were done six months after PTCA. Filling fraction as an index of early diastolic function was significantly lower than that of normal controls. There were no significant changes in left ventricular end-diastolic pressure, peak dp/dt, negative peak dp/dt, ejection fraction, left ventricular systolic pressure/end-systolic volume, between pre- and post-PTCA studies. Filling fraction in a jeopardized area, which was supplied by the left anterior descending artery, increased significantly after PTCA. No significant change was observed in the inferior area. Effect of PTCA during stress test A contrast stress test in eight successful cases without restenosis was performed by injecting 0.7 ml per kilogram of contrast material (76% urografin) at a rate of 13 ml/sec into the left ventricle before and six months after PTCA. The left ventricular end-diastolic pressure increased to 20.1 +/- 3.8 mmHg during stress test before PTCA, and only to 14.3 +/- 5.3 mmHg after PTCA (difference highly significant). Before the procedure, negative peak dp/dt during stress test was 1782 +/- 358 mmHg/sec; it increased significantly to 2342 +/- 702 mmHg/sec after PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon↗
PubMedDate not supplied

Assessment of left ventricular volume by an ambulatory radionuclide monitoring system during head-up tilt in patients with unexplained syncope: relation to autonomic activity assessed by heart rate variability.

BACKGROUND: Decreased left ventricular volume during head-up tilt plays an important role in triggering syncope in patients with neurally mediated syncope. However, precise changes in left ventricular volume during head-up tilt have not been well investigated. This study was conducted to test the hypothesis that the decline in left ventricular volume during tilt could trigger ventricular mechanoreceptor activation. METHODS AND RESULTS: To investigate the mechanisms of tilt-induced syncope, we measured the temporal changes in left ventricular volume, ejection fraction, cardiac output, and heart rate variability indices during head-up tilt in 25 patients with syncope of undetermined etiology. Eleven patients had a cardioinhibitory response (CI group), 7 patients showed a vasodepressor response (VD group), and 7 patients demonstrated a negative response (NG group). Before syncope, ejection fraction increased most in the CI group, the left ventricular end-diastolic volume declined most in the VD group (VD group, -11.0% +/- 3.3%; CI group, -2.8% +/- 4.8%; NG group, -3.4% +/- 2.2%; P <.005), and the high-frequency spectra increased most in the CI group (CI group, 25.0% +/- 21.0%; VD group, -4.1% +/- 11.7%; NG group, -5.3% +/- 12.7%; P <.01). The vasodepressor response was dependent on left ventricular volume, whereas the cardioinhibitory response was related to the vagal activity reflected by high-frequency spectra. CONCLUSIONS: The precise evaluation of left ventricular volume by an ambulatory radionuclide monitoring system combined with a heart rate variability analysis is considered useful for clarifying the pathophysiology of neurally mediated syncope.

Adult↗
PubMedDate not supplied

Determining the temperature distribution of swine aorta with simulated atheromatous plaque under pulsed laser irradiation: an experimental attempt to detect the vulnerability of atherosclerosis.

We developed a method to determine the temperature distribution of swine aortas with simulated atheromatous plaques in order to measure the temperature of atherosclerotic lesions. The inflammation associated with temperature elevation is considered to be one of the aggravating mechanisms of atherosclerosis resulting in fissuring or rupture of atheromatous plaques. The temperature distribution of plaques covered by fibrous caps cannot be measured by conventional thermistors. Indocyanine green (ICG) solution was injected into the subintima of swine aorta to simulate the light absorption coefficient of human atheromatous plaques. The temperature distribution was calculated from measured temperature changes of the aortic intima under pulsed laser irradiation. The aorta was heated from the adventitial side with a halogen lamp to simulate the temperature elevation derived from inflammation. The temperature distribution of the aorta was obtained by solving the heat transfer equation using the surface layer thickness (corresponding to the fibrous cap thickness). The surface layer thickness can be calculated using the following working formula: D(microm)=1363-398DeltaTs+35DeltaTs(2), where AT, denotes intimal surface temperature change under pulsed laser irradiation. The calculated temperature of the ICG layer (corresponding to the atheromatous core) correlated well with the measured temperature (r=0. 97, p<0.0001).

Animals↗
PubMedDate not supplied

Development of a continuous temperature mapping system using a deep body thermometer.

To determine continuous body temperature distribution, an inexpensive temperature mapping system was developed using a deep body thermometer adopting the finite-element method. A stripe with 16 thermocouples was wrapped around the waist of rats to measure body surface temperatures (the boundary conditions). The abdominal deep temperature of the rats was measured from the dorsum using the thermal compensation probe of a deep body thermometer. The abdominal temperature of the rats was mapped by solving a heat conduction equation using surface and deep temperatures obtained in real time. The temperature measured with a thermocouple inserted into the abdominal centre of the rats correlated well with the calculated temperature (r = 0.93, p < 0.01). The system is low cost and simple to use compared with the magnetic resonance temperature mapping system. Our temperature mapping system could potentially result in improved management of patients in critical care medicine.

Abdomen↗
PubMedDate not supplied

Non-invasive estimation of arterial blood pH using exhaled CO/CO2 analyser, microwave radar and infrared thermography for patients after massive haemorrhage.

In order to conduct non-contact estimation of arterial blood pH after massive haemorrhage, we calculated the arterial pH based on linear-regression analysis of exhaled gas concentrations (CO and CO2) and vital signs (heart rate, respiratory rate, and surface temperature) measured using non-contact methods in hypovolemic animals.

Acidosis↗