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Biomedical subjects

E Ino-oka

Publications and source records attributed to E Ino-oka.

5 recordsLinked to original sources
PubMed1997

On an ambulance stretcher suspension concerned with the reduction of patient's blood pressure variation.

The design process and control of an ambulance stretcher suspension to reduce patient's blood pressure variation (BPV) is discussed. The BPV caused by applying the vehicle brakes may lead to deterioration of a patient's condition. The proposed method can reduce BPV by tilting the stretcher and counterbalancing back-to-front acceleration of the ambulance with gravity. The experimental results obtained when using a manually controlled stretcher confirm that BPV is reduced by tilting the stretcher. A continuous control method that varies the tilting angle is investigated through simulation analysis. The results show that this control method reduces the BPV effectively and achieves safe transport of the patient.

Acceleration↗
PubMed1986

The changes in ECG ST segment and mechanical function of regional ischemic myocardium during afterload reduction in isolated dog hearts with coronary stenosis.

By measuring ECG ST segment deviation and regional mechanical dysfunction, we assessed the effects of an alteration in afterload pressure on regional myocardial ischemia due to a partial coronary occlusion of the left circumflex coronary artery (CFX). Eight isolated, perfused and paced dog hearts were loaded with an artificial arterial system which simulated the aortic input impedance of the dog arterial tree. Afterload pressure was altered by stepwise changes in peripheral resistance (Rp), while left ventricular end-diastolic pressure (LVEDP) and heart rate were kept constant. Coronary perfusion pressure (CPP) was kept equal to mean aortic pressure (AoP). ECG and myocardial systolic segment shortening (SS) were measured in both areas perfused by the CFX and the left anterior descending coronary artery (LAD). In the presence of CFX stenosis, mean AoP decreased from 96 +/- 7 to 46 +/- 7 mmHg following a decrease in Rp and cardiac output increased progressively from 465 +/- 30 to 1055 +/- 100 ml/min. In this situation, CFX coronary blood flow decreased from 75 +/- 2 to 28 +/- 6 ml/100 g/min. Epicardial ECG in the ischemic region showed two types of ST segment deviation after CFX stenosis: ST segment elevation and ST segment depression. Moreover, following afterload reduction, these individual ECG ST segment changes showed further deviations. The levels of mean AoP, below which further ST segment deviations significantly occurred, were as follows: 71 +/- 6 mmHg in ST segment elevation cases and 52 +/- 7 mmHg in ST segment depression cases. Myocardial systolic segment shortening in the ischemic region also significantly decreased following CFX stenosis (91 +/- 8% of pre-ischemic control, p less than 0.05). Then, during afterload reduction, SS in the CFX area appeared to be bimodal and it definitely decreased when mean AoP was 46 +/- 7 mmHg. To enhance the sensitivity of detection of further mechanical dysfunction throughout afterload reduction following regional myocardial ischemia, we calculated percentage values of the SS in the CFX area to the SS in the LAD area at each Rp. By this normalization, mechanical dysfunction was found when mean AoP was below 67 +/- 5 mmHg. These results suggest that reduction in afterload pressure below a certain level aggravated the regional ischemia, despite an increase in cardiac output, and to detect this change in the ischemic region during afterload reduction, ECG ST segment deviation seems to be a useful indicator.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

ST segment changes under occlusion of the proximal portion of major coronary arteries in the isolated canine heart.

We studied the mechanisms of ST segment displacement in the ECG recorded from the epi- and subendocardium of ischemic ventricles in the isolated and perfused canine heart. ST segment changes were observed in association with a relatively large area of ischemia produced by occlusion of the left anterior descending and septal arteries (LAD + Sept.) or of the left circumflex artery (LCx). Contrary to previous reports, we found that the amount of subendocardial ST elevation was not always greater than that in the epicardial ECG recorded at the center of ischemia. Also, in the non-ischemic area, the degree of the ST depression in the subendocardial record was nearly the same as the epicardial record. On the other hand, the degree of the epicardial ST elevation on the border zone was always smaller than that at the ischemic center, which seemed to be due to the broadness of the border zone. The amplitude of the ST depression in the non-ischemic area was greater when the recording electrode was near the ischemic border, which supports the solid angle theory. The degrees of both ischemic ST elevation and reciprocal ST depression in the LCx perfused area were always greater than in the LAD + Sept. perfused area. These results strongly suggest that ST segment displacement depends on the relative position of the recording electrode to the electric double layer which exists at the border between the ischemic and non-ischemic area.

Animals↗
PubMed1984

Experimental study on vasodilator therapy and its clinical application.

To evaluate the effects of vasodilator therapy, the quantitative relationships between peripheral resistance, LVEDP, coronary circulation and cardiac output were analyzed by using 23 isolated coronary perfused canine heart which afterload, preload, coronary blood flow and heart rate are able to regulate independently. Peripheral resistance was decreased incrementally to lower mean arterial pressure from 107-97 mmHg to 48-22 mmHg keeping preload and heart rate at constant level. A decrease in mean arterial blood pressure to 72 ( physiologically coronary perfused heart) and 68 mmHg (coronary stenosed model) increased cardiac output, respectively. However, myocardial oxygen consumption in each group decreased under 5.5 ml/min/100g LV which suggested myocardial ischemia worsen and further decrease in blood pressure lowered cardiac output. LVEDP also decreased incrementally from 18-20 mmHg to 5 mmHg keeping afterload at 100 mmHg of mean arterial blood pressure constantly. A decrease in LVEDP from 20 to 14 mmHg reduced stroke work index in normal heart but increased slightly in failing heart. Further lowering in LVEDP resulted decreasing in stroke work index in both group. Thus modest and adequate reduction in preload and afterload has beneficial effects to cardiac function. In contrast, further decrease will worsen myocardial perfusion and cardiac function.

Animals↗