Biomedical subjects

K Hirose

Publications and source records attributed to K Hirose.

At least 487 records · Page 27Linked to original sources

PubMed1979

Effects of intraaortic balloon counterpulsation on regional myocardial function during acute coronary occlusion in the dog.

The effects of intraaortic counterpulsation on regional myocardial function were studied using ultrasonic dimension gauges in 24 open chest dogs. Pairs of ultrasonic crystals were implanted in the subendocardium of the left ventricle in control, marginally ischemic and ischemic segments. After coronary arterial occlusion, the end-diastolic length of all three segments was increased. Segment shortening was rapidly replaced by systolic expansion in the ischemic segment. In the marginal segment, active shortening decreased by 53% and, in the control segment, shortening was augmented by compensatory operation of the Frank-Starling mechanism. Balloon pumping initiated 10 minutes after coronary occlusion resulted in an increase in mean aortic diastolic pressure from 103 to 115 mm Hg without any significant change in peak systolic pressure. In the marginal segment, end-diastolic length decreased by 3%, and previously reduced shortening increased to 82% of control value, deteriorating again with discontinuation of counterpulsation. Balloon pumping produced no change in the dyskinetic motion of the ischemic segment but caused compensatory augmentation of shortening of the control segment. Thus, counterpulsation selectively improved segment function of the marginally ischemic segment, presumably as a result of a regional increase in myocardial blood flow and in availability of oxygen due to augmented perfusion pressure. The systolic unloading effect was counterbalanced by improved cardiac performance.

Acute Disease↗

PubMed1979

Dynamic geometry of the left atrium and left ventricle in acute mitral regurgitation.

The instantaneous transverse diameter of the left atrium, left ventricular free wall segment length (SEG), and the long axis of the anterior papillary muscle (APM) length were measured throughout the cardiac cycle, using ultrasonic dimension gauges together with left atrial and left ventricular pressures in 12 open-chest dogs. During atrial contraction, left atrial diameter decreased from 19.7 to 18.7 mm, while left ventricular dimensions increased simultaneously. During ventricular ejection, percent shortening was 26% in SEG and 10% in APM, while atrial diameter increased continuously to 20.5 mm, with a concomitant rise in the v wave of left atrial pressure. After normal mitral valve opening, left atrial diameter decreased rapidly simultaneously with the y descent of atrial pressure. Graded mitral regurgitation was then produced by sectioning the chordae tendineae. With moderate mitral regurgitation, end-diastolic length of the SEG increased by 27%, while extent of shortening (delta L) was augmented by 96%. End-diastolic length of the APM increased by 7%, and delta L was augmented by 60%. Left atrial pressure was sharply elevated, with a distinct a wave followed by the more prominent v wave. End-diastolic diameter of the left atrium was enlarged to 22.9 mm with increased atrial shortening and expansion. As mitral regurgitation was increased to a severe degree by additional chordal rupture, end-diastolic length and delta L continued to increase both in SEG and APM. Left atrial pressure was further elevated (a wave 25 mm Hg and v wave 47 mm Hg). Left atrial end-diastolic diameter further increased in 24.9 mm. However, the amplitude of left atrial shortening and expansion decreased remarkably. In severe mitral regurgitation, isoproterenol and nitroprusside decreased left atrial pressure and diameter, restoring more forceful atrial shortening.

Acute Disease↗

PubMed1979

HLA in hypertrophic cardiomyopathy and rheumatic heart disease.

1. HLA antigens were determined in 30 Japanese patients with hypertrophic cardiomyopathy. Several antigens were more common in patients compared with controls, but statistically significant differences were not evidenced. In families one and two, six of seven kindred who inherited HLA-A9 and B7 had the disease. None of five kindred lacking HLA-B7 showed evidence of the disease. In families three and four, affecting family members had HLA-A2 and BW-35. Our finding suggest that the HLA system may play some role in the pathogenesis of hypertrophic cardiomyopathy with familial occurrence. 2. Twenty patients with rheumatic valvular heart disease were also studied. There was no significant difference in frequencies of HLA antigens between patients and controls.

Adolescent↗

PubMed1979