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Biomedical subjects

K Shirato

Publications and source records attributed to K Shirato.

At least 271 records · Page 15Linked to original sources
PubMed1988

The effect of sustained stellate ganglion stimulation on left ventricular contractility in the dog.

Although a progressive reduction in left ventricular contractility during sustained left stellate ganglion stimulation has been well documented, there have been no reports on the contractile state after nerve stimulation. Left ventricular contractility after cessation of 60 min of electrical (10 V. 10 Hz. 1 msec) left stellate ganglion stimulation has been assessed in open chest dogs. Before and 15 min after stimulation, left ventricular contractility was evaluated by the end-systolic pressure-segment length relationship using ultrasonic crystals during a stepwise aortic constriction to increase left ventricular afterload. Restimulation of the left stellate ganglion was also performed 15 min after cessation of the first stimulation. After sustained left stellate ganglion stimulation, the end-systolic points shifted to the right from the control and the slope of multiple pressure-segment length coordinates significantly decreased (102.5 +/- 16.1 to 76.5 +/- 10.2 mmHg/mm, mean +/- S.E., p less than 0.05, n = 5), indicating a depression of left ventricular contractility. Increased left ventricular dP/dt max and norepinephrine level in the coronary sinus gradually returned to near base line during 60 min of stimulation. These reduced responses lasted for at least 15 min after cessation of stimulation. The myocardial norepinephrine content was reduced to 0.59 +/- 0.08 (mean +/- S.E.) ng/mg wet tissue from 0.90 +/- 0.15 of the control level (p less than 0.05). These data suggested that left ventricular contractility decreased after sustained cardiac sympathetic nerve stimulation, probably due to norepinephrine reduction in the myocardium.

Animals↗
PubMed1987

The degree of increment in plasma catecholamines in patients with mitral stenosis by mild exercise.

Although sympathetic excitation during mild exercise may readily occur in patients with mitral stenosis (MS), the degree of increment in plasma catecholamines has not been fully investigated. We imposed mild ergometric exercise (50 watts, 300 kg/min for 5 minutes) on five patients with mild MS (mitral valve area greater than or equal to 1.0 cm2) and eight with severe MS (mitral valve area less than 1.0 cm2) while they were undergoing cardiac catheterization. In patients with severe MS, total plasma catecholamine levels during exercise were remarkably higher (2821 +/- 783 [SEM] pg/ml) than in those with mild MS (957 +/- 113 pg/ml, p less than 0.05) and in seven control subjects (612 +/- 75 pg/ml, p less than 0.05). This marked increment could not be predicted by heart rate response, which did not differ between severe and mild MS (166 +/- 5 vs 153 +/- 10 bpm). In contrast with catecholamine change, the cardiac index in severe MS showed a very small increment. Results suggest that mild daily exercise can remarkably increase plasma catecholamine levels in severe MS, and this may accelerate various complications of this disorder.

Adult↗
PubMed1986

Juxtacardiac pressure in closed-chest dogs.

We studied pressure (Ppc)-volume (Vpc) relationships of the pericardial sac by inserting air into it at constant end-diastolic heart volume in six dogs. The lungs were inflated by positive alveolar pressure while pleural pressure was monitored using the esophageal balloon technique. Ppc-Vpc relationships were measured at transpulmonary pressures (PL) of 30, 10, and 5 cmH2O in each of three states: closed chest, open chest with lung separation, and open chest with the pericardium dissected free of its mediastinal attachment. Ppc in the closed-chest condition was more positive than Ppc in the open chest with lung separation, with increase of Vpc and PL, which suggests that the lungs compress the pericardium. Ppc in the open-chest condition with lung separation was also more positive than Ppc in the pericardium after it was dissected free, which suggests that mediastinal attachment compresses the pericardium. It is suggested that lungs in the closed-chest condition as well as mediastinal attachment reduce the heart expansion by a similar magnitude.

Animals↗
PubMed1983

Assessment of the magnitude of aortic regurgitation by dye injection into the descending aorta.

A technique simpler than the angiographic method for estimating aortic regurgitant volume was tried with 31 patients with aortic insufficiency. During cardiac catheterization, we injected dye into the descending aorta while recording the dye dilution curve in the left ear. The distance between the aortic arch and the tip of the catheter at the lowest point from which the injected dye could be detected in the left ear was rated in terms of the number of corresponding vertebral bodies. This "distance score" closely correlated with the regurgitant stroke volume and with the fraction to total stroke volume, which were measured by angiocardiography (r = 0.927, p less than 0.001; and r = 0.900, p less than 0.001, respectively). The correlation coefficients of the aortographic grade to those parameters were not as high as they were in the relationship of the score to the same parameters. Therefore, these results indicate that the "distance score" is a practical method for assessing the magnitude of aortic regurgitant volume.

Adolescent↗
PubMed1983

Influence of the pericardium on left ventricular diastolic pressure-volume curves in dogs with sustained volume overload.

The pericardium is largely responsible for displacement of the left ventricular diastolic pressure-volume curve observed after acute volume loading in dogs. Likewise the pericardium has been considered likely to play a role in displacement of the curve in patients with acute cardiac failure and in shifts following manipulation of afterload. This study was designed to examine the influence of the pericardium on the diastolic pressure-volume relation of the left ventricle when volume load is more sustained, a setting relevant to observations made in patients with heart failure. We measured left ventricular pressure and volume in six conscious dogs with sustained volume overload (mean left ventricular end-diastolic pressure 21 mm Hg, left ventricular end-diastolic volume 149% of the upper limit of normal for our laboratory) produced by aortocaval shunt created 7 to 29 days earlier. Simultaneous left ventriculograms and pressures were obtained before and during nitroprusside infusion with the pericardium intact and in four dogs the studies were repeated 7 to 15 days after pericardiectomy. In all six dogs with intact pericardium, nitroprusside displaced the entire pressure-volume curve downward whereas after pericardiectomy, the pressure-volume data points obtained before and during nitroprusside infusion fell on a single curve. These results were similar to those previously reported for acute volume overload. Nitroprusside did not alter the time course of left ventricular pressure fall during the isovolumic period of diastole either before pericardiectomy (28.8 +/- 10.2 sec,-1, 28.4 +/- 11.9 sec-1) or after (28.8 +/- 6.7 sec-1, 26.1 +/- 7.2 sec-1). These data indicate that in dogs subjected to volume overload sustained for periods of up to 29 days, the pericardium affects the left ventricular diastolic pressure-volume curve and contributes to the elevation of left ventricular filling pressure through upward displacement of this curve.

Animals↗
PubMed1983

The effect of pericardium on the end-systolic pressure-segment length relationship in canine left ventricle in acute volume overload.

The effect of the pericardium on the end-systolic pressure-segment length relationship in the left ventricle was examined with an ultrasonic miniature gauge in open-chest dogs. In 12 dogs, blood was infused until left ventricular (LV) end-diastolic pressure reached about 20 mm Hg, and then the pericardium was opened widely. In the other 12 dogs a pericardiectomy was performed without blood infusion. Stroke volume was measured in six dogs in the former group and in seven dogs in the latter group. After blood infusion, LV systolic, end-systolic, and end-diastolic pressures increased from 120 +/- 14 to 162 +/- 16 mm Hg (mean +/- SD), from 106 +/- 13 to 146 +/- 17 mm Hg, and from 8 +/- 2 to 19 +/- 2 mm Hg, respectively (all p less than .01). End-systolic and end-diastolic segment lengths increased from 8.9 +/- 2.1 to 10.6 +/- 2.2 mm and from 11.6 +/- 2.5 to 14.9 +/- 2.7 mm, respectively (both p less than .01). After pericardiectomy, the segments were further lengthened by 8.9 +/- 4.4% and by 10.0 +/- 6.2%, respectively (both p less than .01). Heart rate, LV systolic and end-systolic pressures, and peak positive dp/dt did not change, although end-diastolic pressure fell from 19 +/- 2 to 18 +/- 2 mm Hg (p less than .01). Stroke volume rose from 13.1 +/- 3.7 to 23.9 +/- 5.0 ml due to volume loading and further increased by 26.7 +/- 9.0% after pericardiectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effects of oxygen breathing on pulmonary vascular input impedance in patients with pulmonary hypertension.

The effect of oxygen breathing on the stiffness of the large pulmonary artery has not been elucidated. We analyzed the proximal pulmonary arterial impedance with a multisensor catheter in ten patients with pulmonary arterial hypertension (PAH), eight patients with pulmonary venous hypertension, and six control subjects. The stiffness of the vessel was quantified by the characteristic impedance (Zo) and compared with the plasma norepinephrine level. Ten minutes of high-oxygen breathing decreased the Zo (from 78 +/- 18 to 57 +/- 14 dynes.sec.cm-5, p less than 0.01) and pulmonary arterial resistance in all the cases with PAH. In this group, norepinephrine also decreased (from 381 +/- 89 to 319 +/- 77 pg/ml, p less than 0.01) following the correction of hypoxemia. Yet, those parameters did not change in the other two groups. These results indicate that in patients with PAH, oxygen breathing can reduce the stiffness of the main pulmonary artery because of the sympatholytic effect.

Biomechanical Phenomena↗
PubMed1982

The effect of pericardium on the diastolic properties of the heart--experimental studies on volume load and on acute ischemia in open chest dogs.

We studied the effect of the pericardium on the end-diastolic pressure-segment length (P-L) relation in volume loading (Experiment I) and in acute ischemia (Experiment II). Experiment I: In 6 open chest dogs, segment length of left and right ventricles were measured using ultrasonic crystals during blood infusion. Drawing end-diastolic pressure (P, on ordinate) against segment length (L, on abscissa), the P-L curve with pericardium positioned upward compared to that without pericardium. The slopes (b) of the exponential curve (P = aebL) with pericardium were steeper than those without pericardium in both ventricles. The difference between the slopes with and without pericardium was significantly larger in the right ventricle (RV, 0.30 +/- 0.10, mean +/- SEM) than in the left ventricle (LV, 0.05 +/- 0.02, p less than 0.05). These results show that the pericardium inhibits the distensibility of the free wall more in RV than in LV, and enhances a mechanical coupling of both ventricles during volume over-load. Experiment II: In 8 open chest dogs, segment lengths of ischemic and non-ischemic regions in LV were measured after left circumflex coronary occlusion. When the segment lengths and LV pressure became stable, a pericardiectomy was performed. After the pericardiectomy, whereas heart rate and LV systolic pressure did not change, end-diastolic segment length in the ischemic region further lengthened (12.0 +/- 0.2 to 12.5 +/- 0.2 mm, p less than 0.01) and that in the non-ischemic region did not change despite the concomitant fall in LV end-diastolic pressure (EDP, 11.9 +/- 0.6 to 9.8 +/- 0.6 mmHg, p less than 0.01). These results suggest that the pericardium alters the LV end-diastolic pressure-volume relation and is one of the factors contributing to an increase in LVEDP during acute ischemia.

Animals↗
PubMed1978

Alteration of the left ventricular diastolic pressure-segment length relation produced by the pericardium. Effects of cardiac distension and afterload reduction in conscious dogs.

Left ventricular pressure and segment length were measured in seven conscious chronically instrumented dogs with the pericardium intact and 3-9 days after pericardiectomy. Diastolic pressure-length plots were obtained under control conditions and after acute volume loading followed by sodium nitroprusside infusion. In all dogs with intact pericardium, volume loading displaced the entire diastolic pressure-length curve upwards and sodium nitroprusside shifted it toward control. After pericardiectomy the pressure-segment length data during control, volume loading and sodium nitroprusside fell on a single curve (intercepts and slopes not statistically different); After dextran infusion, intrapericardial pressure rose from control 1.5 +/- 0.7 mm Hg to 8.2 +/- 0.5 mm Hg, and it fell to 4.8 +/- 0.1 mm Hg after nitroprusside. Therefore, in acute cardiac dilatation the pericardium contributed significantly to the increased left ventricular diastolic pressure and to the fall during sodium nitroprusside infusion and appeared responsible for shifts in the diastolic pressure-segment length relation.

Animals↗
PubMed1978

Cineventriculographic analysis of the ventricular septal motion during stimulation of various pacemaker sites.

By means of cineventriculography, contraction pattern of the ventricular septum was studied during electrical stimulation of the right atrium (RA), outflow tract (RVO) and apex (RVA) of the right ventricle and apex (LVA) and lateral wall (LVL) of the left ventricle. RA pacing produced a monophasic shortening of the septal hemiaxes after initial lengthening for about 40 msec from R wave of ECG. In contrast, ventricular stimulation near the septum (i.e. RVO, RVA and LVA) resulted in a biphasic and decreased contraction of the septal wall, in which an early preejection shortening was followed by a brief lengthening and second shortening. LVL pacing showed a monophasic and increased contraction of the septal wall. The biphasic motion of the septal wall was likely to be related to the abnormal mechanical contraction caused by the abnormal conduction sequence of ventricular depolarization. On the other hand, the lateral wall demonstrated a biphasic and decreased contraction during LVL pacing, and a monophasic and increased contraction during RVO, RVA and LVA pacing. Thus, the biphasic and diminished contraction at the site of electrical stimulation was compensated by the monophasic and forceful contraction of the contralateral wall. It is considered that the ventricular septum plays an important functional role in regulation of cardiac performance.

Animals↗