[Tachycardia, dyspnea, edema of the legs and incomplete paralysis of all extremities (ECG and glycosuria): (diabetes mellitus, ventricular aneurysm and arterioslcerosis)].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Haneda.
Explore the source record for details and available documents.
Plasma catecholamine (CA) levels in the coronary sinus (CS), aorta (Ao) and femoral vein (fv) were simultaneously measured in 22 patients with various heart diseases at rest and during handgrip exercise (IHG). The mean resting levels of plasma norepinephine (NE) in CS, Ao and FV were 359 +/- 49 (SEM) pg/ml, 290 +/- 27 and 234 +/- 24, respectively. The corresponding values of epinephrine (E) were 127 +/- 18 pg/ml, 186+/- 30 and 97 +/- 11, respectively. The E values in Ao were significantly greater than those in CS and in FV (p less than 0.05). IHG exercise induced an obvious elevation of plasma CA levels in every portion of the circulation studied. The mean increments of NE concentration were 81%, 54% and 67% of the resting levels at CS, Ao and FV, respectively, while IHG induced elevation of E were 70% of the resting values at each portion studied. Significant correlations were observed between individual CA concentrations in CS and in Ao, and also between those in Ao and in FV at rest. Under raised sympathoadrenal conditions, however, individual values of NE in CS failed to correlate signficantly to those in Ao and in FV, respectively. The NE output from CS was limited to only 3% and 5% of those in Ao at rest and during IHG, respectively. An actual mean increment of NE on its passing through the coronary circulation was only 2% or less of NE output in ao at both stages. It appears, thus, to be untenable that the cardiac tissue is one of the major source of circulating CA at physiological condition. From these reasons, the direct measurement of NE levels in CS may be mandatory, when plasma CA assay is designed for the purpose of studying the role of the sympathetic nerve activity in the regulation of cardiac function.
Respiratory changes in pleural pressure were recorded simultaneously from the left and right pleural spaces in 6 anesthetized closed-chest dogs in the supine, prone, left lateral and right lateral positions. Saline-filled radiopaque catheters connected to strain-gauge manometers were inserted percutaneously in the left and right pleural spaces by an air tight technique and their tips were placed in the mid-thoracic plane. The esophageal pressure was also recorded with the saline-filled system. The value of respiratory pressure amplitude (deltap, the difference between end-expiratory and minimal inspiratory pressures) in the pleural spaces was significantly greater in the left thorax than in the right in the supine, prone and right lateral positions. In 4 body positions, deltap in pleural pressure was significantly greater than in esophageal pressure. It is concluded that respiratory variations in pleural pressure of the left and right thorax are not the same and that postural change does not produce significant regional difference of the respiratory variations.
The hemodynamic effects of the site of the artificial cardiac stimulation were studied in 17 open chest dogs. The right atrium and five ventricular sites (the inflow and outflow tracts and apex of the right ventricle, apex and lateral wall of the left ventricle) were stimulated electronically at a given rate, ranging from 130 to 190 per min. When cardiac performance during ventricular pacing was compared with those during right atrial pacing, the former uniformly caused a diminution of cardiac output and systemic blood pressure, without reduction of left ventricular end-diastolic pressure. Ventricular function curves, in which left ventricular stroke work was related to left ventricular end-diastolic pressure, shifted downwards and to the right during ventricular pacing. Stimulation frequency did not alter these variables. It was considered that the left ventricular dysfunction in ventricular pacing resulted from the absence of atrial contribution to ventricular filling, mitral regurgitation present and asynchronous ventricular contraction. No significant difference of cardiac performance was demonstrated by changing the site of ventricular pacing, suggesting that the mode of ventricular depolarization itself was not relevant to a decrease in cardiac performance.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effects of long-term treatment with nipradilol, a nitroester-containing beta-blocker, on casual and 24-hour blood pressures were studied in 70 patients with mild-to-moderate essential hypertension. Antihypertensive effects of nipradilol on casual blood pressure were observed in 68% of patients. Nipradilol reduced pulse rates, but no bradycardia was observed. The usefulness of nipradilol in the present study was 65%. The results of ambulatory blood pressure monitoring indicated that nipradilol reduced systolic blood pressure more than diastolic blood pressure, and reduced blood pressure during waking more than during sleep. These results suggest that nipradilol is a safe and useful long-term antihypertensive drug in both young and older patients with mild-to-moderate essential hypertension. When administered twice daily, nipradilol is effective throughout a 24-hour period.
In order to evaluate the relation of cardiac norepinephrine (NE) release to left ventricular function, blood was taken simultaneously from the coronary sinus (CS) and the aorta (A) in 19 patients with heart diseases, at rest and during isometric handgrip exercise (IHG) at 30% of their maximal contraction. Plasma NE was analyzed by Renzini's THI method. The concentrations of plasma NE at rest were 397 +/- 66 (S.E.M.) ng/liter in CS and 292 +/- 50 in A. IHG significantly increased NE to 578 +/- 88 in CS and to 462 +/- 85 in A (p less than 0.001). Estimated NE release from the heart (deltaNE = NECS - NEA) correlated inversely to left ventricular end-diastolic pressure at rest (r = -0.520, p less than 0.05) and during IHG (r= -0.689, p less than 0.01). The changes in deltaNE induced by IHG correlated to the slope of the left ventricular function curve (r=0.618, p less than 0.01). It is concluded that the response of cardiac NE release to exercise is reduced in patients with depressed cardiac function.
The effects of bunazosin on the ischemic myocardium were investigated in isolated, perfused working rat hearts. Ischemia decreased the pressure-rate product and tissue adenosine triphosphate and creatine phosphate levels. Reperfusion did not restore the pressure-rate product nor the adenosine triphosphate levels completely. Bunazosin (5 x 10(-7) and 5 x 10(-6) mol/L) preserved the levels of adenosine triphosphate and creatine phosphate after 20 minutes of ischemia and increased the extent of recovery of the pressure-rate product during reperfusion. The results suggest that bunazosin protects the myocardium against ischemic damage.
Primary cultures of neonatal cardiac myocytes were used to determine the effects of tumor-promoting phorbol esters on ribosomal RNA (rRNA) synthesis during myocyte growth. Treatment of myocytes with phorbol-12, 13-dibutyrate (PDBu) increased protein accumulation by 25% and RNA content by 20%. Rates of rRNA synthesis were measured to assess the mechanism by which rRNA accumulated during myocyte growth. Rates of rRNA synthesis were determined from the incorporation of [3H]uridine into UMP of purified rRNA and the specific radioactivity of the cellular UTP pool. After 24h of PDBu treatment, cellular rates of 18S and 28S rRNA synthesis were accelerated by 67% and 64%, respectively. The increased rate of rRNA synthesis accounted for the net increase in myocyte rRNA content after PDBu treatment.