[The role of vasodilator agents in cardiac insufficiency].
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Cardiac Output↗
Biomedical subjects
E Ino-Oka
Publications and source records attributed to E Ino-Oka.
Experimental study of afterload-reducing therapy: the effects of the reduction of systemic vascular resistance on cardiac output, aortic pressure and coronary circulation in isolated, ejecting canine hearts.
The relationship between cardiac output (CO) and peripheral resistance (Rp) was examined under the following conditions for coronary perfusion: constant coronary flow perfusion; perfusion with a pressure equal to mean aortic pressure (AoP perfusion); and perfusion with a pressure equal to the mean AoP - 30 mm Hg (AoP - 30 mm Hg perfusion). We also examined the coronary pressure-flow relationship. For these studies, we used paced, isolated, ejecting canine hearts, which were loaded by a hydraulic system that simulated the input impedance of a dog's systemic arterial tree. The CO in the constant coronary flow perfusion continued to increase with the reduction of Rp. The CO in the AoP perfusion became maximal at a slightly subphysiologic Rp, or at an average mean AoP of 65 mm Hg. This mean AoP was closely associated with the lower limit of the autoregulation of coronary blood flow. In the AoP - 30 mm Hg perfusion, the mean AoP at which CO became maximal was 72 mm Hg and the corresponding coronary perfusion pressure appeared to be lower than the lower limit of the perfusion pressure range for coronary flow autoregulation. The Rp value at that point was slightly higher than the physiologic range. We conclude that when coronary perfusion pressure changes with mean AoP, and when left ventricular end-diastolic pressure is fixed, there is a clear optimal Rp at which CO becomes maximal, and this optimal Rp is higher if coronary perfusion pressure is biased from mean AoP to a significant degree.
Animals↗
Effects of changes in the aortic input impedance on systolic pressure-ejected volume relationships in the isolated supported canine left ventricle.
We examined the effects of aortic input impedance alteration on left ventricular pressure, aortic flow and ejected volume (integral value of aortic flow), in an isolated blood perfused ejecting canine heart, with special reference to end-systolic values. A hydraulic model which stimulates an aortic input impedance was attached to the aortic root of an excised heart. Left ventricular end-diastolic pressure was kept constant by electrical pacing. Three coronary arteries were perfused with arterial blood from support dogs. When the peripheral resistance in the hydraulic model was changed, there were inverse linear relationships between stroke volume and mean left ventricular systolic pressure and between ejected volume and pressure at end-systole. Time interval from the onset of contraction to end-systole did not change. Thus the relation between stroke volume and mean left ventricular pressure obtained by changes in peripheral resistance is governed by a source resistance, which can be considered as the contractile state of the ventricle. When the capacitance (arterial compliance) was changed, there was no inverse linear relation between stroke volume and mean systolic pressure. In many cases, there was an inverse linear relationship between ejected volume and pressure at end-systole. However, an increase in capacitance prolonged the time interval from the onset of contraction to end-systole. We conclude that the end-systolic pressure-ejected volume relationship in the ejecting heart is governed not only by contractility but also by arterial capacitance.
Animals↗
The effect of graded coronary flow reduction in the left anterior descending and septal arteries on left ventricular function in the canine heart.
WE quantitatively analyzed the effect of graded left anterior descending and septal coronary flow (LAD + septal flow) reduction on left ventricular function with a left ventricular end-diastolic pressure (LVEDP) of 6 mm Hg and 12 mm Hg. We used an isolated, ejecting, canine heart preparation ( n = 8), the coronary flow of which could be controlled independently of the aortic pressure. We kept the other hemodynamic variables - heart rate, left circumflex coronary flow, right coronary flow and aortic input impendance - constant within their normal physiologic range. We considered this reduction in LAD + septal flow to be analogous to that of the most frequent lesion in ischemic heart disease. There was no plateau in the left ventricular work caused by this reduction of the regional coronary flow. Therefore, the plateau commonly reported in previous studies may be partially a result of the compensatory elevation of LVEDP, which is necessary to maintain the left ventricular work.
Animals↗
Effects of verapamil on the contractile force in the glycerinated dog heart muscles.
The effect of Ca-antagonist on the contractile apparatus was investigated in glycerinated cardiac papillary muscle preparations obtained from canine hearts. The results showed that maximal developed tension (P0) was enhanced significantly by 5 mg/liter of verapamil, and the augmentation of contractility was dependent on the concentrations of verapamil. As a conclusion, Ca-antagonist appeared to be a potentiating agent of the contractile force on the contractile apparatus.
Animals↗
Mechanical interaction between the ventricles.
We investigated ventricular interaction by the use of six excised, perfused, canine hearts. In this preparation, we could change the filling pressure of the right and left ventricles independently, thereby breaking the normal series-pump arrangement. We found that mechanical ventricular interaction exists in diastole and in systole. Namely, not only decreased diastolic ventricular compliance, but also the reduced performance in either ventricle was found, when the opposite ventricular pressure was increased. Thus, when the opposite ventricular filling pressure increases, we suspect that systolic ventricular function of either ventricle will be depressed significantly by these two factors; i.e., the Frank-Starling effect due to decreased ventricular diastolic volume following decreased diastolic ventricular compliance, and the depressed systolic ventricular function. Clinically, these findings may be important in considering the mechanism of the occurrence of simultaneous reduced performance of both ventricles in cases when only one side of the ventricle is affected hemodynamically and its filling pressure is greatly increased in various pathological states such as heart failure.
Animals↗
The relationship between myocardial oxygen consumption and total work obtained by a new left ventricular model.
The relationship between myocardial oxygen consumption (MVO2) and left ventricular work was examined experimentally, assuming that the left ventricle is equivalent to an electrical current source generator consisting of parallel source resistance (Ri) and constant generator current (I0). The internal and external work can be calculated as (Ri X I1(2)) and (Rp X I2(2)) in this model, where I1 is current of source resistance, Rp is peripheral resistance and I2 is cardiac output. The experiments were performed with a blood-perfused isolated ejecting canine heart preparation in which the hydraulic model, simulated to an aortic input impedance, was attached to the aortic root. The peripheral resistance was changed in a stepwise fashion and left ventricular pressure, cardiac output and MVO2 were measured. The calculated total work showed a close linear correlation with the MVO2, which suggested that the left ventricle can be regarded as a current source generator and the total work as a main mechanical factor in determining the MVO2.
Animals↗
Pressure-length loop in the ischemic segment during left circumflex coronary artery stenosis and its modification by afterload reducing in excised perfused canine hearts.
By using excised perfused heart preparations, we investigated the regional myocardial functions in the presence of a flow-limiting coronary stenosis of the left circumflex coronary artery (LCX) (approximately low reduction of pre-ischemic control), as well as global cardiac functions during afterload reducing, while keeping left ventricular end-diastolic pressure (LVEDP) and heart rate constant. After inducing the LCX stenosis, cardiac output (CO), peak left ventricular pressure (peak LVP) and stroke work (SW) decreased from pre-ischemic control values, i.e., 81.1 +/- 3.2%, p less than 0.005, 88.1 +/- 3.8%, p less than 0.02 and 72.2 +/- 5.7%, p less than 0.005, respectively (n = 7), whereas pressure-length (P-L) loop areas changed as follows; ischemic control values of the left anterior descending coronary artery (LAD) and LCX regions were 96.6 +/- 6.0%, n.s. and 72.6 +/- 9.0% of pre-ischemic control, p less than 0.02, respectively. Following afterload reducing with LCX stenosis, CO increased gradually, while the ischemic regional function started to further aggravate, and the initial point of further ischemic aggravation obtained in this experiment occurred at 63.5 +/- 6.9 mm Hg of mean aortic pressure (AoP). These results suggested that the increase of total cardiac function such as CO following afterload reducing was probably induced at the expense of aggravated regional ischemia. Therefore it was concluded that the treatment of ischemic myocardium by reducing afterload pressure should be done very carefully.
Animals↗
Effects of OPC-8212, a new positive inotropic agent, and dobutamine on left ventricular global and ischemic regional functions and coronary hemodynamics under coronary artery stenosis.
We have investigated the effects of OPC-8212, a new positive inotropic agent, and dobutamine, a known cardioselective inotropic agent, on global left ventricular (LV) and ischemic regional functions in 14 excised canine hearts with a flow-limiting stenosis of the left circumflex coronary artery (LCX) (i.e., 20-25% of control flow). OPC-8212 infusion (n = 7) under LCX stenosis improved cardiac depression [i.e., peak LV dP/dt increased from 1,295 +/- 143 mm Hg/s to 2,669 +/- 266 mm Hg/s (mean +/- SEM) (p less than 0.001)], while myocardial ischemic injury, assessed by myocardial CO2-tension and electrocardiogram (ECG)-ST changes, improved (i.e., delta CO2-tension and ECG-ST deviation decreased from 21.1 +/- 3.6 mm Hg and 3.8 +/- 0.6 mV to 13.3 +/- 2.8 mm Hg (p less than 0.01) and 2.0 +/- 0.7 mV (p less than 0.05), respectively). On the other hand, dobutamine infusion (n = 7) further increased myocardial CO2-tension and ECG-ST deviation [i.e., delta CO2-tension and ECG-ST deviation increased from 14.4 +/- 4.2 mm Hg and 2.5 +/- 1.2 mV to 29.0 +/- 6.0 mm Hg (p less than 0.01) and 4.9 +/- 1.0 mV (p less than 0.01), respectively]. At the same time, peak LV dP/dt clearly improved, but to a lesser degree; from 1,425 +/- 153 mm Hg/s to 2,393 +/- 245 mm Hg/s (p less than 0.001). There was also an increase in percent systolic segment shortening of each corresponding area as with OPC-8212.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of transdermal therapeutic system-nitroglycerin in patients with heart failure. Influence on hemodynamic changes.
Fourteen patients suffering from severe heart failure with 18 mmHg or higher diastolic pulmonary arterial pressure were given a transdermal therapeutic system of nitroglycerin (TTS-NTG). They were evaluated for changes in the hemodynamic responses over 24 hours. Diastolic pulmonary arterial pressure decreased from 27.1 +/- 2.3 mmHg (mean +/- SE) to 22.4 +/- 1.7 mmHg after 1 hour (p less than 0.01), which was maintained throughout the trial. Cardiac index increased from 2.42 +/- 0.13 l/min/m2 to 2.64 +/- 0.16 l/min/m2 after 1 hour (p less than 0.01). The analysis of cardiac and vascular function curves in individual patients suggested that the improvement of hemodynamics was induced mainly in six patients with an increase of contractility and in four patients with a reduction of afterload. No changes were observed in three patients in either contractility or afterload, and a decrease in contractility was seen in one patient. These results suggest that TTS-NTG can be transcutaneously absorbed well enough to produce improved hemodynamic responses in patients with severe heart failure by several mechanisms and maintain these effects over 24 hours.
Administration, Cutaneous↗