The effect of some hemodynamic factors on the behaviour of the aortic valve.
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Biomedical subjects
Publications and source records attributed to R S Reneman.
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Significant differences between epicardial and endocardial systolic stress in the wall of the left ventricle (LV) have been predicted by various models of LV mechanics. Yet a model incorporating transmural differences in fiber orientation and torsion, defined as a rotation of the apex with respect to the base around the long axis of the LV, predicts transmural equalization of stress and shortening along the fiber direction during the ejection phase. this equalization is due to an interplay between torsion and myocardial contraction. To assess the model hypothesis, predicted epicardial deformation during the ejection phase was compared with that measured experimentally. For this purpose 45 sets of measurements were performed in four open-chest dogs using a triangular array of inductive gauges for the assessment of epicardial circumferential strain (epsilon c), base-to-apex strain (epsilon z), and shear angle (gamma). Changes in shear angle are directly related to LV torsion. LV end-diastolic pressure was varied over a wide range (0-15 mmHg) by volume loading and bleeding. In the control state, the slope of the shear angle vs. volume strain curve (volume strain = 2 epsilon c + epsilon z), which is related to contraction, was found to be 0.74 +/- 0.10 (mean +/- SD). This compares reasonably wih the mathematical model prediction of a slope of 0.67. Due to an interplay between torsion and contraction, left ventricular fiber stress and fiber shortening might be uniformly distributed across the wall.
The effect of ischemia on the myocardial content of nonesterified fatty acids (NEFA), triacylglycerol, cholesteryl esters, and phospholipids assayed with gas-liquid chromatography was studied in an open-chest dog preparation. Ischemia was induced by partial occlusion of the left interventricular coronary artery during 120 minutes (n = 20). Tissue content of the lipid classes was assessed in biopsies taken from ischemic and normoxic areas of the left ventricular free wall. Local venous blood from the concomitant vein of the left interventricular coronary artery was collected to determine myocardial extraction of lipids. In eight other dogs, no ischemia was induced (control group). Under normoxic conditions, NEFA appeared to be present in trace amounts: about 25 nmol/g wet weight of tissue, representing less than 0.1% of total myocardial fatty acids. During ischemia, NEFA increased in the affected area. This accumulation was most pronounced in the least perfused layer: the subendocardium (up to 172 nmol/g). Blood flow, estimated with radioactively labeled microspheres fell from 0.55 to 0.06 ml/min per g in this particular layer. The uptake of NEFA by the ischemic myocardium was decreased, indicating that enhanced lipolysis of endogenous lipids or reduced combustion may be held responsible for the accumulation of NEFA in ischemic tissue. Since arachidonic and linoleic acids showed the highest relative increase, lipolysis of endogenous phospholipids, rich in these fatty acids, seems to be reasonable. Ischemia had no significant effect on the content of triacylglycerol and cholesteryl esters. Phospholipids tended to decrease in the affected subendocardial layers.
In this survey, the effect of fentanyl, a potent morphinomimetic, on myocardial metabolism and some hemodynamic variables during ischemia is described. The data presented were derived from open-chest experiments on dogs. Ischemia was induced by partial occlusion (stenosis) of a coronary artery. Inducing the stenosis twice in the same animal after a certain interval made it possible to use the animal as its own control. Control and compound series are discussed. In the compound series, fentanyl (25 microgram/kg-1) was injected IV 5 minutes before induction of the second stenosis. Fentanyl decreased the oxygen demand of the ischemic myocardium, mainly due to a reduction in heart rate, which resulted in a decrease in the breakdown of energy-rich phosphates and in the anaerobic breakdown of glucose. The latter resulted in a less pronounced production of lactate by the ischemic myocardium and hence in a diminished acidity of this tissue. The release of potassium ions during ischemia was reduced after fentanyl. The uptake of glucose by the ischemic myocardium was not affected by fentanyl, but the uptake of free fatty acids was diminished. During ischemia, the arterial free fatty acid concentration decreased after fentanyl, indicating that the compound may suppress stress responses. Although extrapolation to clinical anesthesia should be handled with care, the described findings suggest that the use of fentanyl may benefit patients with coronary artery disease during anesthesia.
The cardiac dimensions of long-distance runners (LDR), cycle racers (CR), and weight lifters (WL) were determined echocardiographically and were compared with those of control subjects (CS). Left ventricular hypertrophy (LVH) was also assessed from the electrocardiogram. Training information was obtained through a questionnaire. The maximal aerobic performance was assessed on a cycle ergometer. Comparison of the cardiac dimensions revealed that left ventricular mass (LVmass) was significantly increased in LDR and CR as compared to CS. This resulted from thickening of the interventricular septum and left ventricular posterior wall as well as from enlargement of the left ventricular internal diameter. The existence of LVH was confirmed by electrocardiographic investigation. Although the left ventricular wall was enlarged in WL, their LVmass was not significantly increased as compared with CS. These results are in agreement with the training program followed. Weight lifters almost exclusively performed strength training, while LDR and CR were mainly involved in endurance training. The LDR and CR reached significantly higher maximal aerobic performance levels than WL. The present results suggest a close relationship between the type of cardiac enlargement and the training program followed by the athletes.
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In open-chest dogs direct-cinematographic high-speed recordings of aortic valve movement were made using a thin flexible fiberscope. Simultaneously ECG, ascending aortic flow (electromagnetically), and the pressures in the aorta, left ventricle, and left atrium were recorded. Replacement of blood by a transparent liquid (Tyrode solution) was done with two roller pumps, one connected to the left atrium and the other to the femoral artery. Free outflow occurred through a cannula in the pulmonary artery. Comparison of the film frames with the aortic flow signals revealed that 1) the valve was completely open at the moment that aortic flow had reached about 75% of its maximum value; 2) the opening time was 32 ms; 3) valve closure started before the onset of aortic flow deceleration; 4) at least 80% of the closure was completed before aortic flow becomes zero; 5) complete valve closing coincided with the moment of maximum backflow in the valve; 6) the shape of the valvular orifice at complete opening was almost circular; and 7) fluid viscosity had no significant effect on valve closure.
The concentration and composition of fatty acids in four lipid classes in biopsies of dog left ventricular myocardium were determined, using gas-liquid chromatography. When precautions were taken to minimize lipolysis during storage of the tissue and the homogenization process, the following results were obtained: 29 +/- 10 nmol non-esterified fatty acids, 2.98 +/- 2.41 mumol triacylglycerol, 149 +/- 51 nmol cholesteryl esters and 23.76 +/- 3.38 mumol phospholipid (expressed as fatty acid moiety per gram of wet tissue). The concentration of non-esterified fatty acids was 15 to 300 times lower than reported in literature. The main constituents of the non-esterified fatty acids were palmitic, stearic and oleic acid. Triacylglycerol consisted of approximately 40% esterified oleic acid. Linoleic acid accounted for 40% of the fatty acids in the cholesteryl-esters class. More than half of the fatty acid moiety of total phospholipids was linoleic acid and arachidonic acid.
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A new accurate method to determine the deformation of the epicardial surface during the cardiac cycle in vivo is described. Epicardial deformation is determined by a circumferential strain, a base-to-apex strain, and a shear angle. In the measuring setup, one magnetic field-generating coil (MFGC) and two sensor coils are attached to the epicardium, thus forming an approximately right-angled triangle with the MFGC at the right-angled corner and the sides containing the right angle, parallel to the circumferential and base-to-apex direction, respectively. The MFGC generates a magnetic field that rotates around the axis of the coil. The strength of that field decreases with increasing distance. Both strains and the shear angle are derived from the amplitudes of the voltages induced in the sensor coils and their phase difference. In the experimental situation the accuracy of the measurement of strain and shear angle is +/- 0.005 and +/- 1 degree, respectively. The device has a frequency response of 100 Hz (-3 dB) and practically no zero drift. In four open-chest dogs during left ventricular ejection, circumferential natural strain, base-to-apex natural strain, and shear angle at the epicardium of the left ventricular free wall ranged from -0.06 to -0.13, from -0.02 to -0.08, and from 6.8 degrees to 11.5 degrees, respectively.
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The effect of lidoflazine administration (120 mg t.i.d. for 9 weeks) on work tolerance (bicycle ergometer), frequency of anginal attacks, and nitroglycerin consumption was investigated in 28 male patients with stable angina pectoris in a combined single-blind/double-bline study. Lidoflazine increased work tolerance and reduced the frequency of anginal attacks and nitroglycerin consumption. The higher work tolerance level was reached at maximal heart rate and heart rate--systolic blood pressure product values similar to those before treatment. The values of these variables after 3 min of exercise at 60 W, however, were significantly lower after treatment with lidoflazine. These findings indicate that the heart is performing more economically during lidoflazine treatment. The improved work tolerance can probably be ascribed to lidoflazine and not to a training effect because of the significant reduction of this variable in the patients allocated to placebo as compared to those remaining on lidoflazine treatment. The side effects were generally slight. In one patient the prolongation of the QT interval due to lidoflazine resulted in rhythm disturbances.
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The effect of fentanyl 25 micrograms/kg body weight i.v. on left ventricular haemodynamics, myocardial carbohydrate utilization and phosphate release during ischaemia in dogs was investigated. A reproducible degree of ischaemia could be obtained by partial occlusion (stenosis) of the interventricular artery, using an inflatable cuff. Inducing stenosis twice made it possible to use the animal as its own control. Arterio-local venous differences of glucose increased during ischaemia and lactate and inorganic phosphate were released from the ischaemic myocardium. Fentanyl administered before the second stenosis reduced heart rate and, to a lesser extent, mean aortic pressure and left ventricular dP/dt max. The release of lactate and inorganic phosphate was diminished during the period of ischaemia. These findings suggest that fentanyl prevents excessive breakdown of energy-rich phosphates and high anaerobic production rate of lactate by decreasing the energy demand of the ischaemic myocardium.