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Biomedical subjects

R R Taylor

Publications and source records attributed to R R Taylor.

At least 145 records · Page 8Linked to original sources
PubMed1969

Influence of the thyroid state on left ventricular tension-velocity relations in the intact, sedated dog.

The mechanical properties of left ventricular contraction were described in terms of tension, velocity, length, and time in closed-chest, sedated normal, hypothyroid, and hyperthyroid dogs. Heart rate was controlled at 150 beats/min, and instantaneous contractile element velocity was calculated from left ventricular pressure and its first derivative during isovolumic left ventricular contractions, produced by sudden balloon occlusion of the ascending aorta during diastole. Wall tension was derived from ventricular pressure and volume, the latter being obtained from the pressure-volume relation of the arrested ventricle, and tension-velocity relations were analyzed over a range of ventricular endiastolic volumes. At any level of ventricular volume, the hypothyroid state was associated with a displacement of the tension-velocity relation of the left ventricle downwards and to the left, and the time to peak tension was prolonged (154 msec, normal 139 msec). In the hyperthyroid state, the tension-velocity relation of the left ventricle was displaced upwards and to the right, and the time to peak tension was reduced (80 msec). The changes in the tension-velocity relations indicate that the inotropic state of the left ventricle in the intact dog varies directly with the animal's thyroid state. This influence on myocardial contractility necessarily constitutes an important and integral part of the response of the intact circulation to altered thyroid state.

Animals↗
PubMed1969

Autonomic blockade by propranolol and atropine to study intrinsic myocardial function in man.

Blockade of cardiac autonomic nervous activity by an intravenous injection of 0.2 mg/kg propranolol and 0.04 mg/kg atropine was used with cardiac catheterization to study intrinsic cardiac function in 47 patients with normal hearts and known graded myocardial disease. After blockade, significant hemodynamic abnormalities became apparent at rest in the majority of patients with known disease, many of whom had normal control findings. This occurred partly through a reduction in the normal range of cardiac function at rest, and partly through changes in the abnormalities associated with disease: after blockade, diseased hearts had normal stroke volumes, but beat more slowly, and had higher left ventricular filling pressures. The heart rate after blockade was fixed; this was defined as the intrinsic heart rate (IHR); it ranged from 57 to 126 beats/min in different patients. Both the IHR and left ventricular end-diastolic pressure after blockade were sensitively and quantitatively related to the severity of myocardial disease. When, after blockade, arterial pressure was raised by angiotensin, the IHR was unchanged; normal hearts maintained their stroke volume and increased stroke work; diseased hearts maintained stroke volume less well and stroke work was unchanged or fell. Abnormal ventricular responses corresponded well with abnormal ventricular function at rest. In different patients the IHR was significantly related to each available index of left ventricular function. Other studies in animals have shown that the IHR is closely related to intrinsic myocardial contractility in certain forms of experimental heart failure. An analogous relationship existing between the IHR and myocardial function in patients with heart disease is suggested as the explanation for the IHR/ventricular function relationship in this study. If so, the IHR may prove valuable as an index of myocardial function in man, since it can be measured simply and safely in clinical practice.

Atropine↗
PubMed1968

Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention.

The mechanical properties of left ventricular contraction were described in terms of tension, velocity, length, and time in closed-chest, sedated dogs in which a large aorto-caval fistula had resulted in circulatory congestion, and the results were compared with those in normal dogs. Instantaneous contractile element velocity was calculated from left ventricular pressure and its first derivative during isovolumic left ventricular contractions produced by sudden balloon occlusion of the ascending aorta during diastole. A range of ventricular end-diastolic volumes was induced and heart rate was controlled at 150 beats/min. Wall tension (stress) was derived from ventricular pressure and volume, the latter being obtained from the pressure-volume relation of the passive ventricle. Extrapolated velocity at zero tension, V(max), averaged 3.0 circ/sec in the normal dogs and 2.9 circ/sec in the seven dogs with an aorto-caval fistula and fluid retention; in only one of these seven animals was V(max) below the lower limit of normal of 2.7 circ/sec. Isovolumic tension (P(o)) in dogs with aorto-caval fistulas tended to be slightly greater than normal at low ventricular filling pressures, and there was no difference in P(o) between the two groups of animals at high ventricular filling pressures. Time to peak pressure averaged 151 +/- 6 (SE) msec (normal 139 +/- 3). Left ventricular weight averaged 6.32 +/- 0.23 g/kg of initial body weight (normal 5.25 +/- 0.56 g/kg) (P < 0.001), which reflected moderate ventricular hypertrophy, and ventricular internal volume at a given filling pressure was increased proportionally. Therefore, the ventricular contractile state usually was normal in the dog with a large aorto-caval fistula, and it is proposed that mechanisms for fluid retention that results in circulatory congestion were activated because of the large hemodynamic burden despite normal myocardial contractile properties.

Animals↗