Dependence of myocardial blood flow and metabolism on cardiac innervation.
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Biomedical subjects
Publications and source records attributed to M I Noble.
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1. Single fibres from the semitendinosus muscle of Rana temporaria were stretched during fused tetanic contractions and tension and sarcomere length (laser diffraction) responses were recorded. 2. Stretch of the fibres caused proportional increases in length of the sarcomeres. The force increased to a plateau value which was maintained during stretch or increased to a plateau value which was maintained during stretch or increased slightly. 3. The plateau value of force during stretch was dependent upon the velocity of stretch, was independent of the amplitude of stretch and was not proportional to overlap of thick and thin filaments. 4. There was enhancement of force after stretch compared with that produced at the same sarcomere length during isometric tetani. This force enhancement was independent of the velocity at which the stretch had been applied. 5. At sarcomere lengths between 1.9 and 2.3 micrometer, the force enhancement after stretch declayed rapidly, was independent of amplitude of stretch above approximately 25 nm per sarcomere not associated with a shift of the force--velocity curve. At sarcomere lengths above 2.3 micrometer the force enhancement after stretch decayed very slowly and was still present after 4 sec in long tetani. 6. At sarcomere lengths above 2.3 micrometer, force enhancement after stretch increased with amplitude of stretch and increased for any given stretch amplitude with sarcomere length. The force recorded after stretch was thus not proportional to overlap of thick and thin filaments. 7. At sarcomere lengths above 2.3 micrometer, the force enhancement after stretch was associated with a shift towards higher force value of the force--velocity curve. The velocity of shortening and zero load (V max) derived by hyperbolic extrapolation of the force--velocity curve was not affected. 8. Tension enhancement during and after stretch has a stabilizing effect in preventing dispersion of sarcomere length, particularly on the descending limb of the length--tension curve.
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1. The effect of increased aortic pressure on the inotropic state of the left ventricle was studied in isolated cat hearts, perfused with bovine red cells in Tyrode solution, ejecting into a hydraulic model with the same input impedance as that of the cat aorta.2. Inotropic state was assessed at a controlled left ventricular end-diastolic pressure by interpolating single isovolumic beats by means of an occluder in the aortic cannula.3. When such isovolumic beats during periods of raised aortic pressure were compared with those during control periods, the difference in peak isovolumic pressure ranged from -0.3 to +0.5 kPa indicating differences in inotropic state which were small and inconsistent in direction.4. The maximum rate of rise of left ventricular pressure (dP/dt(max).) of ejecting beats was little affected by a rise of aortic pressure and the direction of changes was inconsistent.5. The effect of increased aortic pressure was studied in intact dogs after cardiac denervation; left ventricular end-diastolic pressure was uncontrolled and therefore rose to a higher steady level.6. No consistent change of dP/dt(max). was found during the period of increased aortic pressure.7. All flow and pressure variables remained steady during the period of increased aortic pressure after the higher level of left ventricular end-diastolic pressure had been established.8. These results demonstrate that neither the positive inotropic effect nor the negative inotropic effect of increased load dominates in these preparations. This may be the result of a balance between the two effects, or they may be of unimportant magnitude under physiological conditions.
The measurement of ventricular diastolic compliance is complicated by the presence of viscous properties. To approach this problem, cat papillary muscles contracting isometrically at 15/min at 26 degrees C were stretched at different velocities during diastole. At a given length there was no excess of force above that defined by the static force-length curve until velocity of stretch exceeded 1 muscle length/sec. At greater velocities of stretch there was an increase of force with increasing velocity of stretch denoting viscous resistance to stretch. The viscous characteristic was alinear and increased with muscle length. At a given muscle length potentiation of contractile state by paired pulse stimulation caused a change in the diastolic force-length curve but there was no apparent relationship between viscous resistance to stretch and contractile state or the length of the "series viscous element." These results lead one to expect viscous resistance to stretch during rapid filling of the intact left ventricle.
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1. Single fibre pulmonary stretch receptor discharge was recorded in dogs on cardiopulmonary bypass. 2. Inhalation of CO2 depressed pulmonary stretch receptor discharge despite the absence of changes in arterial PCO2. This effect was particularly marked with airway CO2 levels below 5%. 3. Changing arterial PCO2, without changing airway CO2, had only small and insignificant effects on pulmonary stretch receptor discharge. 4. The effect of changes in airway CO2 on pulmonary stretch receptor discharge was rapid and correlated well in time with the reflex tachypnoea produced when CO2 was inhaled in conditions of cardiopulmonary bypass. 5. Stimulation of the central end of the cut vagus nerve was triggered from simultaneously recorded action potentials from a single pulmonary stretch receptor. 6. In these conditions, the reflex response to CO2 could be simulated provided that the pulmonary stretch receptor had an end-expiratory discharge. 7. It is suggested that the vagally mediated tachypnoeic response to changes in airway CO2 seen in conditions of cardiopulmonary bypass is due to the effect of CO2 on the end-expiratory discharge of pulmonary stretch receptors.
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1. The inhalation of CO(2) produces a tachypnoea only in the presence of intact vagus nerves; the present study was designed to examine the mechanism of this phenomenon in the dog.2. Closed-chest cardiopulmonary bypass was established in dogs weighing 16-24 kg, anaesthetized with chloralose. When the ;bypass' was established pulmonary blood flow ceased, P(A, CO2) was reduced and the respiratory rate slowed. 3-10% CO(2) in O(2) could then be inhaled without change in the level of P(a, CO2) set at the oxygenator.3. The addition of CO(2) in these concentrations to the inspired oxygen resulted in an increase in respiratory frequency, maximal at the first breath and sustained for the 1 min period of exposure. The increase in respiratory frequency was due to a shortening of expiratory duration. Inspiratory duration did not change. The response was absent after vagotomy.4. Inert gases in O(2), given as a control, had no effect on breathing.5. The effect of raising P(a, CO2) (by increasing the concentration of CO(2) in the gas equilibrating the blood in the oxygenator), was primarily to increase tidal volume.6. The ventilatory effect of inspiring CO(2)/O(2) mixtures was shown to be additive to the effect of raising P(a, CO2).7. These experiments show that an afferent vagal reflex originating from the lungs causes tachypnoea, when a dog, on ;bypass', inhales low concentrations of CO(2) in O(2).
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