Pulmonary Vasomotor Fibres in the Sympathetic Chain and Its Associated Ganglia in the Dog

Daly, I. de Burgh; Duke, Helen N.; Hebb, Catherine O.; Weatherall, Josephine A. C.

doi:10.1113/expphysiol.1948.sp000935

Cited by 25 publications

(15 citation statements)

References 1 publication

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“…Thus relatively small variations in pulmonary arterial pressure could reflect changes in blood flow or in pulmonary vasomotor tone (I. de B. Daly, Duke, Hebb & Weatherall, 1948) of considerable physiological significance.…”

Section: Discussionmentioning

confidence: 99%

The effects of stimulation of the carotid sinus baroreceptors upon the pulmonary arterial blood pressure in the dog

Daly¹,

Schweitzer²

1956

The Journal of Physiology

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Compared with the vast literature on the effects of sino-aortic reflexes upon the systemic circulation, few observations have been made on the haemodynamic events occurring in the pulmonary circulation.Schafer (1920) made the first observations using vagotomized rabbits breathing spontaneously. He found that electrical or mechanical stimulation of the aortic (depressor) nerve caused a fall in pulmonary arterial pressure which was followed by an after-rise above the initial level on cessation of the stimulus. Other workers have stimulated the central end of the vagus nerve in the dog and have usually obtained a rise in pulmonary arterial pressure

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Section: Discussionmentioning

confidence: 99%

The effects of stimulation of the carotid sinus baroreceptors upon the pulmonary arterial blood pressure in the dog

Daly¹,

Schweitzer²

1956

The Journal of Physiology

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“…The experiments reported in this paper were intended: (1) to evaluate the influence of sympathetic nerve stimulation on pulmonary vascular input impedance in the anesthetized dog, (2) to determine the effects of beta-receptor blockade on pressure-flow relations in the lung before and during sympathetic nerve stimulation, and (3) to reexamine in the intact preparation existing reports which indicate that the major effects of sympathetic stimulation are exerted on the large pulmonary arteries rather than on small pulmonary vessels.…”

Section: Pacementioning

confidence: 99%

Sympathetic Control of Pulmonary Vascular Impedance in Anesthetized Dogs

Pace

1971

Circulation Research

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The effects of left stellate ganglion stimulation on pulmonary hydraulic input impedance was evaluated in 21 experiments on open-chest dogs anesthetized with chloralose. The stellate ganglion was stimulated at 1, 2, 5, 10, and 20 cps, and impedance spectra were generated at each frequency. Control spectra were characterized by frequency-dependent oscillations in impedance magnitude. Generally, impedance minimums occurred between 2 and 3 cps and maximums between 4 and 6 cps. Stellate ganglion stimulation caused elevations in impedance magnitude and shifted the impedance curve upward. The average control impedance magnitude at the minimum was 4780 dyne sec cm-8 kg ± 262 SE and was increased to 8280 ± 452 during stimulation at 20 cps, while the frequency of the first harmonic in the control averaged 2.50 ± 0.08 SE cps and was 3.10 ± 0.08 during stimulation at 20 cps. Maximum activation of sympathetic outflows (10-20 cps) caused the impedance curve to flatten, attenuating frequency dependent oscillations characteristic of control spectra. The administration of propranolol attenuated cardiogenic increases in pulmonary pressure and flow during stellate ganglion stimulation, but elevations in pulmonary vascular impedance still occurred, indicating that this was not dependent on changes in harmonic content of the flow pulse that attended changes in heart rate and stroke volume. Frequency dependent oscillations in impedance magnitude were usually enhanced during left stellate ganglion stimulation following propranolol. The results indicate that sympathetic nerve stimulation increases the opposition to pulsatile flow; since pulmonary vascular resistance was relatively less affected, the input impedance becomes a greater fraction of the total opposition that must be overcome in moving blood through the lungs. KEY WORDS propranololFourier analysis right ventricular function stellate ganglion stimulation pulmonary arteries• The pioneer studies of I. deB. Daly et al. demonstrated that sympathetic nerve stimulation increased the opposition to steady flow through artificially perfused lungs, thus establishing the existence of a sympathetic innervation to pulmonary vessels which could produce a direct vasomotor response (1 with stellate ganglion stimulation in isolated lung lobes perfused with pulsatile flow was an increase in arterial pulse pressure with an insignificant effect on the level of mean pressure (2). This resulted from generalized stiffening of large pulmonary arteries rather than from constriction of smaller muscular arterioles. Further studies showed that stellate ganglion stimulation reduced the volume distensibility of the main pulmonary artery and increased the elastic modulus of the arterial wall; thus these studies established a physical basis for the observed increases in pulsatile pressure (3).Since stiffening of conduit vessels tends to augment pressure pulsations, a major hemodynamic consequence of activation of sympathetic pathways to the pulmonary vasculature

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“…To date the only evidence on this point is that from anatomical studies and stimulation experiments which show where some of the fibres in the nerves may go. Thus it is known that fibres in the ansae innervate cardiac muscle (Randall & Rhose, 1956), coronary arterioles (Brown, 1968; in the cat), pulmonary blood vessels (Daly, Duke, Hebb & Weatherall, 1948) and airway smooth muscle (Dixon & Ranson, 1912). As well as going to other thoracic structures, some fibres from the ansae pass up the cervical vago-sympathetic trunk.…”

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confidence: 99%

The reflex cardiovascular depression caused by occlusion of the coronary sinus in the dog

Muers¹,

Sleight²

1972

The Journal of Physiology

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4. During occlusions, there was inhibition of activity in single and small multi-fibre preparations of sympathetic efferent nerves in the ansae subclaviae and the cervical sympathetic.5. On the right side, nearly all afferent fibres ran in the recurrent cardiac nerve. There was no concentration of afferents in one cardiac nerve on the left side.6. It was concluded that the cardiovascular depression was reflex, and was caused by the stimulation of nerves or nerve endings in the ventricles of the heart.

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Pulmonary Vasomotor Fibres in the Sympathetic Chain and Its Associated Ganglia in the Dog

Cited by 25 publications

References 1 publication

The effects of stimulation of the carotid sinus baroreceptors upon the pulmonary arterial blood pressure in the dog

The effects of stimulation of the carotid sinus baroreceptors upon the pulmonary arterial blood pressure in the dog

Sympathetic Control of Pulmonary Vascular Impedance in Anesthetized Dogs

The reflex cardiovascular depression caused by occlusion of the coronary sinus in the dog

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