Search for Evidence of Lung Chemoreflexes in Man: Study of Respiratory and Circulatory Effects of Phenyldiguanide and Lobeline

Jain, Sushil K.; Subramanian, Shyamsunder; Julka, Deepinder; Guz, A.

doi:10.1042/cs0420163

Cited by 72 publications

(41 citation statements)

References 16 publications

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“…4). The corresponding means obtained by the exponential least-squares method were 3-6 + 0-2 s and 11I4 + 1-4 s. Direct measurement from this kind of oximeter trace gives values very close to the lung-carotid body delay (Jain, Subramanian, Julka & Guz, 1972 Jlfg llfL End-tidal downward steps, PET 0 was held reasonably constant throughout the step changes in PET, C0 and there were no significant fluctuations in the oximeter trace. Figure 3 between the steps out of hypocapnia (A to B) and out of hypercapnia (C to B).…”

Section: Peripheral Delays Dpmentioning

confidence: 59%

Dynamics of the ventilatory response in man to step changes of end‐tidal carbon dioxide and of hypoxia during exercise.

Macfarlane¹,

Cunningham²

1992

The Journal of Physiology

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SUMMARY1. Four human subjects exercised in hypoxia (end-tidal partial pressure Of 02 (PET, 02) ca 55 Torr; heart rate ca 100-130 beats min-), and the contribution to the respiratory drive of the peripheral and central chemoreflex pathways have been separated on the basis of the latencies and the time courses of the responses to sudden changes of stimulus.2. The subjects were exposed to repeated end-tidal step changes in PCO2 of ca 3-3 5 Torr (at nearly constant PET, 02 ) and P02 (between ca 55 and 230 Torr) at three regions along the expiratory ventilation VE-PET°2 response line (hypocapnia, eucapnia, hypercapnia). The dynamics of the ventilatory responses were calculated using a two-compartment non-linear least-squares optimization method.3. The component of the response attributable to the peripheral chemoreflex loop may in some subjects contribute up to 75% of the ventilatory drive during mild hypocapnic hypoxic exercise and ca 72 % of the total gain following steps Of PET, CO, during hypoxic exercise. These data support the notion that the effectiveness of the peripheral chemoreceptor pathway is enhanced in moderate exercise.4. During hypoxic exercise, the time delays and time constants attributed to the peripheral chemoreflex pathways (ca 3-5 and 9 s respectively) and to the central chemoreflex pathways (ca 9-5 and 47 s respectively) are some of the shortest reported.5. The dynamics of the peripheral and central chemoreflex pathways appeared to be largely independent of each other.6. There was a notable absence of systematic change of inspiratory and expiratory durations during the step-induced transients.

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Section: Peripheral Delays Dpmentioning

confidence: 59%

Dynamics of the ventilatory response in man to step changes of end‐tidal carbon dioxide and of hypoxia during exercise.

Macfarlane¹,

Cunningham²

1992

The Journal of Physiology

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“…In the rat, a mild secondary tachycardia has been demonstrated, but the vasodilatation is apparently absent (26). The limited information available on selective chemoreceptor stimulation in primates, including man, suggests that tachycardia and peripheral vasodilatation secondary to hyperventilation can occur but are weak, the influence of central inspiratory drive on heart rate being more important than the influences of pulmonary stretch receptor stimulation or hypocapnia (27)(28)(29).…”

Section: Species Differencesmentioning

confidence: 99%

Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

Jm¹

1998

Braz J Med Biol Res

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This review describes the ways in which the primary bradycardia and peripheral vasoconstriction evoked by selective stimulation of peripheral chemoreceptors can be modified by the secondary effects of a chemoreceptor-induced increase in ventilation. The evidence that strong stimulation of peripheral chemoreceptors can evoke the behavioural and cardiovascular components of the alerting or defence response which is characteristically evoked by novel or noxious stimuli is considered. The functional significance of all these influences in systemic hypoxia is then discussed with emphasis on the fact that these reflex changes can be overcome by the local effects of hypoxia: central neural hypoxia depresses ventilation, hypoxia acting on the heart causes bradycardia and local hypoxia of skeletal muscle and brain induces vasodilatation. Further, it is proposed that these local influences can become interdependent, so generating a positive feedback loop that may explain sudden infant death syndrome (SIDS). It is also argued that a major contributor to these local influences is adenosine. The role of adenosine in determining the distribution of O 2 in skeletal muscle microcirculation in hypoxia is discussed, together with its possible cellular mechanisms of action. Finally, evidence is presented that in chronic systemic hypoxia, the reflex vasoconstrictor influences of the sympathetic nervous system are reduced and/or the local dilator influences of hypoxia are enhanced. In vitro and in vivo findings suggest this is partly explained by upregulation of nitric oxide (NO) synthesis by the vascular endothelium which facilitates vasodilatation induced by adenosine and other NO-dependent dilators and attenuates noradrenaline-evoked vasoconstriction. Correspondence

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“…Experiments in man have established the presence of sensory receptors in the lung which may be likened to the 'C' fibre endings (Jain, Subramanian, Julka & Guz, 1972). However, these receptors have yet to be assigned a physiological role in either the normal or asthmatic lung.…”

mentioning

confidence: 99%