The effects of stimulation of the carotid body chemoreceptors on pulmonary vascular resistance in the dog

Daly, I. de Burgh; Daly, M. de Burgh

doi:10.1113/jphysiol.1957.sp005825

Cited by 23 publications

(11 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This limits the interpretation of the data in terms of an awake, normally active preparation. On the other hand the older literature contains many studies comparable to the present study (Browse and Shepherd, 1966; Carmody and Scott, 1974; Daly and Daly, 1957; Daly and Ungar, 1966; Krasney, et al, 1973; Parker, et al, 1975). Regarding the potential effect of anesthesia on the sensitivity of the chemoreceptors, Landgren et al in the older literature (1954) reported that intracarotid injections of barbiturates (Dial, Nembutal, Pentothal) had no effect on the chemosensory discharge.…”

Section: Discussionsupporting

confidence: 52%

Autonomic regulation of organ vascular resistances during hypoxemia in the cat

Fitzgerald

Dehghani

Kiihl

2013

Autonomic Neuroscience

View full text Add to dashboard Cite

This study aimed to dissect the roles played by the autonomic interoreceptors, the carotid bodies (cbs) and the aortic bodies (abs) on the vascular resistances of several organs in anesthetized, paralyzed, artificially ventilated cats challenged by systemic hypoxemia. Two 15 min challenges stimulated each of 5 animals in two different groups: (1) In the intact group hypoxic hypoxia (10%O2 in N2; HH) stimulated both abs and cbs, increasing neural output to the nucleus tractus solitarius (NTS); (2) In this group carbon monoxide hypoxia (30%O2 in N2 with the addition of CO; COH) stimulated only the abs, increasing neural output to the NTS. (3) In the second group in which their bilateral aortic depressor nerves had been transected only the cbs increased neural output to the NTS during the HH challenge; (4) In this aortic body resected group during COH neither abs nor cbs increased neural traffic to the NTS. CO and 10%O2 reduced Hb saturation to the same level. With the use of radiolabeled microspheres blood flow was measured in a variety of organs. Organ vascular resistance was calculated by dividing the aortic pressure by that organ’s blood flow. The spleen and pancreas revealed a vasoconstriction in the face of systemic hypoxemia, thought to be sympathetic nervous system(SNS)-mediated. The adrenals and the eyes vasodilated only when cbs were stimulated. Vasodilation in the heart and diaphragm showed no effect of chemoreceptor stimulated increase in SNS output. Different chemoreceptor involvement had different effects on the organs.

show abstract

Section: Discussionsupporting

confidence: 52%

Autonomic regulation of organ vascular resistances during hypoxemia in the cat

Fitzgerald

Dehghani

Kiihl

2013

Autonomic Neuroscience

View full text Add to dashboard Cite

show abstract

“…Previous work indicates that in the dog ventilated with room air, stimulation of the carotid bodies with hypoxic blood causes a primary reflex bradycardia (Bernthal, Greene & Revzin, 1951;Daly & Daly, 1957;Daly & Scott, 1958). In the present study we have shown that, in dogs spontaneously breathing 7% 02 in N2, withdrawal of the hypoxic stimulus to the carotid body chemoreceptors by changing the perfusate from hypoxic to oxygenated blood causes an increase in heart rate.…”

Section: Resultsmentioning

confidence: 99%

The effect of hypoxia on the heart rate of the dog with special reference to the contribution of the carotid body chemoreceptors

Daly¹,

Scott²

1959

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

Daly & Scott (1958) found that in the dog stimulation of the carotid body chemoreceptors by hypoxic blood had variable effects on heart rate. They presented evidence that chemoreceptor stimulation elicited two antagonistic reflexees on the heart, a primary reflex bradycardia from the chemoreceptors themselves and a secondary reflex tachycardia arising from receptors in the lungs as a result of the concomitant increase in respiratory minute volume. It was concluded that the directional change in heart rate depended, among other factors, on which reflex was prepotent. These experiments were made on dogs spontaneously breathing room air, and the blood supplying the medullary centres was therefore fully oxygenated. The aim of the present experiments was to find out what effects, if any, the carotid body chemoreceptors exert on heart rate in systemic hypoxia. Neil (1956) was the first to carry out an experiment of this type. Using cats, he found that the tachycardia of systemic hypoxia was not affected by changing the carotid body perfusate from hypoxic blood to' oxygenated Ringer-Locke's solution. Since some of our results obtained on dogs differ from those of Neil (1956) our experiments will be described in detail. METHODSDogs varying in weight from 10'5 to 17-2 kg were premedicated with morphine hydrochloride (1-2 mg/kg subcutaneously). About half an hour later they were anaesthetized with a mixture of chloralose (0.05 g/kg) and urethane (0-5g/kg) intravenously. Systemic blood pressure was measured in a femoral artery by means of a Hiirthle manometer. Heart rate was counted from the blood pressure record taken on a fast moving paper or was recorded on the kymograph by a Gaddum drop timer (Gaddum & Kwiatkowski, 1938) using the method of Daly & Schweitzer (1950).The animals breathed room air through valves of low resistance. Respiratory minute volume was measured either by collection of expired air in a balanced spirometer for a given period of time or by passing the expired air through a gas meter, every 05 1. expired air being signalled on the * Present address:

show abstract

“…Daly & Scott (1958, 1963 showed that the inconsistent cardiac effects were due, at least in part, to chemoreceptor excitation initiating two opposing mechanisms: the first is a direct or primary reflex effect from the carotid bodies on the heart causing bradyeardia. This response is usually only evident if changes in pulmonary ventilation are excluded (Bernthal et al 1951;Daly & Daly, 1957Daly & Scott, 1958, 1962, 1963aDowning, Remensnyder & Mitchell, 1962), and is mediated by both the vagus and sympathetic nerves (Daly & Scott, 1962;Downing et al 1962). The second mechanism includes various secondary phenomena, important among which are events initiated by reflex stimulation of respiration causing tachycardia (Daly & Scott, 1958, 1963.…”

mentioning

confidence: 99%