Functional asymmetry in carotid sinus cardiac reflexes in humans

Summary The reflex cardiac response to activation (CBA) and inactivation (CBI) of the left and right carotid baroreceptors was studied in 30 healthy subjects, aged between 24 and 38 years. The CBA was evoked by applying negative pressure (from –20 to –60 mmHg) for 10 s to the left and right carotid sinus regions separately or both together, using two small neck capsules. The CBI was produced by applying left and right positive neck pressure (from 20 to 60 mmHg) for 10 s. The blood flow velocity was measured non-invasively with a Doppler scanner placed in the suprasternal notch. Blood flow acceleration was calculated and used as an indication of left cardiac contractility. Heart rate was measured continuously. Differences were found between right and left carotid sinus responses to CBA and CBI. The maximal response of the R-R interval was significantly greater during right CBA than during left CBA (the average gain: R-R·mmHg^–1 2.69 ms·mmHg^–1 and 1.75 ms·mmHg^–1 respectively). Also, the reflex CBI response was significantly greater for the right (3.16 ms·mmHg^–1) than for the left (2.22 ms·mmHg^–1 The reflex decrease/increase in blood-flow acceleration in response to CBA/CBI was significantly greater during left than during right-sided activation/inactivation. It is suggested that the functional asymmetry was related to differences in right/left-sided cardiac innervation as well as to central ipsilateral projection of the carotid baroreceptor afferents to the nuclei tractus solitarii.Research fellow from the A. von Humboldt Foundation from the Department of Physiology, Medical Academy, Warsaw, Poland     

The relation between carotid body chemoreceptor discharge, carotid sinus pressure and carotid body venous flow

1. Activity in forty-two single chemoreceptor afferent fibres from the carotid body in thirty-nine cats was measured when the carotid body was naturally and artificially perfused. In nine of these cats, carotid body venous flow was also measured.     

Central interaction between the baroreceptor reflexes from the carotid sinus and aortic arch.

The cardiovascular response to combined stimulation of the aortic nerve (AN) and carotid sinus nerve (CSN) with trains of electrical stimuli was studied in dogs under morphine-chloralose anesthesia. Combined stimulation of both nerves ipsilaterally resulted in systemic arterial depressor responses and cardiac slowing that were 59% and 77% greater (P less than 0.05) than the respective sum of the responses to separate stimulation of these nerves. The depressor response to combined stimulation of these nerves contralaterally was not different (P greater than 0.05) from the sum of the separate responses. However, cardiac slowing to contralateral stimulation of the nerves remained 43% greater (P less than 0.05) than the sum of the individual responses. The results suggest that an interaction between the aortic and carotid baroreceptor reflexes occurs centrally, which causes a greater than additive effect on the autonomic output. The degree of interaction between the reflexes did not change as the delay between the stimulus trains was varied over an interval of 0 and 100 ms. At intervals greater than 100 ms the reflex responses were additive.     

Interaction between carotid sinus baroreceptor and aortic nerve pressor reflexes in the dog

In dogs anesthetized with morphine-chloralose, strong, low-frequency (2 Hz) electrical stimulation of the aortic nerve (AN) causes pressure in the perfused hindlimbs to rise. This pressor response is followed by a large depressor phase upon cessation of stimulation. Simultaneous stimulation of the ipsilateral carotid sinus nerve (CSN) with intermittent trains of stimuli enhanced the AN pressor response by 113%. Similar stimulation of the contralateral CSN had little effect on the AN pressor response. Constant-frequency stimulation of the ipsilateral CSN also failed to enhance this response. Possible mechanisms of the interaction between these antagonistic reflexes were investigated. The results suggest that the augmentation of the AN pressor response results from a central neuronal interaction between these antagonistic reflexes.     

Effect of adrenoblockers of vascular responses during carotid sinus pressure reflexes

In acute experiments on cats using local anesthesia, listhenon, and artificial respiration, the blood pressure was recorded in the common carotid artery and the tone of the cerebral and femoral vessels was measured by a resistographic method. An increase in pressure in the isolated carotid sinuses was accompanied by a decrease in arterial pressure and tone of the femoral and cerebral vessels. When the pressure in the carotid sinuses fell, the arterial pressure and tone of the femoral and cerebral vessels rose. In both cases the response of the cerebral vessels was less marked than that of the femoral vessels. Blocking -adrenoreceptors with phenatolamine considerably weakened or completely abolished these responses; they were not affected by -adrenergic blockade with obsidan. The role of the carotid baroreceptors in the regulation of the cerebral circulation during orthostatic collapse is discussed.Department of Pharmacology, Pyatigorsk Pharmaceutical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR V. V. Zakusov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 7, pp. 40–42, July, 1979.     

Temporal and spatial interactions between the carotid sinus and vagally mediated baroreflexes in dogs

We investigated the temporal and spatial interactions between the carotid sinus and aortic arch baroreflex control of arterial pressure in 25 dogs anesthetized with pentobarbital sodium. The carotid sinus baroreceptor region was vascularly isolated to control the intracarotid sinus pressure. A hemorrhage catheter was inserted into the aortic arch. The systemic arterial pressure change after quick mild hemorrhage (2 ml/kg body weight within 1-2 s) was monitored. The open-loop gain of the vagally mediated baroreflex system was estimated from the mean arterial pressure response to the hemorrhage. Three protocols were employed to analyze the interactions. In the first protocol, we determined the effect of different levels of intracarotid sinus pressure on the open-loop gain of the vagally mediated baroreflex system. There was no significant effect. In the second protocol, the open-loop gain of the carotid sinus baroreflex system was determined after vagotomy. In the third protocol, the vagally mediated baroreflex system was activated by the hemorrhage without (spatial interaction) or with (temporal interaction) a delay after changing the intracarotid sinus pressure. The spatial interaction was facilitatory. A temporal interaction was found between the carotid sinus and vagally mediated baroreflex systems, when the delay was less than 30 s.     

The role of the carotid body chemoreceptors and carotid sinus baroreceptors in the control of cerebral blood vessels

1. Cerebral blood flow was measured in 17 baboons, anaesthetized with pentobarbitone, paralysed with gallamine and mechanically ventilated and in which the right sinus and both aortic nerves had been cut and the left carotid sinus vascularly isolated. Later in each experiment, the head was artificially perfused with femoral arterial blood via the innominate artery.2. Stimulation of the carotid body chemoreceptors with venous blood invariably caused a rise in regional cerebral blood flow whether the head was naturally or artificially perfused. This response was almost completely abolished if the VIIth cranial nerves were cut intracranially.3. Regional cerebral blood flow varied inversely with carotid sinus pressure.4. After the remaining (left) sinus nerve had been cut, the cerebral vascular response to hypoxia was negligible and the response to hypercapnia was markedly reduced. Blood flow then varied with perfusion pressure.5. These results provide further evidence that cerebral blood vessels are reflexly controlled and that the peripheral arterial receptors are involved. Their action is most conspicuous in the vascular response to hypoxia and together with intrinsic factors in the cerebral vascular bed, they determine the size of the vascular response to changes in CO(2) and pressure.     

Changes in monoamine content of the rabbit carotid body following prolonged electrical stimulation of the carotid sinus nerve

In the anaesthetized, paralysed and artificially ventilated rabbit the carotid sinus nerve (CSN) has been stimulated electrically for 6 h. At the end of the stimulation period, the carotid body (CB) has been removed, frozen and processed for measurement of the monoamines (MA) and of their catabolites with high-pressure liquid chromatography and electrochemical detection (HPLC-ECD). Results show a significant increase of dopamine (DA) and adrenaline (A) content and of all the metabolites. Besides an important augmentation of DA metabolism suggests that CSN efferent activity exerts some regulation on the MA content and turnover of the CB.     

Low glucose effects on rat carotid body chemoreceptor cells' secretory responses and action potential frequency in the carotid sinus nerve

Glucose deprivation (hypoglycaemia) is counterbalanced by a neuroendocrine response in order to induce fast delivery of glucose to blood. Some central neurons can sense glucose, but nevertheless the most important glucose sensors/glycaemia regulators are located outside the brain. Some recent experimental evidence obtained in carotid body (CB) slices and isolated chemoreceptor cells in culture supports a role for the CB in glucose sensing and presumably glucose homeostasis, but this role has been questioned on the basis of a lack of effect of low glucose on the carotid sinus nerve activity. This work was performed in an attempt to clarify if low glucose is or is not a stimulus for the rat CB chemoreceptors. Using freshly isolated intact CB preparations we have monitored the release of catecholamines (CAs) and ATP from chemoreceptor cells in response to several concentrations of glucose, as indices of chemoreceptor cell sensitivity to glycaemia, and the electrical activity in the carotid sinus nerve (CSN), as an index of reflex-triggering output of the CB. We have observed that basal (20% O₂) and hypoxia (7 and 10% O₂)-evoked release of CAs was identical in the presence of normal (5.55 m m ) and low (3, 1 and 0 m m ) glucose concentrations. 0 m m glucose did not activate the release of ATP from the CB, while hypoxia (5% O₂) did. Basal and hypoxia (5% O₂)-induced CSN action potential frequency was identical with 5.55 and 1 m m glucose. Our results indicate that low glucose is not a direct stimulus for the rat carotid body chemoreceptors.