Carotid Sinus/Nerve Stimulation for Treatment of Resistant Hypertension and Heart Failure

Author(s):  
Dali Yin ◽  
Konstantin V. Slavin
1993 ◽  
Vol 265 (4) ◽  
pp. H1310-H1317 ◽  
Author(s):  
W. Wang ◽  
M. Brandle ◽  
I. H. Zucker

In a previous study (Wang, W., J. S. Chen, and I. H. Zucker. Circ. Res. 68: 1294-1301, 1991), we showed a depression in baroreflex gain in dogs with pacing-induced heart failure. This depression was not accompanied by a decrease in the central gain (carotid sinus nerve stimulation vs. renal nerve activity). These previous experiments were carried out on animals that were vagotomized and aortic denervated. In the present study these experiments were repeated, and the data were analyzed both in the intact and vagotomized state. Dogs were cardiac paced at 250 beats/min until heart failure was noted. Sham dogs were used as controls. The carotid sinuses were isolated, and the aortic nerves were sectioned. Activity from a renal sympathetic nerve (RSNA) was recorded with arterial pressure and carotid sinus pressure (CSP) during bilateral step increases in CSP from 25 to 300 mmHg. Mean arterial pressure (MAP) and RSNA responses to carotid sinus pressurization and to carotid sinus nerve stimulation were tested before and after bilateral vagotomy, and curves describing these relationships were constructed. Before vagotomy, the peak response relating stimulation frequency to MAP was significantly depressed in dogs with heart failure (-18.3 +/- 4.7 vs. -37.0 +/- 2.2%, P < 0.001). In addition, the CSP-MAP curves were depressed in dogs with heart failure. Frequency-RSNA curves were not altered in heart failure. There were no significant changes in the baroreflex gain responses to pressurization or electrical stimulation after vagotomy in either sham or heart failure groups.(ABSTRACT TRUNCATED AT 250 WORDS)


Hypertension ◽  
2018 ◽  
Vol 72 (Suppl_1) ◽  
Author(s):  
Aline B Ribeiro ◽  
Patricia G Fernandes ◽  
Fernanda Brognara ◽  
Jaci A Castania ◽  
Carlos A Silva ◽  
...  

1975 ◽  
Vol 8 (3) ◽  
pp. 135-139 ◽  
Author(s):  
John C. Passmore ◽  
Howard L. Strauss ◽  
William Z. Kolozsi

2005 ◽  
Vol 99 (1) ◽  
pp. 189-196 ◽  
Author(s):  
Richard Kinkead ◽  
Roumiana Gulemetova ◽  
Aida Bairam

In awake animals, our laboratory recently showed that the hypoxic ventilatory response of adult male (but not female) rats previously subjected to neonatal maternal separation (NMS) is 25% greater than controls (Genest SE, Gulemetova R, Laforest S, Drolet G, and Kinkead R. J Physiol 554: 543–557, 2004). To begin mechanistic investigations of the effects of this neonatal stress on respiratory control development, we tested the hypothesis that, in male rats, NMS enhances central integration of carotid body chemoafferent signals. Experiments were performed on two groups of adult male rats. Pups subjected to NMS were placed in a temperature-controlled incubator 3 h/day from postnatal day 3 to postnatal day 12. Control pups were undisturbed. At adulthood (8–10 wk), rats were anesthetized (urethane; 1.6 g/kg), paralyzed, and ventilated with a hyperoxic gas mixture [inspired O2 fraction (FiO2) = 0.5], and phrenic nerve activity was recorded. The first series of experiments aimed to demonstrate that NMS-related enhancement of the inspiratory motor output (phrenic) response to hypoxia occurs in anesthetized animals also. In this series, rats were exposed to moderate, followed by severe, isocapnic hypoxia (FiO2 = 0.12 and 0.08, respectively, 5 min each). NMS enhanced both the frequency and amplitude components of the phrenic response to hypoxia relative to controls, thereby validating the use of this approach. In a second series of experiments, NMS increased the amplitude (but not the frequency) response to unilateral carotid sinus nerve stimulation (stimulation frequency range: 0.5–33 Hz). We conclude that enhancement of central integration of carotid body afferent signal contributes to the larger hypoxic ventilatory response observed in NMS rats.


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