Selective Depression of Peripheral Chemoreflex Loop by Sevoflurane in Lightly Anesthetized Cats

Author(s):  
Luc Teppema ◽  
Elise Sarton ◽  
Albert Dahan ◽  
Kees Olievier
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bartłomiej Paleczny ◽  
Rafał Seredyński ◽  
Małgorzata Wyciszkiewicz ◽  
Adrianna Nowicka-Czudak ◽  
Wojciech Łopusiewicz ◽  
...  

AbstractThe aim of this study was to test the utility of haemodynamic and autonomic variables (e.g. peripheral chemoreflex sensitivity [PCheS], blood pressure variability [BPV]) for the prediction of individual performance (marathon time and VO2max) in older men. The post-competition vasodilation and sympathetic vasomotor tone predict the marathon performance in younger men, but their prognostic relevance in older men remains unknown. The peripheral chemoreflex restrains exercise-induced vasodilation via sympathetically-mediated mechanism, what makes it a plausible candidate for the individual performance marker. 23 men aged ≥ 50 year competing in the Wroclaw Marathon underwent an evaluation of: resting haemodynamic parameters, PCheS with two methods: transient hypoxia and breath-holding test (BHT), cardiac barosensitivity, heart rate variability (HRV) and BPV, plasma renin and aldosterone, VO2max in a cardiopulmonary exercise test (CPET). All tests were conducted twice: before and after the race, except for transient hypoxia and CPET which were performed once, before the race. Fast marathon performance and high VO2max were correlated with: low ventilatory responsiveness to hypoxia (r =  − 0.53, r = 0.67, respectively) and pre-race BHT (r =  − 0.47, r = 0.51, respectively), (1) greater SD of beat-to-beat SBP (all p < 0.05). Fast performance was related with an enhanced pre-race vascular response to BHT (r =  − 0.59, p = 0.005). The variables found by other studies to predict the marathon performance in younger men: post-competition vasodilation, sympathetic vasomotor tone (LF-BPV) and HRV were not associated with the individual performance in our population. The results suggest that PCheS (ventilatory response) predicts individual performance (marathon time and VO2max) in men aged ≥ 50 yeat. Although cause-effect relationship including the role of peripheral chemoreceptors in restraining the post-competition vasodilation via the sympathetic vasoconstrictor outflow may be hypothesized to underline these findings, the lack of correlation between individual performance and both, the post-competition vasodilation and the sympathetic vasomotor tone argues against such explanation. Vascular responsiveness to breath-holding appears to be of certain value for predicting individual performance in this population, however.


2020 ◽  
Vol 598 (20) ◽  
pp. 4523-4536 ◽  
Author(s):  
Christopher A. Lear ◽  
Michi Kasai ◽  
Lindsea C. Booth ◽  
Paul P. Drury ◽  
Joanne O. Davidson ◽  
...  

Author(s):  
Marcelle Paula-Ribeiro ◽  
Indyanara C. Ribeiro ◽  
Liliane C. Aranda ◽  
Talita M. Silva ◽  
Camila M. Costa ◽  
...  

The baroreflex integrity in early-stage pulmonary arterial hypertension (PAH) remains uninvestigated. A potential baroreflex impairment could be functionally relevant and possibly mediated by enhanced peripheral chemoreflex activity. Thus, we investigated 1) the cardiac baroreflex in non-hypoxemic PAH; 2) the association between baroreflex indexes and peak aerobic capacity (i.e., V̇O2peak); and 3) the peripheral chemoreflex contribution to the cardiac baroreflex. Nineteen patients and 13 age- and sex-matched healthy adults (HA) randomly inhaled either 100% O2 (peripheral chemoreceptors inhibition) or 21% O2 (control session), while at rest and during a repeated sit-to-stand maneuver. Beat-by-beat analysis of R-R intervals and systolic blood pressure provided indexes of cardiac baroreflex sensitivity (cBRS) and effectiveness (cBEI). The PAH group had lower cBEIALL at rest (mean ± SD: PAH = 0.5 ± 0.2 vs HA = 0.7 ± 0.1 a.u., P = 0.02) and lower cBRSALL (PAH = 6.8 ± 7.0 vs HA = 9.7 ± 5.0 ms mmHg-1, P < 0.01) and cBEIALL (PAH = 0.4 ± 0.2 vs HA= 0.6 ± 0.1 a.u., P < 0.01) during the sit-to-stand maneuver versus the HA group. The cBEI during the sit-to-stand maneuver was independently correlated to V̇O2peak (partial r = 0.45, P < 0.01). Hyperoxia increased cBRS and cBEI similarly in both groups at rest and during the sit-to-stand maneuver. Therefore, cardiac baroreflex dysfunction was observed under spontaneous and, most notably, provoked blood pressure fluctuations in non-hypoxemic PAH, was not influenced by the peripheral chemoreflex, and was associated with lower V̇O2peak suggesting it could be functionally relevant.


Author(s):  
W.-X. Huang ◽  
S. Lahiri ◽  
C. Di Giulio ◽  
A. Mokashi ◽  
A. K. Sherpa ◽  
...  

2010 ◽  
Vol 1351 ◽  
pp. 141-149 ◽  
Author(s):  
Fabíola C. Nunes ◽  
Thaís P. Ribeiro ◽  
Maria S. França-Silva ◽  
Isac A. Medeiros ◽  
Valdir A. Braga

2003 ◽  
Vol 9 (5) ◽  
pp. 380-383 ◽  
Author(s):  
Sonia Velez-Roa ◽  
Philippe van de Borne ◽  
Virend K Somers

2008 ◽  
Vol 105 (1) ◽  
pp. 14-23 ◽  
Author(s):  
Yanfeng Ding ◽  
Yu-Long Li ◽  
Harold D. Schultz

Peripheral chemoreflex sensitivity is potentiated in clinical and experimental chronic heart failure (CHF). Downregulation of nitric oxide (NO) synthase (NOS) in the carotid body (CB) is involved in this effect. However, it remains poorly understood whether carbon monoxide (CO) also contributes to the altered peripheral chemoreflex sensitivity in CHF. This work highlights the effect of NO and CO on renal sympathetic nerve activity (RSNA) in response to graded hypoxia in conscious rabbits. Renal sympathetic nerve responses to graded hypoxia were enhanced in CHF rabbits compared with sham rabbits. The NO donor S-nitroso- N-acetylpenicillamine (SNAP, 1.2 μg·kg−1·min−1) and the CO-releasing molecule tricarbonyldichlororuthenium (II) dimer {[Ru(CO)3Cl2]2, 3.0 μg·kg−1·min−1} each attenuated hypoxia-induced RSNA increases in CHF rabbits ( P < 0.05), but the degree of attenuation of RSNA induced by SNAP or [Ru(CO)3Cl2]2 was smaller than that induced by SNAP + [Ru(CO)3Cl2]2. Conversely, treatment with the NOS inhibitor Nω-nitro-l-arginine (30 mg/kg) + the heme oxygenase (HO) inhibitor Cr (III) mesoporphyrin IX chloride (0.5 mg/kg) augmented the renal sympathetic nerve response to hypoxia in sham rabbits to a greater extent than treatment with either inhibitor alone and was without effect in CHF rabbits. In addition, using immunostaining and Western blot analyses, we found that expression of neuronal NOS, endothelial NOS, and HO-2 protein (expressed as the ratio of NOS or HO-2 expression to β-tubulin protein expression) was lower in CBs from CHF (0.19 ± 0.04, 0.17 ± 0.06, and 0.15 ± 0.02, respectively) than sham (0.63 ± 0.04, 0.56 ± 0.06, and 0.27 ± 0.03, respectively) rabbits ( P < 0.05). These results suggest that a deficiency of NO and CO in the CBs augments peripheral chemoreflex sensitivity to hypoxia in CHF.


2014 ◽  
pp. n/a-n/a ◽  
Author(s):  
Piotr Niewinski ◽  
Stanislaw Tubek ◽  
Waldemar Banasiak ◽  
Julian F.R. Paton ◽  
Piotr Ponikowski

2003 ◽  
Vol 81 (8) ◽  
pp. 765-773 ◽  
Author(s):  
James Duffin ◽  
Safraaz Mahamed

Exposure to hypoxia, whether for short or prolonged periods or for repeated episodes, produces alterations in the ventilatory responses. This review presents evidence that these adaptations are likely to be mediated by adaptations in the respiratory chemoreflexes, particularly the peripheral chemoreflex, and proposes models of respiratory control explaining the observed changes in ventilation. After a brief introduction to the respiratory control system, a graphical model is developed that illustrates the operation of the system in the steady state, which will be used later. Next, the adaptations in ventilatory responses to hypoxia that have been observed are described, and methods of measuring the alterations in the chemoreflexes that might account for them are discussed. Finally, experimental data supporting the view that changes in the activity of the peripheral chemoreflex can account for the ventilatory adaptations to hypoxia are presented and incorporated into models of chemoreflex behaviour during exposures to hypoxia of various durations.Key words: respiration, chemoreflexes, hypoxia, adaptation, models.


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