Carotid body chemosensitivity is not attenuated during cold water diving

2021 ◽  
Author(s):  
Hayden W. Hess ◽  
David Hostler ◽  
Brian M. Clemency ◽  
Erika St. James ◽  
Blair D. Johnson
Keyword(s):  
Cold Stress ◽  
Carotid Body ◽  
Cold Water ◽  
Ventilatory Response ◽  
Water Immersion ◽  
Hypoxic Ventilatory Response ◽  
Hyperbaric Chamber ◽  
Time Points ◽  
Hypercapnic Ventilatory Response ◽  
End Tidal

Introduction: Tonic carotid body (CB) activity is reduced during exposure to cold and hyperoxia. We tested the hypotheses that cold water diving lowers CB chemosensitivity and augments CO2 retention more than thermoneutral diving. Methods: Thirteen subjects (age: 26±4 y; BMI: 26±2 kg/m2) completed two, four-hour head out water immersion protocols in a hyperbaric chamber (1.6 ATA) in cold (15°C) and thermoneutral (25°C) water. CB chemosensitivity was assessed using brief hypercapnic ventilatory response (CBCO2) and hypoxic ventilatory response (CBO2) tests pre-dive, 80 and 160 min into the dives (D80 and D160, respectively), immediately following and 60 min post-dive. Data are reported as an absolute mean (SD) change from pre-dive. Results: End-tidal CO2 pressure increased during both the thermoneutral water dive (D160: +2(3) mmHg; p=0.02) and cold water dive (D160: +1(2) mmHg; p=0.03). Ventilationincreased during the cold water dive (D80: 4.13(4.38) and D160: 7.75(5.23) L·min-1; both p<0.01) and was greater than the thermoneutral water dive at both time points (both p<0.01). CBCO2 was unchanged during the dive (p=0.24) and was not different between conditions (p=0.23). CBO2 decreased during the thermonutral water dive (D80: -3.45(3.61) and D160: -2.76(4.04) L·min·mmHg-1; p<0.01 and p=0.03, respectively), but not the cold water dive. However, CBO2 was not different between conditions (p=0.17). Conclusion: CB chemosensitivity was not attenuated during the cold stress diving condition and does not appear to contribute to changes in ventilation or CO2 retention.

Attenuated carotid body hypoxic sensitivity after prolonged hypoxic exposure

1991 ◽  
Vol 70 (2) ◽  
pp. 748-755 ◽  
Author(s):  
K. Tatsumi ◽  
C. K. Pickett ◽  
J. V. Weil
Keyword(s):  
Carotid Body ◽  
Prolonged Exposure ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Exposure ◽  
Control Group ◽  
Hypoxic Ventilatory Response ◽  
End Tidal ◽  
Awake Cats ◽  
Body Response

Prolonged exposure to hypoxia is accompanied by decreased hypoxic ventilatory response (HVR), but the relative importance of peripheral and central mechanisms of this hypoxic desensitization remain unclear. To determine whether the hypoxic sensitivity of peripheral chemoreceptors decreases during chronic hypoxia, we measured ventilatory and carotid sinus nerve (CSN) responses to isocapnic hypoxia in five cats exposed to simulated altitude of 5,500 m (barometric pressure 375 Torr) for 3-4 wk. Exposure to 3-4 wk of hypobaric hypoxia produced a decrease in HVR, measured as the shape parameter A in cats both awake (from 53.9 +/- 10.1 to 14.8 +/- 1.8; P less than 0.05) and anesthetized (from 50.2 +/- 8.2 to 8.5 +/- 1.8; P less than 0.05). Sustained hypoxic exposure decreased end-tidal CO2 tension (PETCO2, 33.3 +/- 1.2 to 28.1 +/- 1.3 Torr) during room-air breathing in awake cats. To determine whether hypocapnia contributed to the observed depression in HVR, we also measured eucapnic HVR (PETCO2 33.3 +/- 0.9 Torr) and found that HVR after hypoxic exposure remained lower than preexposed value (A = 17.4 +/- 4.2 vs. 53.9 +/- 10.1 in awake cats; P less than 0.05). A control group (n = 5) was selected for hypoxic ventilatory response matched to the baseline measurements of the experimental group. The decreased HVR after hypoxic exposure was associated with a parallel decrease in the carotid body response to hypoxia (A = 20.6 +/- 4.8) compared with that of control cats (A = 46.9 +/- 6.3; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of pregnancy on ventilatory and carotid body neural output responsiveness to hypoxia in cats

1989 ◽  
Vol 67 (2) ◽  
pp. 797-803 ◽  
Author(s):  
B. Hannhart ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
L. G. Moore
Keyword(s):  
Carotid Body ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Air Ventilation ◽  
Near Term ◽  
End Tidal ◽  
Neural Influences ◽  
End Tidal Co2 ◽  
Ventilatory Response To Hypoxia

Pregnancy increases ventilation and ventilatory sensitivity to hypoxia and hypercapnia. To determine the role of the carotid body in the increased hypoxic ventilatory response, we measured ventilation and carotid body neural output (CBNO) during progressive isocapnic hypoxia in 15 anesthetized near-term pregnant cats and 15 nonpregnant females. The pregnant compared with nonpregnant cats had greater room-air ventilation [1.48 +/- 0.24 vs. 0.45 +/- 0.05 (SE) l/min BTPS, P less than 0.01], O2 consumption (29 +/- 2 vs. 19 +/- 1 ml/min STPD, P less than 0.01), and lower end-tidal PCO2 (30 +/- 1 vs. 35 +/- 1 Torr, P less than 0.01). Lower end-tidal CO2 tensions were also observed in seven awake pregnant compared with seven awake nonpregnant cats (28 +/- 1 vs. 31 +/- 1 Torr, P less than 0.05). The ventilatory response to hypoxia as measured by the shape of parameter A was twofold greater (38 +/- 5 vs. 17 +/- 3, P less than 0.01) in the anesthetized pregnant compared with nonpregnant cats, and the CBNO response to hypoxia was also increased twofold (58 +/- 11 vs. 29 +/- 5, P less than 0.05). The increased CBNO response to hypoxia in the pregnant compared with the nonpregnant cats persisted after cutting the carotid sinus nerve while recording from the distal end, indicating that the increased hypoxic sensitivity was not due to descending central neural influences. We concluded that greater carotid body sensitivity to hypoxia contributed to the increased hypoxic ventilatory responsiveness observed in pregnant cats.

Ventilatory responses to hypercapnia and hypoxia during continuous aspirin ingestion

1977 ◽  
Vol 43 (6) ◽  
pp. 971-976 ◽  
Author(s):  
D. J. Riley ◽  
B. A. Legawiec ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Carbon Dioxide Tension ◽  
Base Line ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Responses ◽  
Hypercapnic Ventilatory Response ◽  
The Central Nervous System ◽  
End Tidal

Hypercapnic and hypoxic ventilatory responses were serially measured in nine normal subjects given 3.9 g aspirin (ASA) per day for 9 days. Minute ventilation (VE), end-tidal carbon dioxide tension (PETCO2), venous bicarbonate concentration [HCO3-], oxygen consumption (VO2), hypercapnic ventilatory response (deltaVE/deltaPCO2), and isocapnic hypoxic ventilatory response (A) were determined before, 2 h after the first dose, and at 72-h intervals during the next 14 days. Serum salicylate levels averaged 18.6 +/- 2.0 mg/dl. VE increased (P less than 0.05, PETCO2 decreased (P less than 0.05), and [HCO3-] did not change significantly during drug ingestion. deltaVE/deltaPCO2 increased gradually to a value 37% greater than control by day 3 and remained constant (P less 0.01). A increased by 251% and VO2 by 18% within 2 h and remained constant for the remainder of the ASA period (P less than 0.01). All values returned to base line within 24 h following cessation of ASA. We conclude that during continuous ASA ingestion there is a gradual increase of hypercapnic ventilatory response. This may reflect slow entrance of ASA into the central nervous system. In contrast, there is a rapid rise in hypoxic ventilatory response which may be mechanically linked to changes in metabolic rate.

Effect of hypercapnia on hypoxic ventilatory drive in carotid body-resected man

1978 ◽  
Vol 45 (6) ◽  
pp. 971-977 ◽  
Author(s):  
George D. Swanson ◽  
Brian J. Whipp ◽  
Robert D. Kaufman ◽  
Kamel A. Aqleh ◽  
Benjamin Winter ◽  
...  
Keyword(s):  
Carotid Body ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Hypoxic Ventilatory Response ◽  
Small Component ◽  
Ventilatory Drive ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Hypoxia

Steplike end-tidal hypoxic drives (Petcoco2, = 53 Torr) lasting for 5 min were generated in a group of normal subjects and a group of carotid body-resected subjects when end-tidal CO2, was maintained constant under eucapnic (Petcoco2 = 39 Torr) and hypercapnic (Petcoco2 = 49 Torr) conditions. The hypoxic ventilatory response of the normal subjects was prompt and significant in eucapnia and was enhanced in the hypercapnic state, evidencing CO2-O2 interaction. In contrast, the carotid body-resected subjects did not respond to eucapnic hypoxia but did demonstrate a small but significant ventilatory response to hypoxia against the hypercapnic background. This suggests that the aortic bodies in man may contribute a small component of the hypoxic ventilatory drive under hypercapnic conditions, although the possibility of neuromalike ending regeneration cannot be excluded.

The relationship of deep and surface skin temperatures to the ventilatory responses elicited during cold water immersion

1978 ◽  
Vol 56 (6) ◽  
pp. 999-1004 ◽  
Author(s):  
Sheilagh Martin ◽  
K. E. Cooper
Keyword(s):  
Skin Temperature ◽  
Cold Water ◽  
Ventilatory Response ◽  
Water Immersion ◽  
Cold Water Immersion ◽  
Rate Of Change ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Relationship Of ◽  
Skin Temperatures

Subjects were immersed for 10 min in water at 14.5 °C, after exposure either to ambient temperature or sauna heating. During the immersions, total ventilation, end-tidal [Formula: see text], the mean of three surface skin temperatures, and deep skin temperatures were measured. There was a statistically significant correlation between the rate of change of deep skin temperature and the initial ventilatory responses evoked during both cold water immersions. After the sauna heating and cold water exposure, the temperature gradient through the skin appeared to be related to the ventilatory response. There was no significant correlation between the rate of change of mean surface skin temperature and the ventilatory response. The results suggest that the primary drive to increased ventilation during cold water immersion is the rate of change of deep skin temperature.

Living high-training low increases hypoxic ventilatory response of well-trained endurance athletes

2002 ◽  
Vol 93 (4) ◽  
pp. 1498-1505 ◽  
Author(s):  
Nathan E. Townsend ◽  
Christopher J. Gore ◽  
Allan G. Hahn ◽  
Michael J. McKenna ◽  
Robert J. Aughey ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Endurance Athletes ◽  
Hypoxic Exposure ◽  
Dependent Manner ◽  
Hypoxic Ventilatory Response ◽  
Ambient Conditions ◽  
Altitude Exposure ◽  
End Tidal

This study determined whether “living high-training low” (LHTL)-simulated altitude exposure increased the hypoxic ventilatory response (HVR) in well-trained endurance athletes. Thirty-three cyclists/triathletes were divided into three groups: 20 consecutive nights of hypoxic exposure (LHTLc, n = 12), 20 nights of intermittent hypoxic exposure (four 5-night blocks of hypoxia, each interspersed with 2 nights of normoxia, LHTLi, n = 10), or control (Con, n = 11). LHTLc and LHTLi slept 8–10 h/day overnight in normobaric hypoxia (∼2,650 m); Con slept under ambient conditions (600 m). Resting, isocapnic HVR (ΔV˙e/ΔSpO2 , whereV˙e is minute ventilation and SpO2 is blood O2 saturation) was measured in normoxia before hypoxia (Pre), after 1, 3, 10, and 15 nights of exposure (N1, N3, N10, and N15, respectively), and 2 nights after the exposure night 20 (Post). Before each HVR test, end-tidal Pco 2(Pet CO2 ) and V˙e were measured during room air breathing at rest. HVR (l · min−1 · %−1) was higher ( P < 0.05) in LHTLc than in Con at N1 (0.56 ± 0.32 vs. 0.28 ± 0.16), N3 (0.69 ± 0.30 vs. 0.36 ± 0.24), N10 (0.79 ± 0.36 vs. 0.34 ± 0.14), N15 (1.00 ± 0.38 vs. 0.36 ± 0.23), and Post (0.79 ± 0.37 vs. 0.36 ± 0.26). HVR at N15 was higher ( P < 0.05) in LHTLi (0.67 ± 0.33) than in Con and in LHTLc than in LHTLi. Pet CO2 was depressed in LHTLc and LHTLi compared with Con at all points after hypoxia ( P < 0.05). No significant differences were observed for V˙e at any point. We conclude that LHTL increases HVR in endurance athletes in a time-dependent manner and decreases Pet CO2 in normoxia, without change inV˙e. Thus endurance athletes sleeping in mild hypoxia may experience changes to the respiratory control system.

scholarly journals Lethal avian influenza A (H5N1) virus replicates in pontomedullary chemosensitive neurons and depresses hypercapnic ventilatory response in mice

2019 ◽  
Vol 316 (3) ◽  
pp. L525-L536 ◽  
Author(s):  
Jianguo Zhuang ◽  
Na Zang ◽  
Chunyan Ye ◽  
Fadi Xu
Keyword(s):  
Viral Infection ◽  
Carotid Body ◽  
Influenza A ◽  
Tryptophan Hydroxylase ◽  
Ventilatory Response ◽  
Severe Depression ◽  
Infection Period ◽  
Hypercapnic Ventilatory Response ◽  
H5n1 Influenza ◽  
Neurokinin 1

The highly pathogenic H5N1 (HK483) viral infection causes a depressed hypercapnic ventilatory response (dHCVR, 20%↓) at 2 days postinfection (dpi) and death at 7 dpi in mice, but the relevant mechanisms are not fully understood. Glomus cells in the carotid body and catecholaminergic neurons in locus coeruleus (LC), neurokinin 1 receptor (NK1R)-expressing neurons in the retrotrapezoid nucleus (RTN), and serotonergic neurons in the raphe are chemosensitive and responsible for HCVR. We asked whether the dHCVR became worse over the infection period with viral replication in these cells/neurons. Mice intranasally inoculated with saline or the HK483 virus were exposed to hypercapnia for 5 min at 0, 2, 4, or 6 dpi, followed by immunohistochemistry to determine the expression of nucleoprotein of H5N1 influenza A (NP) alone and coupled with 1) tyrosine hydroxylase (TH) in the carotid body and LC, 2) NK1R in the RTN, and 3) tryptophan hydroxylase (TPH) in the raphe. HK483 viral infection blunted HCVR by ∼20, 50, and 65% at 2, 4, and 6 dpi. The NP was observed in the pontomedullary respiratory-related nuclei (but not in the carotid body) at 4 and 6 dpi, especially in 20% of RTN NK1R, 35% of LC TH, and ∼10% raphe TPH neurons. The infection significantly reduced the local NK1R or TPH immunoreactivity and population of neurons expressing NK1R or TPH. We conclude that the HK483 virus infects the pontomedullary respiratory nuclei, particularly chemosensitive neurons in the RTN, LC, and raphe, contributing to the severe depression of HCVR and respiratory failure at 6 dpi.

64 HYPOXIC VENTILATORY RESPONSE IN EARLY LUNG INJURY IS AUGMENTED BY OXYGEN-INDEPENDENT SENSITIZATION OF THE CAROTID BODY.

2006 ◽  
Vol 54 (2) ◽  
pp. S354.2-S354
Author(s):  
F. J. Jacono ◽  
Y. Peng ◽  
D. Nethery ◽  
J. A. Faress ◽  
J. A. Kern ◽  
...  
Keyword(s):  
Lung Injury ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of intravenous dopamine on hypercapnic ventilatory response in humans

1983 ◽  
Vol 55 (5) ◽  
pp. 1418-1425 ◽  
Author(s):  
D. S. Ward ◽  
J. W. Bellville
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Carbon Dioxide Concentration ◽  
Carbon Dioxide Tension ◽  
Model Parameters ◽  
Loop Gain ◽  
Loop Contribution ◽  
Dopamine Infusion ◽  
Hypercapnic Ventilatory Response ◽  
End Tidal

This study assessed the effect of low-dose intravenous dopamine (3 micrograms X kg-1 X min-1) on the hypercapnic ventilatory response in humans. Six normal healthy subjects were studied. By manipulating the inspired carbon dioxide concentration, the end-tidal carbon dioxide tension was raised in a stepwise fashion from 41 to 49 Torr and held at this level for 4 min. The end-tidal CO2 tension was then lowered back to 41 Torr in a stepwise fashion. The end-tidal O2 tension was held constant at 106 Torr throughout the experiment. The ventilatory response to this normoxic hypercapnic stimulus was analyzed by fitting two exponential functions, allowing the response to be separated into slow and fast chemoreflex loops. Each loop is described by a gain, time constant, and time delay. A single eupneic threshold was used for both loops. Nine control experiments and eight experiments performed during dopamine infusion were analyzed. The dopamine infusion caused the fast loop gain to be significantly (P less than 0.05) reduced from 0.64 to 0.19 l X min-1 X Torr-1, while the slow loop gain was unchanged. The fast loop contribution was reduced from 28 to 11% of the total ventilatory response. None of the other model parameters were significantly affected by the dopamine infusion. Exogenously administered dopamine substantially reduces the sensitivity of the fast chemoreflex loop to carbon dioxide.

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