scholarly journals (336) Ventilator Hypercapnic Response (VHR) methodology

2017 ◽  
Vol 18 (4) ◽  
pp. S59
Author(s):  
L. Webster ◽  
R. Grunspan
Keyword(s):  
Hypercapnic Response

Computer simulation of experiments in responses to intravenous and inhaled CO2

1981 ◽  
Vol 50 (4) ◽  
pp. 835-843 ◽  
Author(s):  
W. S. Yamamoto
Keyword(s):  
Venous Return ◽  
Neural Signal ◽  
Set Point ◽  
Ventilatory Responses ◽  
Operating Level ◽  
Excitatory State ◽  
Co2 Level ◽  
Neural Excitation ◽  
Low Levels ◽  
Hypercapnic Response

A simulation of ventilatory responses to infused and inhaled CO2 at controlled cardiac output and high and low levels of neural excitation mimics comparable experiments in animals. The model suggests that at low levels of endogenous and exogenous CO2 load the alert quiescent animal will show hyperpnea to both test states associated with hypercapnia. The nonalert quiescent animal simulated will show an isocapnic response to endogenous load and hypercapnic response to exogenous load. The explanation of this behavior lies in the model formulation, which allows the neural signal from metabolically active sources to drive the proportional component of the controller below an operating level established by its set point. By this reasoning the excited but metabolically inactive animal should be paradoxically less sensitive to small changes in CO2, whether exogenous or endogenous, than the quiescent animal. The model demonstrates further that a neural "exercise" signal in proportion to venous return better simulates observations in which CO2 load and venous return are dissociated than one in which the neural signal is computed from metabolism. The use of delta V/delta P slopes as estimates of sensitivity go awry in experiment and simulation when blood flow, CO2 level, and neural excitatory state are dissociated. This is particularly true when the organism is operating at and below the hypothesized set point.

scholarly journals Volatile Anaesthetic Depression of the Carotid Body Chemoreflex-Mediated Ventilatory Response to Hypoxia: Directions for Future Research

Scientifica ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
J. J. Pandit
Keyword(s):  
Quantitative Analysis ◽  
Carotid Body ◽  
Meta Analysis ◽  
Future Research ◽  
Inclusion Criteria ◽  
Molecular Processes ◽  
Similar Dose ◽  
Hypercapnic Response ◽  
Ventilatory Response To Hypoxia ◽  
Body Response

In assessing whether volatile anaesthetics directly depress the carotid body response to hypoxia it is necessary to combine in meta-analysis studies of when it is “functionally isolated” (e.g., recordings are made from its afferent nerve). Key articles were retrieved (full papers in English) and subjected to quantitative analysis to yield an aggregate estimate of effect. Results from articles that did not use such methodology were assessed separately from this quantitative approach, to see what could be learned also from a nonquantitative overview. Just 7 articles met the inclusion criteria for hypoxia and just 6 articles for hypercapnia. Within these articles, the anaesthetic (mean dose 0.75, standard deviation (SD) 0.40 minimum alveolar concentration, MAC) statistically significantly depressed carotid body hypoxic response by 24% (P=0.041), but a similar dose (mean 0.81 (0.42) MAC) did not affect the hypercapnic response. The articles not included in the quantitative analysis (31 articles), assessed qualitatively, also indicated that anaesthetics depress carotid body function. This conclusion helps direct future research on the anaesthetic effects on putative cellular/molecular processes that underlie the transduction of hypoxia in the carotid body.

scholarly journals Consequences of a Maternal Vitamin B6 Deficiency on Hypercapnic Response in Rat Pups

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Jessica Lynn St. Laurent ◽  
Kimberly Iceman ◽  
Michael Bruce Harris
Keyword(s):  
Vitamin B6 ◽  
Maternal Vitamin ◽  
Rat Pups ◽  
Vitamin B6 Deficiency ◽  
Hypercapnic Response

Permissive and obligatory roles of NO in cerebrovascular responses to hypercapnia and acetylcholine

1996 ◽  
Vol 271 (4) ◽  
pp. R990-R1001 ◽  
Author(s):  
C. Iadecola ◽  
F. Zhang
Keyword(s):  
Basal Forebrain ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Doppler Flowmetry ◽  
No Donors ◽  
Nos Inhibitors ◽  
Fusion Site ◽  
Nos Inhibitor ◽  
Hypercapnic Response ◽  
Major Mediator

Inhibition of nitric oxide (NO) synthesis attenuates the hypercapnic cerebrovasodilation or the increases in cerebral blood flow (CBF) produced by acetylcholine (ACh), either topically applied or endogenously released in neocortex by stimulation of the basal forebrain cholinergic system. We investigated whether exogenous administration of NO, using NO donors, can reverse the attenuation of these responses by NO synthase (NOS) inhibitors. In halothane-anesthetized, ventilated rats the frontoparietal cortex was exposed and superfused with Ringer. CBF was monitored at the super fusion site by laser-Doppler flowmetry. The basal forebrain was stimulated (100 microA; 50 Hz) with microelectrodes stereotaxically implanted. Superfusion with the NOS inhibitor NG-nitro-L-arginine (L-NNA; 1 mM) reduced resting CBF (-38 +/- 2%; mean +/- SE) and attenuated the vasodilation elicited by hypercapnia (Pco2, 50-60 mmHg; -79 +/- 3%), ACh (10 microM; -83 +/- 7%), or basal forebrain stimulation (-44 +/- 2%) (P < 0.05, analysis of variance and Tukey's test). After L-NNA, topical application of 3-morpholinosydnonimine (SIN-1) (n = 7), S-nitroso-N-acetylpenicillamine (SNAP) (n = 6), or 8-bromoguanosine 3',5'-monophosphate (8-BrcGMP, n = 4) reestablished resting CBF (P > 0.05 from Ringer) and reversed the attenuation of the response to hypercapnia (P > 0.05 from Ringer). However, SIN-1 or SNAP failed to reverse the attenuation of the response to basal forebrain stimulation or topical ACh (P > 0.05 from L-NNA). After L-NNA, the NO-independent vasodilator papaverine (n = 4) reestablished resting CBF (P > 0.05 from Ringer) but failed to restore the hypercapnic vasodilation (P > 0.05 from L-NNA). The attenuation of hypercapnic response by the neuronal NOS inhibitor 7-nitroindazole was counteracted only partially by SIN-1 (n = 4) or 8-BrcGMP (n = 4). The data support the hypothesis that the vasodilation elicited by hypercapnia requires resting levels of NO for its expression, whereas the response to endogenous or exogenous ACh depends on agonist-induced NOS activation. In hypercapnia NO may act as a permissive factor by facilitating the action of other vasodilators, whereas in the vascular response initiated by ACh NO is likely to be the major mediator of smooth muscle relaxation.

scholarly journals Evidence from high-altitude acclimatization for an integrated cerebrovascular and ventilatory hypercapnic response but different responses to hypoxia

2017 ◽  
Vol 123 (6) ◽  
pp. 1477-1486 ◽  
Author(s):  
Zachary M. Smith ◽  
Erin Krizay ◽  
Rui Carlos Sá ◽  
Ethan T. Li ◽  
Miriam Scadeng ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Control Mechanism ◽  
Integrated Control ◽  
Acute Hypoxia ◽  
Absolute Value ◽  
Ventilatory Responses ◽  
Two Systems ◽  
Hypercapnic Response ◽  
Sustained Hypoxia

Ventilation and cerebral blood flow (CBF) are both sensitive to hypoxia and hypercapnia. To compare chemosensitivity in these two systems, we made simultaneous measurements of ventilatory and cerebrovascular responses to hypoxia and hypercapnia in 35 normal human subjects before and after acclimatization to hypoxia. Ventilation and CBF were measured during stepwise changes in isocapnic hypoxia and iso-oxic hypercapnia. We used MRI to quantify actual cerebral perfusion. Measurements were repeated after 2 days of acclimatization to hypoxia at 3,800 m altitude (partial pressure of inspired O2 = 90 Torr) to compare plasticity in the chemosensitivity of these two systems. Potential effects of hypoxic and hypercapnic responses on acute mountain sickness (AMS) were assessed also. The pattern of CBF and ventilatory responses to hypercapnia were almost identical. CO2 responses were augmented to a similar degree in both systems by concomitant acute hypoxia or acclimatization to sustained hypoxia. Conversely, the pattern of CBF and ventilatory responses to hypoxia were markedly different. Ventilation showed the well-known increase with acute hypoxia and a progressive decline in absolute value over 25 min of sustained hypoxia. With acclimatization to hypoxia for 2 days, the absolute values of ventilation and O2 sensitivity increased. By contrast, O2 sensitivity of CBF or its absolute value did not change during sustained hypoxia for up to 2 days. The results suggest a common or integrated control mechanism for CBF and ventilation by CO2 but different mechanisms of O2 sensitivity and plasticity between the systems. Ventilatory and cerebrovascular responses were the same for all subjects irrespective of AMS symptoms. NEW & NOTEWORTHY Ventilatory and cerebrovascular hypercapnic response patterns show similar plasticity in CO2 sensitivity following hypoxic acclimatization, suggesting an integrated control mechanism. Conversely, ventilatory and cerebrovascular hypoxic responses differ. Ventilation initially increases but adapts with prolonged hypoxia (hypoxic ventilatory decline), and ventilatory sensitivity increases following acclimatization. In contrast, cerebral blood flow hypoxic sensitivity remains constant over a range of hypoxic stimuli, with no cerebrovascular acclimatization to sustained hypoxia, suggesting different mechanisms for O2 sensitivity in the two systems.

Somatostatin inhibits the ventilatory response to hypoxia in humans

1986 ◽  
Vol 60 (3) ◽  
pp. 997-1002 ◽  
Author(s):  
D. L. Maxwell ◽  
P. Chahal ◽  
K. B. Nolop ◽  
J. M. Hughes
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Open Circuit ◽  
Co2 Production ◽  
Adult Males ◽  
Hypoxic Response ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Hypercapnic Response ◽  
Ventilatory Response To Hypoxia

The effects of a 90-min infusion of somatostatin (1 mg/h) on ventilation and the ventilatory responses to hypoxia and hypercapnia were studied in six normal adult males. Minute ventilation (VE) was measured with inductance plethysmography, arterial 02 saturation (SaO2) was measured with ear oximetry, and arterial PCO2 (Paco2) was estimated with a transcutaneous CO2 electrode. The steady-state ventilatory response to hypoxia (delta VE/delta SaO2) was measured in subjects breathing 10.5% O2 in an open circuit while isocapnia was maintained by the addition of CO2. The hypercapnic response (delta VE/delta PaCO2) was measured in subjects breathing first 5% and then 7.5% CO2 (in 52–55% O2). Somatostatin greatly attenuated the hypoxic response (control mean -790 ml x min-1.%SaO2 -1, somatostatin mean -120 ml x min-1.%SaO2 -1; P less than 0.01), caused a small fall in resting ventilation (mean % fall - 11%), but did not affect the hypercapnic response. In three of the subjects progressive ventilatory responses (using rebreathing techniques, dry gas meter, and end-tidal Pco2 analysis) and overall metabolism were measured. Somatostatin caused similar changes (mean fall in hypoxic response -73%; no change in hypercapnic response) and did not alter overall O2 consumption nor CO2 production. These results show an hitherto-unsuspected inhibitory potential of this neuropeptide on the control of breathing; the sparing of the hypercapnic response is suggestive of an action on the carotid body but does not exclude a central effect.

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